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  1. Pulmonary edema

    MedlinePlus

    ... congestion; Lung water; Pulmonary congestion; Heart failure - pulmonary edema ... Pulmonary edema is often caused by congestive heart failure . When the heart is not able to pump efficiently, blood ...

  2. Pulmonary edema of scuba divers.

    PubMed

    Hampson, N B; Dunford, R G

    1997-01-01

    A syndrome of acute pulmonary edema has been previously reported among scuba divers in cold, European waters. Because of the temperatures involved, the name "cold-induced pulmonary edema" was coined in the original 1989 description. We report six individuals who developed the identical syndrome, five while diving in Puget Sound and one in the Gulf of Mexico. The four women and two men ranged in age from 24 to 60 yr. They experienced one to six episodes apiece, each with the development severe dyspnea at depth without excessive exertion. Associated symptoms included cough, weakness, expectoration of froth, chest discomfort, orthopnea, wheezing, hemoptysis, and dizziness. Emergency medical evaluation of four divers revealed rales on examination and pulmonary edema on chest radiograph. In one diver with pulmonary edema on chest radiograph, pulmonary capillary wedge pressure was normal when measured acutely. Symptoms resolved either spontaneously over 1-2 days or with standard medial treatment for pulmonary edema. Prior history of cardiovascular disease was negative except for hypertension and mitral valve prolapse in one diver. Cardiac evaluations following recovery from the acute episodes were normal. Episodes in the cold waters of Puget Sound sometimes occurred despite the use of dry suits. Furthermore, one diver developed recurrent episodes in 27 degrees C water off Cozumel, Mexico. Development of pulmonary edema while scuba diving constitutes a distinct clinical entity which may occur in either "cold" or "warm" water. It is not associated with a decompression mechanism. Personnel caring for divers should be aware of the syndrome in order to provide optimal medical management.

  3. Unilateral pulmonary edema following acute subglottic edema.

    PubMed

    Morisaki, H; Ochiai, R; Takeda, J; Nagano, M

    1990-01-01

    Presented here is a case of unilateral pulmonary edema following acute subglottic edema after removal of an endotracheal tube. A 3-year-old boy, diagnosed as having nondiphtheric croup and pectus excavatum deformity, was scheduled for repair of a cleft lip. No complication occurred during the operation. After removal of the endotracheal tube, he showed dyspnea and cyanosis and was later found to have acute subglottic edema. After reintubation of the trachea, frothy pink fluid was discharged from the tube, and chest roentgenogram showed a right-sided alveolar infiltrate. Many factors may cause unilateral pulmonary edema, but it is suggested that acute subglottic edema and unilateral bronchial fragility strongly affected this episode.

  4. [Hyponatremic encephalopathy with non-cardiogenic pulmonary edema. Development following marathon run].

    PubMed

    Wellershoff, G

    2013-04-01

    This article presents the case of a 52-year-old woman who developed exercise-associated hyponatremia (EAH) complicated by non-cardiogenic pulmonary edema after a marathon run. The condition of EAH is a potentially life-threatening complication of endurance exercise. The main cause seems to be inadequate intake of free water during or following exercise with enduring antidiuresis due to nonosmotic stimulation of ADH secretion. Known risk factors are female gender, slow running pace and lack of weight loss. Emergency therapy is fluid restriction and bolus infusion of 3% NaCl solution to rapidly reduce brain edema. PMID:23381723

  5. The Curious Question of Exercise-Induced Pulmonary Edema

    PubMed Central

    Bates, Melissa L.; Farrell, Emily T.; Eldridge, Marlowe W.

    2011-01-01

    The question of whether pulmonary edema develops during exercise on land is controversial. Yet, the development of pulmonary edema during swimming and diving is well established. This paper addresses the current controversies that exist in the field of exercise-induced pulmonary edema on land and with water immersion. It also discusses the mechanisms by which pulmonary edema can develop during land exercise, swimming, and diving and the current gaps in knowledge that exist. Finally, this paper discusses how these fields can continue to advance and the areas where clinical knowledge is lacking. PMID:21660232

  6. Naloxone-induced pulmonary edema.

    PubMed

    Schwartz, J A; Koenigsberg, M D

    1987-11-01

    We present the case of a 68-year-old woman with acute pulmonary edema secondary to the administration of naloxone to reverse an inadvertent narcotic overdose. The patient presented following a 12-hour history of increasingly bizarre behavior and confusion. A total IV dose of 1.6 mg naloxone was administered in an attempt to reverse the suspected overconsumption of a codeine-containing cough suppressant. She immediately became agitated, tachycardic, and diaphoretic; a clinical diagnosis of acute pulmonary edema was made. Following treatment with furosemide, nitroglycerin, and morphine sulfate, the patient recovered completely without further incident. Although naloxone is thought to be a safe drug with few complications, it should not be used indiscriminantly, and the smallest doses necessary to elicit the desired response should be used. PMID:3662194

  7. Scuba diving-induced pulmonary edema in a swimming pool.

    PubMed

    Gnadinger, C A; Colwell, C B; Knaut, A L

    2001-11-01

    SCUBA diving-induced pulmonary edema is a rare syndrome that has been previously reported to occur in cold water. We present a case of SCUBA diving-induced pulmonary edema in a 52-year-old man diving in a warm swimming pool. The pathophysiology of this syndrome is unclear, but it is unrelated to either barotrauma or decompression illness. This patient developed frank pulmonary edema while submerged, which resolved after surfacing. As with other patients who have had this syndrome, he did not have any cardiorespiratory disease. The presentation and pathophysiology of SCUBA diving-induced pulmonary edema are discussed.

  8. [High-altitude pulmonary edema in Japan].

    PubMed

    Kobayashi, T

    1995-12-01

    To understand the pathophysiology of high-altitude pulmonary edema (HAPE), we examined the pathway of adaptation to high altitude in lifelong of Tibet. The Tibetan natives had higher exercise performance, but lower maximal oxygen uptake and lower blood lactate concentrations than did acclimatized Han newcomers. Clinical and basic studies done to determine the pathophysiologic characteristics of 47 patients with HAPE and of subjects susceptible to HAPE. The altitude of onset was 2,680 m to 3,190 m above sea level. Results of hemodynamic studies and the presence of protein-rich edema fluid indicated that HAPE is noncardiogenic and is a type of increased permeability edema. The levels of IL-1 beta, IL-6, IL-8, and TNF-alpha in bronchoalveolar lavage fluid from subjects with HAPE were high on admission. The subjects susceptible to HAPE had much greater increases in an index of pulmonary vascular resistance than did the controls, which resulted in much higher levels of pulmonary arterial pressure during both acute hypoxia and hypobaria. The subjects susceptible to HAPE also has blunted hypoxic ventilatory drives. We studied whether human leukocyte antigen DR-6 functions as a genetic predisposition to HAPE. The frequency of DR-6 was increased in the subjects susceptible to HAPE, which suggests that they have a constitutional abnormality in the pulmonary circulatory, and ventilatory responses to hypoxia and hypobaria, and that genetic factors may be involved in the development of HAPE.

  9. Reexpansion pulmonary edema in children

    PubMed Central

    Rodrigues, Antonio Lucas L.; Lopes, Carlos Eduardo; Romaneli, Mariana Tresoldi das N.; Fraga, Andrea de Melo A.; Pereira, Ricardo Mendes; Tresoldi, Antonia Teresinha

    2013-01-01

    OBJECTIVE To present a case of a patient with clinical and radiological features of reexpansion pulmonary edema, a rare and potentially fatal disease. CASE DESCRIPTION An 11-year-old boy presenting fever, clinical signs and radiological features of large pleural effusion initially treated as a parapneumonic process. Due to clinical deterioration he underwent tube thoracostomy, with evacuation of 3,000 mL of fluid; he shortly presented acute respiratory insufficiency and needed mechanical ventilation. He had an atypical evolution (extubated twice with no satisfactory response). Computerized tomography findings matched those of reexpansion edema. He recovered satisfactorily after intensive care, and pleural tuberculosis was diagnosed afterwards. COMMENTS Despite its rareness in the pediatric population (only five case reports gathered), the knowledge of this pathology and its prevention is very important, due to high mortality rates. It is recommended, among other measures, slow evacuation of the pleural effusion, not removing more than 1,500 mL of fluid at once. PMID:24142327

  10. [Cardiogenic and non cardiogenic pulmonary edema: pathomechanisms and causes].

    PubMed

    Glaus, T; Schellenberg, S; Lang, J

    2010-07-01

    The development of pulmonary edema is divided in cardiogenic and non-cardiogenic. Cardiogenic edema pathogenically is caused by elevated hydrostatic pressure in the pulmonary capillaries due to left sided congestive heart failure. Non-cardiogenic pulmonary edema is categorized depending on the underlying pathogenesis in low-alveolar pressure, elevated permeability or neurogenic edema. Some important examples of causes are upper airway obstruction like in laryngeal paralysis or strangulation for low alveolar pressure, leptospirosis and ARDS for elevated permeability, and epilepsy, brain trauma and electrocution for neurogenic edema. The differentiation between cardiogenic versus non-cardiogenic genesis is not always straightforward, but most relevant, because treatment markedly differs between the two. Of further importance is the identification of the specific underlying cause in non-cardiogenic edema, not only for therapeutic but particularly for prognostic reasons. Depending on the cause the prognosis ranges from very poor to good chance of complete recovery. PMID:20582896

  11. Acute pulmonary edema associated with naphazoline ingestion.

    PubMed

    Fukushima, Hidetada; Norimoto, Kazunobu; Seki, Tadahiko; Nishiguchi, Takashi; Nakamura, Tatsuya; Konobu, Toshifumi; Nishio, Kenji; Okuchi, Kazuo

    2008-03-01

    In published reports of naphazoline ingestion, clinical effects are hypertension, bradycardia, pallor, diaphoresis, and respiratory distress. We report three cases of acute pulmonary edema after the intentional ingestion of naphazoline-containing antiseptic first aid liquid. These cases presented with altered mental status, hypertension, bradycardia, and diaphoresis. Chest x-ray on admission revealed acute pulmonary edema. Two cases required mechanical ventilation. All of these clinical effects resolved within 24 hours and the patients were discharged with no sequelae. Since naphazoline stimulates the peripheral alpha-2 adrenergic receptor, we speculate that intense vasoconstriction may have elevated cardiac afterload and left atrial-ventricular blood volume and caused acute pulmonary edema.

  12. Synthetic smoke with acrolein but not HCl produces pulmonary edema

    SciTech Connect

    Hales, C.A.; Barkin, P.W.; Jung, W.; Trautman, E.; Lamborghini, D.; Herrig, N.; Burke, J.

    1988-03-01

    The chemical toxins in smoke and not the heat are responsible for the pulmonary edema of smoke inhalation. We developed a synthetic smoke composed of carbon particles (mean diameter of 4.3 microns) to which toxins known to be in smoke, such as HCl or acrolein, could be added one at a time. We delivered synthetic smoke to dogs for 10 min and monitored extravascular lung water (EVLW) accumulation thereafter with a double-indicator thermodilution technique. Final EVLW correlated highly with gravimetric values (r = 0.93, P less than 0.01). HCl in concentrations of 0.1-6 N when added to heated carbon (120 degrees C) and cooled to 39 degrees C produced airway damage but no pulmonary edema. Acrolein, in contrast, produced airway damage but also pulmonary edema, whereas capillary wedge pressures remained stable. Low-dose acrolein smoke (less than 200 ppm) produced edema in two of five animals with a 2- to 4-h delay. Intermediate-dose acrolein smoke (200-300 ppm) always produced edema at an average of 147 +/- 57 min after smoke, whereas high-dose acrolein (greater than 300 ppm) produced edema at 65 +/- 16 min after smoke. Thus acrolein but not HCl, when presented as a synthetic smoke, produced a delayed-onset, noncardiogenic, and peribronchiolar edema in a roughly dose-dependent fashion.

  13. Serotonin syndrome presenting as pulmonary edema

    PubMed Central

    Shah, Nilima Deepak; Jain, Ajay B.

    2016-01-01

    Serotonin syndrome (SS) is a potentially life-threatening condition resulting from excessive central and peripheral serotonergic activity. Clinically, it is a triad of mental-status changes, neuromuscular abnormalities, and autonomic disturbances. It can be caused by intentional self-poisoning, overdose, or inadvertent drug interactions. We report the case of a 58-year-old male with type 2 diabetes mellitus and obsessive compulsive disorder who developed pulmonary edema as a possible complication of SS. SS was caused by a combination of three specific serotonin re-uptake inhibitors (fluoxetine, fluvoxamine, and sertraline), linezolid, and fentanyl. The hospital course was further complicated by difficult weaning from the ventilator. SS was identified and successfully treated with cyproheptadine and lorazepam. The case highlights the importance of effective consultation-liaison and prompt recognition of SS as the presentation may be complex in the presence of co-morbid medical illness. PMID:26997733

  14. An uncommon cause of acute pulmonary edema.

    PubMed

    Nepal, Santosh; Giri, Smith; Bhusal, Mohan; Siwakoti, Krishmita; Pathak, Ranjan

    2016-09-01

    Acute cardiogenic pulmonary edema secondary to catecholamine-induced cardiomyopathy is a very uncommon and fatal initial presentation of pheochromocytoma. However, with early clinical suspicion and aggressive management, the condition is reversible. This case report describes a patient who presented with hypertension, dyspnea, and cough with bloody streaks, and who recovered within 48 hours after appropriate treatment. PMID:27575897

  15. Negative pressure pulmonary edema following choking on a cookie.

    PubMed

    Toukan, Yazeed; Gur, Michal; Bentur, Lea

    2016-07-01

    A 12-year-old boy developed severe acute respiratory distress during a school break requiring resuscitative measures. The episode started shortly after a short choking episode with a cookie. History, physical examination, laboratory results, chest X-ray, and clinical course supported the diagnosis of negative pressure pulmonary edema (NPPE). NPPE occurring outside a hospital setting, especially following a short episode of choking on a cookie, is rarely reported in children. Understanding the pathophysiological mechanisms contributing to pulmonary edema can help in distinguishing NPPE from other causes of fulminant respiratory distress, and especially from other causes of noncardiogenic pulmonary edema. Pediatr Pulmonol. 2016;51:E25-E27. © 2016 Wiley Periodicals, Inc.

  16. Pulmonary edema associated with scuba diving : case reports and review.

    PubMed

    Slade, J B; Hattori, T; Ray, C S; Bove, A A; Cianci, P

    2001-11-01

    Acute pulmonary edema has been associated with cold-water immersion in swimmers and divers. We report on eight divers using a self-contained underwater breathing apparatus (scuba) who developed acute pulmonary edema manifested by dyspnea, hypoxemia, and characteristic chest radiographic findings. All cases occurred in cold water. All scuba divers were treated with complete resolution, and three have returned to diving without further episodes. Mechanisms that would contribute to a raised capillary transmural pressure or to a reduced blood-gas barrier function or integrity are discussed. Pulmonary edema in scuba divers is multifactorial, and constitutional factors may play a role. Physicians should be aware of this potential, likely underreported, problem in scuba divers.

  17. The evolution of scuba divers pulmonary edema.

    PubMed

    Edmonds, Carl

    2016-01-01

    The evolution of scuba divers pulmonary edema is described. When discovered in 1981, it was believed to be a cold-induced response in a submerged, otherwise healthy, scuba diver. The clinical features are described and discussed, as are the demographics. An alleged prevalence of 1.1% was complicated by problematic statistics and an apparent increase in reported cases. Recurrences both while diving and swimming or snorkeling were common. More recent case reports and surveys are described, identifying predisposing factors and associations, including cardiac pathology. Stress cardiomyopathies, reversible myocardial disorder or Takotsubo cardiomyopathy, may complicate the presentation, especially in older females. Relevant cardiac investigations and autopsy findings are reviewed. Disease severity and potential lethality of scuba divers pulmonary edema became more apparent early this century, and these influence our current recommendations to survivors. First aid and treatment are also discussed. PMID:27265985

  18. Influenza leaves a TRAIL to pulmonary edema.

    PubMed

    Brauer, Rena; Chen, Peter

    2016-04-01

    Influenza infection can cause acute respiratory distress syndrome (ARDS), leading to poor disease outcome with high mortality. One of the driving features in the pathogenesis of ARDS is the accumulation of fluid in the alveoli, which causes severe pulmonary edema and impaired oxygen uptake. In this issue of the JCI, Peteranderl and colleagues define a paracrine communication between macrophages and type II alveolar epithelial cells during influenza infection where IFNα induces macrophage secretion of TRAIL that causes endocytosis of Na,K-ATPase by the alveolar epithelium. This reduction of Na,K-ATPase expression decreases alveolar fluid clearance, which in turn leads to pulmonary edema. Inhibition of the TRAIL signaling pathway has been shown to improve lung injury after influenza infection, and future studies will be needed to determine if blocking this pathway is a viable option in the treatment of ARDS. PMID:26999598

  19. The evolution of scuba divers pulmonary edema.

    PubMed

    Edmonds, Carl

    2016-01-01

    The evolution of scuba divers pulmonary edema is described. When discovered in 1981, it was believed to be a cold-induced response in a submerged, otherwise healthy, scuba diver. The clinical features are described and discussed, as are the demographics. An alleged prevalence of 1.1% was complicated by problematic statistics and an apparent increase in reported cases. Recurrences both while diving and swimming or snorkeling were common. More recent case reports and surveys are described, identifying predisposing factors and associations, including cardiac pathology. Stress cardiomyopathies, reversible myocardial disorder or Takotsubo cardiomyopathy, may complicate the presentation, especially in older females. Relevant cardiac investigations and autopsy findings are reviewed. Disease severity and potential lethality of scuba divers pulmonary edema became more apparent early this century, and these influence our current recommendations to survivors. First aid and treatment are also discussed.

  20. Treatment of Acute Low Pressure Pulmonary Edema in Dogs

    PubMed Central

    Prewitt, R. M.; McCarthy, J.; Wood, L. D. H.

    1981-01-01

    Severe pulmonary edema sometimes develops despite normal pulmonary capillary wedge pressure (Ppw). The equation describing net transvascular flux of lung liquid predicts decreased edema when hydrostatic pressure is reduced or when colloid osmotic pressure is increased in the pulmonary vessels. We tested these predictions in a model of pulmonary capillary leak produced in 35 dogs by intravenous oleic acid. 1 h later, the dogs were divided into five equal groups and treated for 4 h in different ways: (a) not treated, to serve as the control group (Ppw = 11.1 mm Hg); (b) given albumin to increase colloid osmotic pressure by 5 mm Hg (Ppw = 10.6 mm Hg); (c) ventilated with 10 cm H2O positive end-expiratory pressure (Peep) (transmural Ppw = 10.4 mm Hg); (d) phlebotomized to reduce Ppw to 6 mm Hg; (e) infused with nitroprusside, which also reduced Ppw to 6 mm Hg. Phlebotomy and nitroprusside reduced the edema in excised lungs by 50% (P< 0.001), but Peep and albumin did not affect the edema. Pulmonary shunt decreased on Peep and increased on nitroprusside, and lung compliance was not different among the treatment groups, demonstrating that these variables are poor indicators of changes in edema. Cardiac output decreased during the treatment period in all but the nitroprusside group, where Ppw decreased and cardiac output did not. We conclude that canine oleic acid pulmonary edema is reduced by small reductions in hydrostatic pressure, but not by increased colloid osmotic pressure, because the vascular permeability to liquid and protein is increased. These results suggest that low pressure pulmonary edema may be reduced by seeking the lowest Ppw consistent with adequate cardiac output enhanced by vasoactive agents like nitroprusside. Further, colloid infusions and Peep are not helpful in reducing edema, so they may be used in the lowest amount that provides adequate circulating volume and arterial O2 saturation on nontoxic inspired O2. Until these therapeutic principles

  1. Subclinical pulmonary edema in endurance athletes.

    PubMed

    Bussotti, M; Di Marco, S; Marchese, G; Agostoni, P G

    2012-06-01

    Strenuous exercise may cause progressive and proportional haemodynamic overload damage to the alveolar membrane, even in athletes. Despite the high incidence of arterial desaturation reported in endurance athletes has been attributed, into other factors, also to the damage of the alveolar-capillary membrane this evidence is equivocal. Some studies demonstrated flood of the interstitial space and consequent increase in pulmonary water content, but most of them were able to show this through indirect signs of interstitial oedema. The present review illustrates the literature's data in favour or against pulmonary interstitial edema due to intense exercise in athletes.

  2. High altitude pulmonary edema in mountain climbers.

    PubMed

    Korzeniewski, Krzysztof; Nitsch-Osuch, Aneta; Guzek, Aneta; Juszczak, Dariusz

    2015-04-01

    Every year thousands of ski, trekking or climbing fans travel to the mountains where they stay at the altitude of more than 2500-3000m above sea level or climb mountain peaks, often exceeding 7000-8000m. High mountain climbers are at a serious risk from the effects of adverse environmental conditions prevailing at higher elevations. They may experience health problems resulting from hypotension, hypoxia or exposure to low temperatures; the severity of those conditions is largely dependent on elevation, time of exposure as well as the rate of ascent and descent. A disease which poses a direct threat to the lives of mountain climbers is high altitude pulmonary edema (HAPE). It is a non-cardiogenic pulmonary edema which typically occurs in rapidly climbing unacclimatized lowlanders usually within 2-4 days of ascent above 2500-3000m. It is the most common cause of death resulting from the exposure to high altitude. The risk of HAPE rises with increased altitude and faster ascent. HAPE incidence ranges from an estimated 0.01% to 15.5%. Climbers with a previous history of HAPE, who ascent rapidly above 4500m have a 60% chance of illness recurrence. The aim of this article was to present the relevant details concerning epidemiology, pathophysiology, clinical symptoms, prevention, and treatment of high altitude pulmonary edema among climbers in the mountain environment.

  3. Pulmonary tissue volume in dogs during pulmonary edema.

    PubMed

    Peterson, B T; Petrini, M F; Hyde, R W; Schreiner, B F

    1978-05-01

    Pulmonary tissue volume (Vt) and pulmonary capillary blood flow (Qc) were measured in anesthetized dogs by analyzing end-expiratory concentrations of dimethyl ether (DME), acetylene (C2H2), and sulfur hexafluoride during a 30-s rebreathing maneuver. Vt was compared to the postmortem lung weight of control dogs and dogs with hemodynamic and nonhemodynamic (alloxan) pulmonary edema. Qc was compared to the cardiac output measured by dye dilution. A 100-ml increase in alveolar volume (VA) in the range of 1-2 liters resulted in a 9 +/- 3 ml increase in Vt. Vt measured at a VA of 1.9 liters measures 114 +/- 18% of the postmortem lung weight in 20 control dogs and in 6 dogs with moderate edema (lung weight < 250% of predicted). Vt measured only 53 +/- 14% of the lung weight in 11 dogs with more severe edema. DME and C2H2 gave the smae mean values of Vt, but the reproducibility of a series of 3-7 measurements was greater with DME (coefficient of variation was 5% with DME and 8% C2H2). Qc measured 96 +/ 15% of the cardiac output during the rebreathing maneuver, but the maneuver caused a 4-40% fall in the cardiac output. These data show that Vt determined by rebreathing DME is between 86% and 135% of the lung weight in dogs with pulmonary edema until the lung weight is greater than 250% of the predicted value.

  4. A patient with possible TRALI who developed pulmonary hypertensive crisis and acute pulmonary edema during cardiac surgery.

    PubMed

    Kojima, Taiki; Nishisako, Ryo; Sato, Hideo

    2012-06-01

    There are very few case reports of transfusion-related acute lung injury (TRALI) under close hemodynamic monitoring. We encountered a case of possible TRALI during on-pump coronary artery bypass grafting (CABG). A 66-year-old man who had undergone on-pump CABG was administered fresh frozen plasma (FFP). One hour after FFP transfusion, pulmonary hypertensive crisis and subsequent hypoxic decompensation occurred. A second cardiopulmonary bypass (CPB) was needed for circulatory and respiratory deterioration. Extracorporeal life support (ECLS), intraaortic balloon pumping (IABP), and nitric oxide therapy were required after the surgery. Despite the severity of the initial state, his recovery was comparatively smooth. ECLS and IABP were removed on postoperative day (POD)1; the patient was extubated and discharged from the ICU on POD7 and POD12, respectively. The diagnosis of TRALI was confirmed by human leukocyte antigen antibody detection in the administered FFP. In addition, lymphocytic immunofluorescence test showed that a cross-match of the plasma from the pooled FFP against the recipient leukocytes was positive. The clinical course of the pulmonary artery hypertension was followed by a decrease in dynamic lung compliance. The mechanism of this phenomenon is unclear. However, it might suggest the possibility of vasoconstriction or obstruction of the peripheral pulmonary artery preceding lung damage, as in the case in animal models reported previously.

  5. Smoke aldehyde component influences pulmonary edema

    SciTech Connect

    Hales, C.A.; Musto, S.W.; Janssens, S.; Jung, W.; Quinn, D.A.; Witten, M. , Massachusetts General Hospital, Boston )

    1992-02-01

    The pulmonary edema of smoke inhalation is caused by the toxins of smoke and not the heat. We investigated the potential of smoke consisting of carbon in combination with either acrolein or formaldehyde (both common components of smoke) to cause pulmonary edema in anesthetized sheep. Seven animals received acrolein smoke, seven animals received a low-dose formaldehyde smoke, and five animals received a high-dose formaldehyde smoke. Pulmonary arterial pressure, pulmonary capillary wedge pressure, and cardiac output were not affected by smoke in any group. Peak airway pressure increased after acrolein (14 +/- 1 to 21 +/- 2 mmHg; P less than 0.05) and after low- and high-dose formaldehyde (14 +/- 1 to 21 +/- 1 and 20 +/- 1 mmHg, respectively; both P less than 0.05). The partial pressure of O2 in arterial blood fell sharply after acrolein (219 +/- 29 to 86 +/- 9 (SE) Torr; P less than 0.05) but not after formaldehyde. Only acrolein resulted in a rise in lung lymph flow (6.5 +/- 2.2 to 17.9 +/- 2.6 ml/h; P less than 0.05). Lung lymph-to-plasma protein ratio was unchanged for all three groups, but clearance of lymph protein was increased after acrolein. After acrolein, the blood-free extravascular lung water-to-lung dry weight ratio was elevated (P less than 0.05) compared with both low- and high-dose formaldehyde groups (4.8 +/- 0.4 to 3.3 +/- 0.2 and 3.6 +/- 0.2, respectively). Lymph clearance (ng/h) of thromboxane B2, leukotriene B4, and the sulfidopeptide leukotrienes was elevated after acrolein but not formaldehyde.(ABSTRACT TRUNCATED AT 250 WORDS)

  6. New Compton densitometer for measuring pulmonary edema

    SciTech Connect

    Loo, B.W.; Goulding, F.S.; Simon, D.S.

    1985-10-01

    Pulmonary edema is the pathological increase of extravascular lung water found most often in patients with congestive heart failure and other critically ill patients who suffer from intravenous fluid overload. A non-invasive lung density monitor that is accurate, easily portable, safe and inexpensive is needed for clinical evaluation of pulmonary edema. Other researchers who have employed Compton scattering techniques generally used systems of extended size and detectors with poor energy resolution. This has resulted in significant systematic biases from multiply-scattered photons and larger errors in counting statistics at a given radiation dose to the patient. We are proposing a patented approach in which only backscattered photons are measured with a high-resolution HPGe detector in a compact system geometry. By proper design and a unique data extraction scheme, effects of the variable chest wall on lung density measurements are minimized. Preliminary test results indicate that with a radioactive source of under 30 GBq, it should be possible to make an accurate lung density measurement in one minute, with a risk of radiation exposure to the patient a thousand times smaller than that from a typical chest x-ray. The ability to make safe, frequent lung density measurements could be very helpful for monitoring the course of P.E. at the hospital bedside or outpatient clinics, and for evaluating the efficacy of therapy in clinical research. 6 refs., 5 figs.

  7. Glyphosate poisoning with acute pulmonary edema.

    PubMed

    Thakur, Darshana Sudip; Khot, Rajashree; Joshi, P P; Pandharipande, Madhuri; Nagpure, Keshav

    2014-01-01

    GlySH-surfactant herbicide (GlySH), one of the most commonly used herbicides worldwide, has been considered as minimally toxic to humans. However, clinical toxicologists occasionally encounter cases of severe systemic toxicity. The US Environmental Protection Agency (EPA) states that 'GlySH' is of relatively low oral and acute dermal toxicity. It does not have anticholinesterase effect and no organophosphate-like central nervous system (CNS) effects. The clinical features range from skin and throat irritation to hypotension and death. Severe GlySH-surfactant poisoning is manifested by gastroenteritis, respiratory disturbances, altered mental status, hypotension refractory to the treatment, renal failure, and shock.[1] GlySH intoxication has a case fatality rate 3.2-29.3%. Pulmonary toxicity and renal toxicity seem to be responsible for mortality. Metabolic acidosis, abnormal chest X-ray, arrhythmias, and elevated serum creatinine levels are useful prognostic factors for predicting GlySH mortality.[2] There is no antidote and the mainstay of treatment for systemic toxicity is decontamination and aggressive supportive therapy. We report a case of acute pulmonary edema, which is a rare but severe manifestation of oral GlySH poisoning, where patient survived with aggressive supportive therapy. PMID:25948977

  8. Unusual ventilation perfusion scintigram in a case of immunologic pulmonary edema clinically simulating pulmonary embolism

    SciTech Connect

    Campeau, R.J.; Faust, J.M.; Ahmad, S.

    1987-11-01

    A case of immunologic pulmonary edema secondary to hydrochlorothiazide allergy developed in a 55-year-old woman that clinically simulated pulmonary embolism. The patient had abnormal washin images with normal washout images on an Xe-133 ventilation study. On the perfusion study, large bilateral central and posterior perfusion defects were present that showed an unusual mirror image pattern on the lateral and posterior oblique views. Resolution of radiographic and scintigraphic abnormalities occurred over a 3-day period in conjunction with corticosteroid therapy.

  9. Exercise-Induced Pulmonary Edema in a Triathlon.

    PubMed

    Yamanashi, Hirotomo; Koyamatsu, Jun; Nobuyoshi, Masaharu; Murase, Kunihiko; Maeda, Takahiro

    2015-01-01

    Introduction. Family physicians have more opportunities to attend athletic competitions as medical staff at first-aid centers because of the increasing popularity of endurance sports. Case. A 38-year-old man who participated in a triathlon race experienced difficulty in breathing after swimming and was moved to a first-aid center. His initial oxygen saturation was 82% and a thoracic computed tomography scan showed bilateral ground glass opacity in the peripheral lungs. His diagnosis was noncardiogenic pulmonary edema associated with exercise or swimming: exercise-induced pulmonary edema (EIPE) or swimming-induced pulmonary edema (SIPE). Treatment with furosemide and corticosteroid relieved his symptoms of pulmonary edema. Discussion. Noncardiogenic pulmonary edema associated with endurance sports is not common, but knowledge about EIPE/SIPE or neurogenic pulmonary edema associated with hyponatremia, which is called Ayus-Arieff syndrome, is crucial. Knowledge and caution for possible risk factors, such as exposure to cold water or overhydration, are essential for both medical staff and endurance athletes. Conclusion. To determine the presence of pulmonary edema associated with strenuous exercise, oxygen saturation should be used as a screening tool at a first-aid center. To avoid risks for EIPE/SIPE, knowledge about these diseases is essential for medical staff and for athletes who perform extreme exercise.

  10. Exercise-Induced Pulmonary Edema in a Triathlon

    PubMed Central

    Yamanashi, Hirotomo; Koyamatsu, Jun; Nobuyoshi, Masaharu; Murase, Kunihiko; Maeda, Takahiro

    2015-01-01

    Introduction. Family physicians have more opportunities to attend athletic competitions as medical staff at first-aid centers because of the increasing popularity of endurance sports. Case. A 38-year-old man who participated in a triathlon race experienced difficulty in breathing after swimming and was moved to a first-aid center. His initial oxygen saturation was 82% and a thoracic computed tomography scan showed bilateral ground glass opacity in the peripheral lungs. His diagnosis was noncardiogenic pulmonary edema associated with exercise or swimming: exercise-induced pulmonary edema (EIPE) or swimming-induced pulmonary edema (SIPE). Treatment with furosemide and corticosteroid relieved his symptoms of pulmonary edema. Discussion. Noncardiogenic pulmonary edema associated with endurance sports is not common, but knowledge about EIPE/SIPE or neurogenic pulmonary edema associated with hyponatremia, which is called Ayus-Arieff syndrome, is crucial. Knowledge and caution for possible risk factors, such as exposure to cold water or overhydration, are essential for both medical staff and endurance athletes. Conclusion. To determine the presence of pulmonary edema associated with strenuous exercise, oxygen saturation should be used as a screening tool at a first-aid center. To avoid risks for EIPE/SIPE, knowledge about these diseases is essential for medical staff and for athletes who perform extreme exercise. PMID:26229538

  11. Hemodynamic and alveolar protein studies in noncardiac pulmonary edema.

    PubMed

    Gelb, A F; Klein, E

    1976-11-01

    Hemodynamic data were obtained within 15 hours of admission in 11 previously healthy patients (20 to 51 years of age, 7 men and 4 women) who had developed transient, reversible pulmonary edema without cardiac dilation in association with near-death from freshwater drowning (2 cases), pentobarbital overdose, heroin overdose (2 cases), smoke inhalation, chest trauma, sepsis (2 cases), pancreatitis, or prolonged abdominal surgery with suspected sepsis. Using a balloon-tipped flow-directed catheter, the pulmonary artery systolic/diastolic pressures (in mm Hg) were 25/12, 22/9, 31/11, 26/15, 20/10, 35/15, 40/15, 32/18, 20/10, 24/10, and 20/7; the corresponding pulmonary capillary wedge pressures (in mm Hg) were 8, 9, 6, 14, 6, 6, 15, 15, 10, 10, and 5, respectively. Plasma colloidal osmotic pressures measured in the latter 5 cases were 26, 18, 18, 18, and 15 mm Hg, respectively. In addition, the protein content of the alveolar fluid was 5.1, 3.4, 4.0, and 7.1 g per 100 ml in 4 patients. The concentration and distribution of the protein in plasma and alveolar fluid were very similar. These findings provide strong efidence that altered capillary permeability is responsible for the pulmonary edema.

  12. Pulmonary edema after photocoagulation of the endometrium with the Nd:YAG laser. A case report.

    PubMed

    Feinberg, B I; Gimpelson, R J; Godier, D E

    1989-06-01

    A woman developed pulmonary edema as a result of fluid overload during Nd:YAG ablation of endometrial tissue. As a result of a miscalculation of fluid administration and collection, she was overhydrated with irrigation fluid. The clinical picture of pulmonary edema was noted in the immediate postoperative period and responded to positive pressure ventilation and diuretic therapy. The mechanism of pulmonary edema is postulated to have been the result of the absorption of irrigating fluid through open venous channels resulting from the laser ablation. PMID:2661818

  13. An orally active TRPV4 channel blocker prevents and resolves pulmonary edema induced by heart failure.

    PubMed

    Thorneloe, Kevin S; Cheung, Mui; Bao, Weike; Alsaid, Hasan; Lenhard, Stephen; Jian, Ming-Yuan; Costell, Melissa; Maniscalco-Hauk, Kristeen; Krawiec, John A; Olzinski, Alan; Gordon, Earl; Lozinskaya, Irina; Elefante, Lou; Qin, Pu; Matasic, Daniel S; James, Chris; Tunstead, James; Donovan, Brian; Kallal, Lorena; Waszkiewicz, Anna; Vaidya, Kalindi; Davenport, Elizabeth A; Larkin, Jonathan; Burgert, Mark; Casillas, Linda N; Marquis, Robert W; Ye, Guosen; Eidam, Hilary S; Goodman, Krista B; Toomey, John R; Roethke, Theresa J; Jucker, Beat M; Schnackenberg, Christine G; Townsley, Mary I; Lepore, John J; Willette, Robert N

    2012-11-01

    Pulmonary edema resulting from high pulmonary venous pressure (PVP) is a major cause of morbidity and mortality in heart failure (HF) patients, but current treatment options demonstrate substantial limitations. Recent evidence from rodent lungs suggests that PVP-induced edema is driven by activation of pulmonary capillary endothelial transient receptor potential vanilloid 4 (TRPV4) channels. To examine the therapeutic potential of this mechanism, we evaluated TRPV4 expression in human congestive HF lungs and developed small-molecule TRPV4 channel blockers for testing in animal models of HF. TRPV4 immunolabeling of human lung sections demonstrated expression of TRPV4 in the pulmonary vasculature that was enhanced in sections from HF patients compared to controls. GSK2193874 was identified as a selective, orally active TRPV4 blocker that inhibits Ca(2+) influx through recombinant TRPV4 channels and native endothelial TRPV4 currents. In isolated rodent and canine lungs, TRPV4 blockade prevented the increased vascular permeability and resultant pulmonary edema associated with elevated PVP. Furthermore, in both acute and chronic HF models, GSK2193874 pretreatment inhibited the formation of pulmonary edema and enhanced arterial oxygenation. Finally, GSK2193874 treatment resolved pulmonary edema already established by myocardial infarction in mice. These findings identify a crucial role for TRPV4 in the formation of HF-induced pulmonary edema and suggest that TRPV4 blockade is a potential therapeutic strategy for HF patients.

  14. Acute pulmonary edema following inflation of arterial tourniquet.

    PubMed

    Santhosh, M C B; Pai, R B; Rao, R P

    2014-10-01

    Arterial tourniquets are used as one of the methods for reducing blood loss and for allowing blood free surgical field. A 20-year-old, 45 kg healthy female with a sphere shaped pendunculated hemangioma in the popliteal fossa of her left lower limb was applied with arterial tourniquet after exsanguination. The procedure was performed under general anesthesia. Soon after exsanguination and tourniquet inflation, the patient developed pulmonary edema which subsided after deflating the tourniquet. The clinical evolution, treatment and pathophysiology of this complication are described.

  15. Post extubation negative pressure pulmonary edema due to posterior mediastinal cyst in an infant.

    PubMed

    Dubey, Prakash Kumar

    2014-01-01

    A 3-month-old male child underwent uneventful inguinal herniotomy under general anesthesia. After extubation, airway obstruction followed by pulmonary edema appeared for which the baby was reintubated and ventilated. The baby made a complete recovery and extubated after about 2 h. A post-operative computed tomography scan revealed a posterior mediastinal cystic mass abutting the tracheal bifurcation. Presumably, extrinsic compression by the mass on the tracheal bifurcation led to the development of negative pressure pulmonary edema.

  16. PATIENT-VENTILATION ASYNCHRONY CAUSING NEGATIVE PRESSURE PULMONARY EDEMA IN AN INTUBATED OBESE PATIENT.

    PubMed

    Siddik-Sayyid, Sahar M; AlFahel, Waseem; El-Khatib, Mohamad F

    2016-02-01

    Negative pressure pulmonary edema is a potentially life-threatening condition that may occur when a large negative intrathoracic pressure is generated against a 'physically' obstructed upper airway during emergence from anesthesia. We report a 35 year old male patient who is morbidly obese and undergoing laparoscopic gastric bypass who developed negative pressure pulmonary edema without any evidence of a 'physical' upper airway obstruction. In our patient, the negative pressure pulmonary edema occurred after complete reversal of neuromuscular blockade and during manual positive pressure ventilation with the endotracheal tube still in place and in the presence of an oral airway. Since the patient was still intubated and had an airway in place with no possibility for physical obstruction, we speculate that the occurrence of the negative pressure pulmonary edema was mainly due to a 'functional' obstruction secondary to the severe patient-ventilation asynchrony that ensued upon reversal of the neuromuscular blockade. PMID:27382824

  17. Hemoptysis and pulmonary edema in a scuba diver using diclofenac.

    PubMed

    Van Renterghem, Dirk; Depuydt, Charlotte

    2012-01-01

    Hemoptysis and pulmonary edema associated with nonsteroidal anti-inflammatory drug use is a known condition, but is probably underreported. The mechanisms of induction of pulmonary toxicity are still not well understood. We describe a case of hemoptysis and dyspnea in a scuba diver who was taking diclofenac.

  18. The pathogenesis of pulmonary edema in acute pancreatitis.

    PubMed Central

    Warshaw, A L; Lesser, P B; Rie, M; Cullen, D J

    1975-01-01

    Acute pulmonary edema appeared 3 or more days after the onset of acute pancreatitis in 7 patients, an approximate incidence of 8%. The severity of pancreatitis in these patients was characterized by massive requirements for intravenous colloid and by marked hypocalcemia. In addition, at least 5 of the 7 patients had very high serum levels of triglycerides at the time of hospital admission. Hemodynamic studies during pulmonary edema showed normal central venous pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and pulmonary vascular resistance. Cardiac index was appropriately elevated. Respiratory treatment, consisting of endotracheal intubation and controlled ventilation with PEEP, was successful in allowing reversal of the pulmonary injury and recovery of respiratory function within 1-2 weeks in all cases. Two patients died later from pancreatic abscesses. The findings indicate that a distinct form of pulmonary injury may occur in acute pancreatitis, characterized by loss of integrity of the alveolar-capilllary membrane, leading to pulmonary edema. The mechanism of injury is not known but may be caused by circulating free fatty acids, phospholipase A, or vasoactive substances. The pulmonary membrane lesion appears to heal during the period of intensive respiratory support. Images Fig. 1. PMID:1101836

  19. High altitude pulmonary edema. Epidemiologic observations in Peru.

    PubMed

    Hultgren, H N; Marticorena, E A

    1978-10-01

    The incidence of high altitude pulmonary edema was examined by a survey (via questionnaire) of residents living at 3,750 meters (12,303 feet) in the mining community of La Oroya, Peru. Ninety-seven subjects made a total of 1,157 ascents to high altitude after a stay at sea level of longer than 14 days. Sixty-four subjects experienced at least one episode of high-altitude pulmonary edema. The incidence was higher in subjects aged 13 to 20 years, where 17 percent (15) of 90 ascents resulted in episodes of high-altitude pulmonary edema, than in subjects 21 years or older (3 percent; 18/686 ascents). Young subjects (2 to 12 years old) had more severe episodes of high-altitude pulmonary edema (81 percent; 30/37 episodes) than adults (22 percent; 4/18 episodes). No episodes were observed in children under two years old. Five subjects under 21 years of age experienced recurrent episodes. Our estimated incidence of severe episodes of high altitude pulmonary edema per ascent in adults (0.6 percent; 4/686) is similar to that reported by other workers (incidence of 0.15 to 0.57 percent) in various parts of the world. PMID:699645

  20. The risk factors and prognostic implication of acute pulmonary edema in resuscitated cardiac arrest patients

    PubMed Central

    Kang, Dae-hyun; Kim, Joonghee; Rhee, Joong Eui; Kim, Taeyun; Kim, Kyuseok; Jo, You Hwan; Lee, Jin Hee; Lee, Jae Hyuk; Kim, Yu Jin; Hwang, Seung Sik

    2015-01-01

    Objective Pulmonary edema is frequently observed after a successful resuscitation in out-of-hospital cardiac arrest (OHCA) patients. Currently, its risk factors and prognostic implications are mostly unknown. Methods Adult OHCA patients with a presumed cardiac etiology who achieved sustained return of spontaneous circulation (ROSC) in emergency department were retrospectively analyzed. The patients were grouped according to the severity of consolidation on their initial chest X-ray (group I, no consolidation; group II, patchy consolidations; group III, consolidation involving an entire lobe; group IV, total white-out of any lung). The primary objective was to identify the risk factors of developing severe pulmonary edema (group III or IV). The secondary objective was to evaluate the association between long-term prognosis and the severity of pulmonary edema. Results One hundred and seven patients were included. Total duration of cardiopulmonary resuscitation (CPR) and initial pCO2 level were both independent predictors of developing severe pulmonary edema with their odds ratio (OR) being 1.02 (95% confidence interval [CI], 1.00 to 1.04; per 1 minute) and 1.04 (95% CI, 1.01 to 1.07; per 1 mmHg), respectively. The long term prognosis was significantly poor in patients with severe pulmonary edema with a OR for good outcome (6-month cerebral performance category 1 or 2) being 0.22 (95% CI, 0.06 to 0.79) in group III and 0.16 (95% CI, 0.04 to 0.63) in group IV compared to group I. Conclusion The duration of CPR and initial pCO2 level were both independent predictors for the development of severe pulmonary edema after resuscitation in emergency department. The severity of the pulmonary edema was significantly associated with long-term outcome.

  1. The Endothelial Glycocalyx: Emerging Concepts in Pulmonary Edema and Acute Lung Injury

    PubMed Central

    Collins, Stephen R.; Blank, Randal S.; Deatherage, Lindy S.; Dull, Randal O.

    2013-01-01

    The endothelial glycocalyx is a dynamic layer of macromolecules at the luminal surface of vascular endothelium that is involved in fluid homeostasis and regulation. Its role in vascular permeability and edema formation is emerging but is still not well understood. In this special article, we highlight key concepts of endothelial dysfunction with regards to the glycocalyx and provide new insights into the glycocalyx as a mediator of processes central to the development of pulmonary edema and lung injury. PMID:23835455

  2. Bilateral pulmonary edema after endoscopic sympathectomy in a patient with glucose-6-phosphate dehydrogenase deficiency.

    PubMed

    Lan, C J; Luk, H N; Wu, C T; Chang, W K; Tsou, M Y; Lui, P W; Lee, T Y

    2001-01-01

    Transaxillary endoscopic sympathectomy of thoracic ganglia (T2-T3) has recently gained wider acceptance as the treatment of choice for palmar hyperhidrosis. It requires one-lung ventilation to facilitate the surgery. One-lung ventilation, however, is not without complications, among which acute pulmonary edema has been reported. In this case report, we present a patient with palmar hyperhidrosis complicated by glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, who received bilateral endoscopic sympathectomy under alternate one-lung anesthesia, and developed acute pulmonary edema immediately after recruitment of the successive collapsed lung. The effects of hypoxemia, G-6-PD deficiency and sympathectomy might all add to the development of acute pulmonary edema secondary to reexpansion of each individual lung after alternate one-lung ventilation. The possibilities of the inferred causes are herein discussed. PMID:11152024

  3. Pulmonary edema following closed-circuit oxygen diving and strenuous swimming.

    PubMed

    Shupak, Avi; Guralnik, Ludmila; Keynan, Yoav; Yanir, Yoav; Adir, Yochai

    2003-11-01

    Acute pulmonary edema may be induced by diving and strenuous swimming. We report the case of a diver using closed-circuit, scuba equipment who developed acute dyspnea, hemoptysis, and hypoxemia following a dive in 18 degreesC (64.4 degrees F) water and physical exertion during the swim back to shore. With the growing popularity of recreational scuba diving, emergency physicians are liable to be faced with increasing numbers of diving-related medical problems. Diving-induced pulmonary edema should be included in the differential diagnosis of acute hypoxemia, sometimes accompanied by acid-base abnormalities, when this is seen in a diver.

  4. [Acute heart failure: acute cardiogenic pulmonary edema and cardiogenic shock].

    PubMed

    Sánchez Marteles, Marta; Urrutia, Agustín

    2014-03-01

    Acute cardiogenic pulmonary edema and cardiogenic shock are two of the main forms of presentation of acute heart failure. Both entities are serious, with high mortality, and require early diagnosis and prompt and aggressive management. Acute pulmonary edema is due to the passage of fluid through the alveolarcapillary membrane and is usually the result of an acute cardiac episode. Correct evaluation and clinical identification of the process is essential in the management of acute pulmonary edema. The initial aim of treatment is to ensure hemodynamic stability and to correct hypoxemia. Other measures that can be used are vasodilators such as nitroglycerin, loop diuretics and, in specific instances, opioids. Cardiogenic shock is characterized by sustained hypoperfusion, pulmonary wedge pressure > 18 mmHg and a cardiac index < 2.2l/min/m(2). The process typically presents with hypotension (systolic blood pressure < 90 mmHg or a decrease in mean arterial pressure > 30 mmHg) and absent or reduced diuresis (< 0.5 ml/kg/h). The most common cause is left ventricular failure due to acute myocardial infarction. Treatment consists of general measures to reverse acidosis and hypoxemia, as well as the use of vasopressors and inotropic drugs. Early coronary revascularization has been demonstrated to improve survival in shock associated with ischaemic heart disease.

  5. Aripiprazole induced non-cardiogenic pulmonary edema: a case report.

    PubMed

    Cetin, Mustafa; Celik, Mustafa; Cakıcı, Musa; Polat, Mustafa; Suner, Arif

    2014-01-01

    Aripiprazole is a second-generation antipsychotic drug with partial dopamine agonistic activity. Although the adverse cardiovascular effects of both typical and atypical antipsychotics are well known, similar data on aripiprazole, which was recently introduced, are scarce. Herein we report a 35-year-old female that presented to our emergency department with non-cardiogenic pulmonary edema. Chest X-ray and thoracic CT showed pulmonary edema and bilateral pleural effusion. Anamnesis showed that she had been taking sertraline 200 mg d-1 for obsessive-compulsive disorder for a long time and that aripiprazole10 mg d-1 was added for augmentation 2 months prior to presentation. We think that the CYP 2D6 inhibitor sertraline might have played a role in increasing the plasma concentration and toxicity of aripiprazole in the presented patient. PMID:25487626

  6. Pulmonary edema in scuba divers: recurrence and fatal outcome.

    PubMed

    Cochard, G; Arvieux, J; Lacour, J M; Madouas, G; Mongredien, H; Arvieux, C C

    2005-01-01

    Pulmonary edema occurring in divers using a self-contained underwater breathing apparatus (scuba) is an uncommon, probably under-reported, but potentially life-threatening and recurrent condition. We report six episodes of pulmonary edema in five scuba divers seen during a period of 15 months. The four men and one woman ranged in age from 37 to 56 years and two were treated for hypertension. Symptoms were mostly dyspnea onset at depth, cough, hemoptysis and hypoxemia, which in the recurrent case led to cardiac arrest and death. All cases occurred in rather cold water. Findings on thoracic computed tomography (CT) scanning ranged from pleural effusion to ground-glass opacities restricted to a few areas of the lung. The complex underlying mechanisms that would contribute to a raised transalveolar pressure or to a disruption of the blood-gas barrier are discussed. It is important for emergency care providers to be aware of this syndrome for prompt recognition and optimal treatment.

  7. Role of posterior hypothalamus in hypobaric hypoxia induced pulmonary edema.

    PubMed

    Sharma, R K; Choudhary, R C; Reddy, M K; Ray, A; Ravi, K

    2015-01-01

    To investigate the role of posterior hypothalamus and central neurotransmitters in the pulmonary edema due to hypobaric hypoxia, rats were placed in a high altitude simulation chamber (barometric pressure-294.4 mmHg) for 24 h. Exposure to hypobaric hypoxia resulted in increases in mean arterial blood pressure, renal sympathetic nerve activity, right ventricular systolic pressure, lung wet to dry weight ratio and Evans blue dye leakage. There was a significant attenuation in these responses to hypobaric hypoxia (a) after lesioning posterior hypothalamus and (b) after chronic infusion of GABAA receptor agonist muscimol into posterior hypothalamus. No such attenuation was evident with the chronic infusion of the nitric oxide donor SNAP into the posterior hypothalamus. It is concluded that in hypobaric hypoxia, there is over-activity of posterior hypothalamic neurons probably due to a local decrease in GABA-ergic inhibition which increases the sympathetic drive causing pulmonary hypertension and edema. PMID:25448396

  8. Marathon-induced pulmonary edema of a patient with transient dyspnea.

    PubMed

    Miyazawa, Ryo; Morita, Yuka; Okajima, Yuka; Matsusako, Masaki; Kurihara, Yasuyuki

    2015-10-01

    We report a case of a 31-year-old healthy man with marathon-induced pulmonary edema. Chest radiograph revealed pulmonary edema without cardiomegaly. Contrast-enhanced chest computed tomography (CT) revealed transient pulmonary edema without filling-defect in pulmonary arteries. As marathon running increases in popularity, radiologists and emergency physicians should be familiar with diagnosis of this entity on chest radiograph, avoiding unnecessary CT examination without additional clinical information.

  9. Marathon-induced pulmonary edema of a patient with transient dyspnea.

    PubMed

    Miyazawa, Ryo; Morita, Yuka; Okajima, Yuka; Matsusako, Masaki; Kurihara, Yasuyuki

    2015-10-01

    We report a case of a 31-year-old healthy man with marathon-induced pulmonary edema. Chest radiograph revealed pulmonary edema without cardiomegaly. Contrast-enhanced chest computed tomography (CT) revealed transient pulmonary edema without filling-defect in pulmonary arteries. As marathon running increases in popularity, radiologists and emergency physicians should be familiar with diagnosis of this entity on chest radiograph, avoiding unnecessary CT examination without additional clinical information. PMID:26324381

  10. Pulmonary Edema Assessed by Ultrasound: Impact in Cardiology and Intensive Care Practice.

    PubMed

    Blanco, Pablo A; Cianciulli, Tomás F

    2016-05-01

    Pulmonary edema is a frequent condition found in adult patients hospitalized in cardiology wards and intensive care units. Ultrasonography is a diagnostic modality with a high sensitivity for the detection of extravascular lung water, visualized as B lines, and usually caused by cardiogenic or noncardiogenic pulmonary edema. This paper highlights a simple method for the assessment of patients with pulmonary edema, which allows for a differential diagnosis of its possible mechanism and contributes to therapeutic intervention guiding and monitoring. PMID:26841270

  11. Is High Altitude Pulmonary Edema Relevant to Hawai‘i?

    PubMed Central

    2014-01-01

    High altitude clinical syndromes have been described in the medical literature but may be under recognized in the state of Hawai‘i. As tourism increases, high altitude injuries may follow given the easy access to high altitude attractions. Visitors and clinicians should be aware of the dangers associated with the rapid ascent to high altitudes in the perceived comfort of a vehicle. This paper will review the basic pathophysiology, prevention, and treatment of the most serious of the high altitude clinical syndromes, high altitude pulmonary edema. PMID:25478294

  12. Pulmonary Edema in Healthy Subjects in Extreme Conditions

    PubMed Central

    Garbella, Erika; Catapano, Giosuè; Pratali, Lorenza; Pingitore, Alessandro

    2011-01-01

    There are several pieces of evidence showing occurrence of pulmonary edema (PE) in healthy subjects in extreme conditions consisting of extreme psychophysical demand in normal environment and psychophysical performances in extreme environment. A combination of different mechanisms, such as mechanical, hemodynamic, biochemical, and hypoxemic ones, may underlie PE leading to an increase in lung vascular hydrostatic pressure and lung vascular permeability and/or a downregulation of the alveolar fluid reabsorption pathways. PE can be functionally detected by closing volume measurement and lung diffusing capacity test to different gases or directly visualized by multiple imaging techniques. Among them chest ultrasonography can detect and quantify the extravascular lung water, creating “comet-tail” ultrasound artefacts (ULCs) from water-thickened pulmonary interlobular septa. In this paper the physiopathological mechanisms of PE, the functional and imaging techniques applied to detect and quantify the phenomenon, and three models of extreme conditions, that is, ironman athletes, climbers and breath-hold divers, are described. PMID:21766015

  13. Pulmonary edema: an MR study of permeability and hydrostatic types in animals.

    PubMed

    Schmidt, H C; Tsay, D G; Higgins, C B

    1986-02-01

    Permeability pulmonary edema was induced in ten rats by intravenous injection of oleic acid. Hydrostatic pulmonary edema was induced in another ten rats by continuous infusion of saline. Permeability pulmonary edema was detected as increased signal intensity in all animals on images obtained with repetition times (TR) of 2.0 sec and echo times (TE) of 28 and 56 msec. Hydrostatic pulmonary edema was perceivable only in seven of ten rats. It was best seen on spin-echo TR = 2.0 sec, TE = 28 msec images as increased intensity either throughout the whole lung or in a predominant central distribution. The slopes of the relationships between the mean signal intensity and water content of both lungs were lower for hydrostatic pulmonary edema than for permeability pulmonary edema. Hydrostatic pulmonary edema demonstrated similar T1 but markedly shorter T2 relaxation times than permeability edema. Magnetic resonance imaging can be used to estimate severity of hydrostatic and permeability pulmonary edemas. PMID:3941856

  14. Inhibition of chlorine-induced pulmonary inflammation and edema by mometasone and budesonide.

    PubMed

    Chen, Jing; Mo, Yiqun; Schlueter, Connie F; Hoyle, Gary W

    2013-10-15

    Chlorine gas is a widely used industrial compound that is highly toxic by inhalation and is considered a chemical threat agent. Inhalation of high levels of chlorine results in acute lung injury characterized by pneumonitis, pulmonary edema, and decrements in lung function. Because inflammatory processes can promote damage in the injured lung, anti-inflammatory therapy may be of potential benefit for treating chemical-induced acute lung injury. We previously developed a chlorine inhalation model in which mice develop epithelial injury, neutrophilic inflammation, pulmonary edema, and impaired pulmonary function. This model was used to evaluate nine corticosteroids for the ability to inhibit chlorine-induced neutrophilic inflammation. Two of the most potent corticosteroids in this assay, mometasone and budesonide, were investigated further. Mometasone or budesonide administered intraperitoneally 1h after chlorine inhalation caused a dose-dependent inhibition of neutrophil influx in lung tissue sections and in the number of neutrophils in lung lavage fluid. Budesonide, but not mometasone, reduced the levels of the neutrophil attractant CXCL1 in lavage fluid 6h after exposure. Mometasone or budesonide also significantly inhibited pulmonary edema assessed 1 day after chlorine exposure. Chlorine inhalation resulted in airway hyperreactivity to inhaled methacholine, but neither mometasone nor budesonide significantly affected this parameter. The results suggest that mometasone and budesonide may represent potential treatments for chemical-induced lung injury.

  15. Inhibition of chlorine-induced pulmonary inflammation and edema by mometasone and budesonide

    SciTech Connect

    Chen, Jing; Mo, Yiqun; Schlueter, Connie F.; Hoyle, Gary W.

    2013-10-15

    Chlorine gas is a widely used industrial compound that is highly toxic by inhalation and is considered a chemical threat agent. Inhalation of high levels of chlorine results in acute lung injury characterized by pneumonitis, pulmonary edema, and decrements in lung function. Because inflammatory processes can promote damage in the injured lung, anti-inflammatory therapy may be of potential benefit for treating chemical-induced acute lung injury. We previously developed a chlorine inhalation model in which mice develop epithelial injury, neutrophilic inflammation, pulmonary edema, and impaired pulmonary function. This model was used to evaluate nine corticosteroids for the ability to inhibit chlorine-induced neutrophilic inflammation. Two of the most potent corticosteroids in this assay, mometasone and budesonide, were investigated further. Mometasone or budesonide administered intraperitoneally 1 h after chlorine inhalation caused a dose-dependent inhibition of neutrophil influx in lung tissue sections and in the number of neutrophils in lung lavage fluid. Budesonide, but not mometasone, reduced the levels of the neutrophil attractant CXCL1 in lavage fluid 6 h after exposure. Mometasone or budesonide also significantly inhibited pulmonary edema assessed 1 day after chlorine exposure. Chlorine inhalation resulted in airway hyperreactivity to inhaled methacholine, but neither mometasone nor budesonide significantly affected this parameter. The results suggest that mometasone and budesonide may represent potential treatments for chemical-induced lung injury. - Highlights: • Chlorine causes lung injury when inhaled and is considered a chemical threat agent. • Corticosteroids may inhibit lung injury through their anti-inflammatory actions. • Corticosteroids inhibited chlorine-induced pneumonitis and pulmonary edema. • Mometasone and budesonide are potential rescue treatments for chlorine lung injury.

  16. TEVAR for Flash Pulmonary Edema Secondary to Thoracic Aortic Aneurysm to Pulmonary Artery Fistula.

    PubMed

    Bornak, Arash; Baqai, Atif; Li, Xiaoyi; Rey, Jorge; Tashiro, Jun; Velazquez, Omaida C

    2016-01-01

    Enlarging aneurysms in the thoracic aorta frequently remain asymptomatic. Fistulization of thoracic aortic aneurysms (TAA) to adjacent structures or the presence of a patent ductus arteriosus and TAA may lead to irreversible cardiopulmonary sequelae. This article reports on a large aneurysm of the thoracic aorta with communication to the pulmonary artery causing pulmonary edema and cardiorespiratory failure. The communication was ultimately closed after thoracic endovascular aortic aneurysm repair allowing rapid symptom resolution. Early diagnosis and closure of such communication in the presence of TAA are critical for prevention of permanent cardiopulmonary damage.

  17. Three plasma metabolite signatures for diagnosing high altitude pulmonary edema

    NASA Astrophysics Data System (ADS)

    Guo, Li; Tan, Guangguo; Liu, Ping; Li, Huijie; Tang, Lulu; Huang, Lan; Ren, Qian

    2015-10-01

    High-altitude pulmonary edema (HAPE) is a potentially fatal condition, occurring at altitudes greater than 3,000 m and affecting rapidly ascending, non-acclimatized healthy individuals. However, the lack of biomarkers for this disease still constitutes a bottleneck in the clinical diagnosis. Here, ultra-high performance liquid chromatography coupled with Q-TOF mass spectrometry was applied to study plasma metabolite profiling from 57 HAPE and 57 control subjects. 14 differential plasma metabolites responsible for the discrimination between the two groups from discovery set (35 HAPE subjects and 35 healthy controls) were identified. Furthermore, 3 of the 14 metabolites (C8-ceramide, sphingosine and glutamine) were selected as candidate diagnostic biomarkers for HAPE using metabolic pathway impact analysis. The feasibility of using the combination of these three biomarkers for HAPE was evaluated, where the area under the receiver operating characteristic curve (AUC) was 0.981 and 0.942 in the discovery set and the validation set (22 HAPE subjects and 22 healthy controls), respectively. Taken together, these results suggested that this composite plasma metabolite signature may be used in HAPE diagnosis, especially after further investigation and verification with larger samples.

  18. Using ultrasound lung comets in the diagnosis of high altitude pulmonary edema: fact or fiction?

    PubMed

    Wimalasena, Yashvi; Windsor, Jeremy; Edsell, Mark

    2013-06-01

    High altitude pulmonary edema is a life-threatening condition that remains a concern for climbers and clinicians alike. Within the last decade, studies have shown ultrasonography to be valuable in the accurate diagnosis of a variety of lung pathologies, including cardiogenic pulmonary edema, pleural effusion, pneumothorax, and lung consolidation. Recently, studies conducted in remote areas have demonstrated that ultrasound lung comets can be used as a measure of subacute pulmonary edema and high altitude pulmonary edema in climbers ascending to altitude. This clinical review article provides an overview of lung ultrasonography and its relevance as a diagnostic aid to respiratory pathology. In addition, we describe a standardized technique for identifying ultrasound lung comets and its utility in recognizing the presence of extravascular lung water, as well as the results of studies that have used this approach at sea level and high altitude. PMID:23453728

  19. Refractory Pulmonary Edema Caused by Late Pulmonary Vein Thrombosis After Lung Transplantation: A Rare Adverse Event.

    PubMed

    Denton, Eve J; Rischin, Adam; McGiffin, David; Williams, Trevor J; Paraskeva, Miranda A; Westall, Glen P; Snell, Greg

    2016-09-01

    After lung transplantation, pulmonary vein thrombosis is a rare, potentially life-threatening adverse event arising at the pulmonary venous anastomosis that typically occurs early and presents as graft failure and hemodynamic compromise with an associated mortality of up to 40%. The incidence, presentation, outcomes, and treatment of late pulmonary vein thrombosis remain poorly defined. Management options include anticoagulant agents for asymptomatic clots, and thrombolytic agents or surgical thrombectomy for hemodynamically significant clots. We present a rare case highlighting a delayed presentation of pulmonary vein thrombosis occurring longer than 2 weeks after lung transplantation and manifesting clinically as graft failure secondary to refractory pulmonary edema. The patient was treated successfully with surgical thrombectomy and remains well. We recommend a high index of suspicion of pulmonary vein thrombosis when graft failure after lung transplantation occurs and is not responsive to conventional therapy, and consideration of investigation with transesophageal echocardiography or computed tomography with venous phase contrast in such patients even more than 2 weeks after lung transplantation.

  20. Edema

    MedlinePlus

    ... involve your entire body. Causes of edema include Eating too much salt Sunburn Heart failure Kidney disease Liver problems from cirrhosis Pregnancy Problems with lymph nodes, especially after mastectomy Some ...

  1. Use of the Gamow Bag by EMT-basic park rangers for treatment of high-altitude pulmonary edema and high-altitude cerebral edema.

    PubMed

    Freeman, Kimberly; Shalit, Marc; Stroh, Geoffrey

    2004-01-01

    As part of an emergency medical system protocol, national park service rangers certified at the level of an emergency medical technician-basic (EMT-B) are taught to recognize and treat high-altitude pulmonary edema and high-altitude cerebral edema. In Sequoia and Kings Canyon National Parks, this is done with the assistance of physician on-line medical control as a backup. High-altitude pulmonary edema and high-altitude cerebral edema are both potentially fatal altitude illnesses that can be particularly problematic in the backcountry, where evacuation may be delayed. We report a case of high-altitude pulmonary edema and high-altitude cerebral edema occurring at moderate altitude that was successfully treated by park rangers with the Gamow Bag.

  2. Postobstructive Pulmonary Edema following Tonsillectomy/Adenoidectomy in a 2-Year-Old with Poland-Moebius Syndrome

    PubMed Central

    Powell, Tanisha; Sharma, Nirupma; McKie, Kathleen T.

    2016-01-01

    A 2-year-old male with Poland-Moebius syndrome was transferred from a local hospital to the Pediatric ICU at Children's Hospital of Georgia for suspected postobstructive pulmonary edema (POPE) after tonsillectomy/adenoidectomy (T&A). The patient's respiratory status ultimately declined and he developed respiratory failure. Imaging suggested pulmonary edema as well as a left-sided pneumonia. Echocardiogram showed pulmonary hypertension and airway exam via direct fiberoptic bronchoscopy revealed tracheomalacia and bronchomalacia. He developed acute respiratory distress syndrome (ARDS) and remained intubated for ten days. This case highlights the association between congenital upper body abnormalities with cranial nerve dysfunction and the development of POPE with delayed resolution of symptoms. Patients with upper body abnormalities as above are at great risk of postoperative complications and should therefore be managed in a tertiary-care facility. PMID:26942029

  3. A new Compton densitometer for measuring pulmonary edema

    SciTech Connect

    Loo, B.W.; Goulding, F.S.; Simon, S.

    1986-02-01

    Pulmonary edema (PE) is the pathological increase of extravascular lung water found most often in patients with congestive heart failure and other critically ill patients who suffer from intravenous fluid overload. The chest x-ray, the standard method for validating the presence of PE, is neither quantitative nor sensitive. A non-invasive lung density monitor that is accurate, easily portable, safe and inexpensive is needed for clinical use. To deal with the problem of attenuation along the beam paths, previous gamma-ray techniques require simultaneous measurement of transmitted and scattered beams. Since multiple scattering is a strong function of the density of the scattering medium and the mass distribution within the detection geometry, there will be inherent uncertainties in the system calibration unless it is performed on a body structure closely matched to that of each individual patient. Other researchers who have employed Compton scattering techniques generally used systems of extended size and detectors with poor energy resolution. This has resulted in significant systematic biases from multiply-scattered photons and larger errors in counting statistics at a given radiation dose to the patient. We are proposing a patented approach in which only backscattered photons are measured with a high-resolution HPGe detector in a compact system geometry. By proper design and a unique data extraction scheme, effects of the variable chest wall on lung density measurements are minimized. Preliminary test results indicate that with a radioactive source of under 30 GBq, it should be possible to make an accurate lung density, measurement in one minute, with a risk of radiation exposure to the patient a thousand times smaller than that from a typical chest x-ray.

  4. Analysis of proteins in bronchoalveolar lavage fluids during pulmonary edema resulting from nitrogen dioxide and cadmium exposure

    SciTech Connect

    Gurley, L.R.; London, J.E.; Dethloff, L.A.; Lehnert, B.E.

    1988-01-01

    We have developed a new HPLC method by which quantitative measurements can be made on the biochemical constituents of the extracellular fluid lining of the lung as sampled by bronchoalveolar lavage. Nine of the fractions are proteins, two are phospholipids, and two fractions remained unidentified. Rats were subjected to the intrapulmonary deposition of cadmium, a treatment model known to induce pulmonary edema and cause a translocation of blood compartment proteins into the lung's alveolar space compartment. Resulting pulmonary edema was hallmarked by /approximately/25-fold increases in three major blood compartment-derived HPLC protein fractions, two of which have been identified as albumin and immunoglobulin(s). Analysis of lavage fluid from rats exposed to 100 ppM NO/sub 2/ for 15 min, an exposure regimen which also produces pulmonary edema, indicated that the three blood compartment proteins in the lavage fluids were elevated 35- to 72-fold over controls 24 h after exposure. These results demonstrate that HPLC can be used to provide a highly sensitive method for detection and quantitation of pulmonary edema that can occur in acute lung injuries resulting from environmental insults.

  5. Noninvasive mechanical ventilation in chronic obstructive pulmonary disease and in acute cardiogenic pulmonary edema.

    PubMed

    Rialp Cervera, G; del Castillo Blanco, A; Pérez Aizcorreta, O; Parra Morais, L

    2014-03-01

    Noninvasive ventilation (NIV) with conventional therapy improves the outcome of patients with acute respiratory failure due to hypercapnic decompensation of chronic obstructive pulmonary disease (COPD) or acute cardiogenic pulmonary edema (ACPE). This review summarizes the main effects of NIV in these pathologies. In COPD, NIV improves gas exchange and symptoms, reducing the need for endotracheal intubation, hospital mortality and hospital stay compared with conventional oxygen therapy. NIV may also avoid reintubation and may decrease the length of invasive mechanical ventilation. In ACPE, NIV accelerates the remission of symptoms and the normalization of blood gas parameters, reduces the need for endotracheal intubation, and is associated with a trend towards lesser mortality, without increasing the incidence of myocardial infarction. The ventilation modality used in ACPE does not affect the patient prognosis.

  6. Pioglitazone-induced congestive heart failure and pulmonary edema in a patient with preserved ejection fraction.

    PubMed

    Jearath, Vaneet; Vashisht, Rajan; Rustagi, Vipul; Raina, Sujeet; Sharma, Rajesh

    2016-01-01

    Pioglitazone-induced heart failure is known in patients with underlying heart disease, but is not well documented in patients with normal left ventricular function. Pioglitazone has been very popular as it is an insulin sensitizer and insulin resistance is prevalent among Indians. Fluid retention exacerbates pre-existing heart failure or precipitates heart failure in a patient with underlying left ventricular dysfunction. However, pathogenesis of heart failure in a patient with normal left ventricular function is not known. Probably it is due to dose-related effect on pulmonary endothelial permeability, rather than alterations in left ventricular mass or ejection fraction. We report a patient who developed congestive heart failure and pulmonary edema with normal left ventricular function within 1 year of starting pioglitazone therapy. We have to be careful in monitoring all possible side effects during followup when patients are on pioglitazone therapy.

  7. Pioglitazone-induced congestive heart failure and pulmonary edema in a patient with preserved ejection fraction

    PubMed Central

    Jearath, Vaneet; Vashisht, Rajan; Rustagi, Vipul; Raina, Sujeet; Sharma, Rajesh

    2016-01-01

    Pioglitazone-induced heart failure is known in patients with underlying heart disease, but is not well documented in patients with normal left ventricular function. Pioglitazone has been very popular as it is an insulin sensitizer and insulin resistance is prevalent among Indians. Fluid retention exacerbates pre-existing heart failure or precipitates heart failure in a patient with underlying left ventricular dysfunction. However, pathogenesis of heart failure in a patient with normal left ventricular function is not known. Probably it is due to dose-related effect on pulmonary endothelial permeability, rather than alterations in left ventricular mass or ejection fraction. We report a patient who developed congestive heart failure and pulmonary edema with normal left ventricular function within 1 year of starting pioglitazone therapy. We have to be careful in monitoring all possible side effects during followup when patients are on pioglitazone therapy. PMID:27127397

  8. Increased pulmonary vascular permeability as a cause of re-expansion edema in rabbits

    SciTech Connect

    Pavlin, D.J.; Nessly, M.L.; Cheney, F.W.

    1981-01-01

    In order to study the mechanism(s) underlying re-expansion edema, we measured the concentration of labeled albumin (RISA) in the extravascular, extracellular water (EVECW) of the lung as a measure of pulmonary vascular permeability. Re-expansion edema was first induced by rapid re-expansion of rabbit lungs that had been collapsed for 1 wk by pneumothorax. The RISA in EVECW was expressed as a fraction of its plasma concentration: (RISA)L/(RISA)PL. The volume of EVECW (ml/gm dry lung) was measured using a /sup 24/Na indicator. Results in re-expansion edema were compared with normal control lungs and with oleic acid edema as a model of permeability edema. In re-expanded lungs, EVECW (3.41 +/- SD 1.24 ml/g) and (RISA)L/(RISA)PL 0.84 +/- SD 0.15) were significantly increased when compared with normal control lungs (2.25 +/- 0.41 ml/g and 0.51 +/- 0.20, respectively). Results in oleic acid edema (5.66 +/- 2.23 ml/g and 0.84 +/- 0.23) were similar to re-expansion edema. This suggested that re-expansion edema is due to increased pulmonary vascular permeability caused by mechanical stresses applied to the lung during re-expansion.

  9. Swimming-induced immersion pulmonary edema while snorkeling can be rapidly life-threatening: case reports.

    PubMed

    Cochard, G; Henckes, A; Deslandes, S; Noël-Savina, E; Bedossa, M; Gladu, G; Ozier, Y

    2013-01-01

    It is well known that immersion pulmonary edema can be life-threatening for divers using a self-contained underwater breathing apparatus (scuba). Swimming-induced pulmonary edema in otherwise healthy individuals is not an object of dispute but its real severity is not well known and is probably underestimated. We report two cases of life-threatening acute respiratory distress while swimming and snorkeling, one of which is well documented for swimming-induced pulmonary edema. The interest of these case reports lies in the suddenness of these life-threatening events. Such accidents can mimic a loss of consciousness due to cardiac dysrhythmia and lead to drowning. In the case of swimming-induced pulmonary edema, the prognosis is far better than for a cardiac disorder, but it is also dependent on the efficiency of the supervision. Swimmers, divers, race organizers and supervising physicians should be given knowledge of this pathology and its potentially acute occurrence. Adequate organizational dispositions are mandatory to prevent swimming-induced pulmonary edema-related deaths. PMID:24224285

  10. The Effects of Aquaporin-1 in Pulmonary Edema Induced by Fat Embolism Syndrome

    PubMed Central

    Zhang, Yiwei; Tian, Kun; Wang, Yan; Zhang, Rong; Shang, Jiawei; Jiang, Wei; Wang, Aizhong

    2016-01-01

    This study was designed to investigate the role of aquaporin1 (AQP1) in the pathologic process of pulmonary edema induced by fat embolism syndrome (FES) and the effects of a free fatty acid (FFA) mixture on AQP1 expression in pulmonary microvascular endothelial cells (PMVECs). In vivo, edema was more serious in FES mice compared with the control group. The expression of AQP1 and the wet-to-dry lung weight ratio (W/D) in the FES group were significantly increased compared with the control group. At the same time, inhibition of AQP1 decreased the pathological damage resulting from pulmonary edema. Then we performed a study in vitro to investigate whether AQP1 was induced by FFA release in FES. The mRNA and protein level of AQP1 were increased by FFAs in a dose- and time-dependent manner in PMVECs. In addition, the up-regulation of AQP1 was blocked by the inhibitor of p38 kinase, implicating the p38 MAPK pathway as involved in the FFA-induced AQP1 up-regulation in PMVECs. Our results demonstrate that AQP1 may play important roles in pulmonary edema induced by FES and can be regarded as a new therapy target for treatment of pulmonary edema induced by FES. PMID:27455237

  11. Assessment of lung water by magnetic resonance in three types of pulmonary edema.

    PubMed

    Vinitski, S; Steiner, R M; Wexler, H R; Rifkin, M

    1988-01-01

    Pulmonary edema was produced in nine mongrel dogs by: (a) saline lavage; (b) intravenous injection of oleic acid; and (c) intravenous injection of propranolol followed by ureteral ligation. The resulting effect could be characterized by varying the protein concentration in the pulmonary edema fluid. After induction, all dogs were killed and 20 samples from each passively deflated lung were obtained. Proton T1 and T2 values were measured on a Praxis II NMR spectrometer operated at 10.7 MHz and 37 degrees C. The water content of all samples was determined gravimetrically. Correlation between T1 or T2 measured in vitro and the ratio of wet to dry weight was highly significant (r greater than 0.95, P less than 0.001) in each pathological state. Regression curves indicate that although all three types of pulmonary edema can be characterized by slightly different slopes, the differences are statistically insignificant. Moreover, the slopes of previous studies, when recast in the same format, are very similar to our findings despite the use of different magnetic field strengths and different animal models. This study indicates that quantitation of pulmonary edema is possible, but in vitro measurements do not give useful information for characterizing the etiology of pulmonary edema. PMID:3253274

  12. Swimming-induced immersion pulmonary edema while snorkeling can be rapidly life-threatening: case reports.

    PubMed

    Cochard, G; Henckes, A; Deslandes, S; Noël-Savina, E; Bedossa, M; Gladu, G; Ozier, Y

    2013-01-01

    It is well known that immersion pulmonary edema can be life-threatening for divers using a self-contained underwater breathing apparatus (scuba). Swimming-induced pulmonary edema in otherwise healthy individuals is not an object of dispute but its real severity is not well known and is probably underestimated. We report two cases of life-threatening acute respiratory distress while swimming and snorkeling, one of which is well documented for swimming-induced pulmonary edema. The interest of these case reports lies in the suddenness of these life-threatening events. Such accidents can mimic a loss of consciousness due to cardiac dysrhythmia and lead to drowning. In the case of swimming-induced pulmonary edema, the prognosis is far better than for a cardiac disorder, but it is also dependent on the efficiency of the supervision. Swimmers, divers, race organizers and supervising physicians should be given knowledge of this pathology and its potentially acute occurrence. Adequate organizational dispositions are mandatory to prevent swimming-induced pulmonary edema-related deaths.

  13. Negative pressure pulmonary edema after craniotomy through the endonasal transsphenoidal approach

    PubMed Central

    Ou, Mengchan; Luo, Zhen; Liu, Juan; Yang, Yaoxin; Li, Yu

    2015-01-01

    We describe a case of negative pressure pulmonary edema that occurred in the post-anesthesia care unit in a patient who had undergone transsphenoidal resection of a pituitary adenoma. Negative pressure pulmonary edema is an uncommon complication of general anesthesia. In this case, the patient’s nasal cavity had been filled with surgical packs and she had not become accustomed to breathing through her mouth, in addition to her large tongue and small oropharyngeal cavity, residual effect of anesthetic may resulting in tongue falling which caused airway obstruction. The main causative factor is excessive negative intrathoracic pressure generated by the patient’s spontaneous forced inspiration in an effort to overcome the airway obstruction. It typically developed rapidly, and may be life threatening if not diagnosed promptly. After re-intubation for a short period of mechanical ventilation with positive end expiratory pressure (PEEP 10 cm H2O) and a bolus of intravenous furosemide, the patient recovered rapidly and discharged 8 days after surgery. PMID:26131257

  14. Acute Pulmonary Edema in an Eclamptic Pregnant Patient: A Rare Case of Takotsubo Syndrome

    PubMed Central

    Karamchandani, Kunal; Bortz, Brandon; Vaida, Sonia

    2016-01-01

    Patient: Female, 35 Final Diagnosis: Takotsubo cardiomyopathy Symptoms: Seizures Medication: — Clinical Procedure: Cesarean section Specialty: Critical Care Medicine Objective: Rare co-existance of disease or pathology Background: Acute pulmonary edema in a pregnant patient is associated with significant morbidity and mortality. Takotsubo syndrome, or stress-induced cardiomyopathy, is a rare cause of acute pulmonary edema in a pregnant patient, especially prior to delivery of the fetus. Case Report: We describe a case of a pregnant patient who presented with acute pulmonary edema and eclampsia and was found to have Takotsubo syndrome. To the best of our knowledge, eclampsia as a precipitating factor for Takotsubo syndrome has not been described in literature. Conclusions: Clinicians taking care of pregnant patients should be aware of the potential link between eclampsia and Takotsubo cardiomyopathy. Prompt correction of the precipitating cause along with supportive management as described is the key to a successful outcome. PMID:27658947

  15. Brain natriuretic peptide levels in six basic underwater demolitions/SEAL recruits presenting with swimming induced pulmonary edema (SIPE).

    PubMed

    Shearer, Damon; Mahon, Richard

    2009-01-01

    Swimming induced pulmonary edema (SIPE) is associated with both SCUBA diving and strenuous surface swimming; however, the majority of reported cases and clinically observed cases tend to occur during or after aggressive surface swimming. Capillary stress failure appears to be central to the pathophysiology of this disorder. Regional pulmonary capillaries are exposed to relatively high pressures secondary to increased vascular volume, elevation of pulmonary vascular resistance, and regional differences in perfusion secondary to forces of gravity and high cardiac output. Acute pulmonary edema can be classified as either cardiogenic or noncardiogenic or both. Cardiogenic pulmonary edema occurs when the pulmonary capillary hydrostatic pressure exceeds plasma oncotic pressure. Noncardiogenic pulmonary edema occurs when pulmonary capillary permeability is increased. Given the pathophysiology noted above, SIPE can be described as a cardiogenic pulmonary edema, at least in part, since an increased transalveolar pressure gradient has been implicated in the pathogenesis of SIPE. Brain natriuretic peptide (BNP) is used in the clinical setting to differentiate cardiac from pulmonary sources of dyspnea, specifically to diagnose cardiogenic pulmonary edema. During clinical management, BNP levels were drawn on six BUD/S recruits simultaneously presenting with pulmonary complaints consistent with SIPE, after an extended surface bay swim. This paper analyzes that data after de-identification and reviews the pathophysiology and clinical management of SIPE.

  16. Fumonisin toxicosis in swine: an overview of porcine pulmonary edema and current perspectives.

    PubMed Central

    Haschek, W M; Gumprecht, L A; Smith, G; Tumbleson, M E; Constable, P D

    2001-01-01

    Fumonisin toxicosis in swine was named porcine pulmonary edema (PPE) after outbreaks of a fatal disease in pigs fed Fusarium verticillioides (F. moniliforme)-contaminated corn screenings from the 1989 corn crop in Iowa, Illinois, and Georgia. Pigs that died had severe pulmonary edema, which has not been identified in other species after exposure to fumonisins. The disease has been reproduced experimentally by feeding of naturally contaminated corn, F. verticillioides culture material, and by intravenous administration of fumonisin B1 (FB1). Hepatic lesions consisting of apoptosis, necrosis, and hepatocyte proliferation also are observed. As in other species, alterations in clinical pathology reflect hepatic injury as well as elevated serum cholesterol concentration. In chronic studies, esophageal plaques, hyperplastic hepatic nodules, and right ventricular hypertrophy were found. In pigs, as in other species, fumonisin alters sphingolipid biosynthesis, with the greatest alterations in sphingosine and sphinganine concentrations in kidney, liver, lung, and heart. Our recent studies on fumonisin toxicosis in pigs have focused on immune effects and the pathogenesis of pulmonary edema. The specific immune system was not affected; however, FB1 inhibited phagocytosis and sphingolipid biosynthesis in pulmonary macrophages. Fumonisin induced an accumulation of membranous material in pulmonary capillary endothelial cells; this change appears specific to this cell type and to swine. In short-term cardiovascular studies, fumonisin decreased left ventricular dP/dt(max) (an index of cardiac contractility), mean systemic arterial pressure, heart rate, and cardiac output, and increased mean pulmonary artery pressure and pulmonary artery wedge pressure. These changes are compatible with the inhibition of L-type calcium channels by increased sphingosine and/or sphinganine concentration. Therefore, fumonisin-induced pulmonary edema in swine appears to result from acute left

  17. VA/Q distribution during heavy exercise and recovery in humans: implications for pulmonary edema

    NASA Technical Reports Server (NTRS)

    Schaffartzik, W.; Poole, D. C.; Derion, T.; Tsukimoto, K.; Hogan, M. C.; Arcos, J. P.; Bebout, D. E.; Wagner, P. D.

    1992-01-01

    Ventilation-perfusion (VA/Q) inequality has been shown to increase with exercise. Potential mechanisms for this increase include nonuniform pulmonary vasoconstriction, ventilatory time constant inequality, reduced large airway gas mixing, and development of interstitial pulmonary edema. We hypothesized that persistence of VA/Q mismatch after ventilation and cardiac output subside during recovery would be consistent with edema; however, rapid resolution would suggest mechanisms related to changes in ventilation and blood flow per se. Thirteen healthy males performed near-maximal cycle ergometry at an inspiratory PO2 of 91 Torr (because hypoxia accentuates VA/Q mismatch on exercise). Cardiorespiratory variables and inert gas elimination patterns were measured at rest, during exercise, and between 2 and 30 min of recovery. Two profiles of VA/Q distribution behavior emerged during heavy exercise: in group 1 an increase in VA/Q mismatch (log SDQ of 0.35 +/- 0.02 at rest and 0.44 +/- 0.02 at exercise; P less than 0.05, n = 7) and in group 2 no change in VA/Q mismatch (n = 6). There were no differences in anthropometric data, work rate, O2 uptake, or ventilation during heavy exercise between groups. Group 1 demonstrated significantly greater VA/Q inequality, lower vital capacity, and higher forced expiratory flow at 25-75% of forced vital capacity for the first 20 min during recovery than group 2. Cardiac index was higher in group 1 both during heavy exercise and 4 and 6 min postexercise. However, both ventilation and cardiac output returned toward baseline values more rapidly than did VA/Q relationships. Arterial pH was lower in group 1 during exercise and recovery. We conclude that greater VA/Q inequality in group 1 and its persistence during recovery are consistent with the hypothesis that edema occurs and contributes to the increase in VA/Q inequality during exercise. This is supported by observation of greater blood flows and acidosis and, presumably therefore

  18. Severe preeclampsia, pulmonary edema, and peripartum cardiomyopathy in a primigravida patient.

    PubMed

    Cunningham, Curt; Rivera, Jesse; Spence, Dennis

    2011-06-01

    Peripartum cardiomyopathy (PPCM) is a rare form of heart failure of unknown etiology that is associated with late pregnancy and the early postpartum period. Although the complete pathogenesis of PPCM is not completely understood, the signs and symptoms are identical to those of left ventricular heart failure. The diagnosis of PPCM is made in a parturient only after other causes of heart failure are ruled out. Management of PPCM is similar to that of congestive heart failure with a few exceptions, such as avoiding the use of angiotensin-converting enzyme inhibitors during pregnancy. This report describes the presentation and anesthetic management of a parturient who was admitted with a diagnosis of severe preeclampsia in whom pulmonary edema and heart failure developed, necessitating emergency cesarean delivery under general anesthesia. The patient was subsequently given a diagnosis of PPCM.

  19. Transpulmonary Thermodilution-Based Management of Neurogenic Pulmonary Edema After Subarachnoid Hemorrhage.

    PubMed

    Mutoh, Tatsushi; Kazumata, Ken; Ueyama-Mutoh, Tomoko; Taki, Yasuyuki; Ishikawa, Tatsuya

    2015-11-01

    Neurogenic pulmonary edema (NPE) is a potentially catastrophic but treatable systemic event after subarachnoid hemorrhage (SAH). The development of NPE most frequently occurs immediately after SAH, and the severity is usually self-limiting. Despite extensive research efforts and a breadth of collective clinical experience, accurate diagnosis of NPE can be difficult, and effective hemodynamic treatment options are limited. Recently, a bedside transpulmonary thermodilution device has been introduced that traces physiological patterns consistent with current theories regarding the mechanism (hydrostatic or permeability PE) of NPE. This article provides an overview of the clinical usefulness of the advanced technique for use in the neurointensive care unit for the diagnosis and management of post-SAH NPE.

  20. Diagnosis and treatment of presumptive postobstructive pulmonary edema in a Florida panther (Puma concolor coryi).

    PubMed

    Fiorello, Christine V; Cunningham, Mark W; Cantwell, Shauna L; Levy, Julie K; Neer, Erin M; Conley, Kenneth; Rist, Paul M

    2007-06-01

    A free-ranging, adult male Florida panther (Puma concolor coryi) was immobilized and evaluated for hematuria following routine capture. Prior to anesthetic recovery, the panther was fitted with a telemetry collar. After an initially quiet recovery, the panther began thrashing in the transport cage, and was again immobilized. Pink foam was evident from the nostrils, and crackles were ausculted over the chest, indicating pulmonary edema. Postobstructive pulmonary edema was diagnosed based on history, clinical signs, radiographic evaluation, and blood gas analysis. The animal was treated intensively for several hours with diuretics, oxygen, and manual ventilation. The panther responded rapidly to therapy and was released back into the wild 48 hr after presentation. Postobstructive pulmonary edema, also called negative-pressure pulmonary edema, may be underrecognized in veterinary medicine. In this case, the telemetry collar, in conjunction with anesthetic recovery in a small transport crate, may have contributed to tracheal obstruction. Wildlife veterinarians and biologists should be aware of the risk of airway obstruction when placing tracking collars, and animals should be continuously monitored during anesthetic recovery to ensure the presence of a patent airway.

  1. High altitude pulmonary edema-clinical features, pathophysiology, prevention and treatment.

    PubMed

    Paralikar, Swapnil J

    2012-05-01

    High altitude pulmonary edema (HAPE) is a noncardiogenic pulmonary edema which typically occurs in lowlanders who ascend rapidly to altitudes greater than 2500-3000 m. Early symptoms of HAPE include a nonproductive cough, dyspnoea on exertion and reduced exercise performance. Later, dyspnoea occurs at rest. Clinical features are cyanosis, tachycardia, tachypnoea and elevated body temperature generally not exceeding 38.5°C. Rales are discrete initially and located over the middle lung fields. HAPE mainly occurs due to exaggerated hypoxic pulmonary vasoconstriction and elevated pulmonary artery pressure. It has been observed that HAPE is a high permeability type of edema occurring also due to leaks in the capillary wall ('stress failure'). Slow descent is the most effective method for prevention; in addition, graded ascent and time for acclimatization, low sleeping altitudes, avoidance of alcohol and sleeping pills, and avoidance of exercise are the key to preventing HAPE. Treatment of HAPE consists of immediate improvement of oxygenation either by supplemental oxygen, hyperbaric treatment, or by rapid descent. PMID:23580834

  2. Genetic delivery of bevacizumab to suppress vascular endothelial growth factor-induced high-permeability pulmonary edema.

    PubMed

    Watanabe, Masaki; Boyer, Julie L; Crystal, Ronald G

    2009-06-01

    High-permeability pulmonary edema causing acute respiratory distress syndrome is associated with high mortality. Using a model of intratracheal adenovirus (Ad)-mediated overexpression of human vascular endothelial growth factor (VEGF)-A(165) in mouse lung to induce alveolar permeability and consequent pulmonary edema, we hypothesized that systemic administration of a second adenoviral vector expressing an anti-VEGF antibody (AdalphaVEGFAb) would protect the lung from pulmonary edema. Pulmonary edema was induced in mice by intratracheal administration of AdVEGFA165. To evaluate anti-VEGF antibody therapy, the mice were treated intravenously with AdalphaVEGFAb, an adenoviral vector encoding the light and heavy chains of an anti-human VEGF antibody with the bevacizumab (Avastin) antigen-binding site. Lung VEGF-A(165) and phosphorylated VEGF receptor (VEGFR)-2 levels, histology, lung wet-to-dry weight ratios, and bronchoalveolar lavage fluid (BALF) levels of total protein were assessed. Administration of AdalphaVEGFAb to mice decreased AdVEGFA165-induced levels of human VEGF-A(165) and phosphorylated VEGFR-2 in the lung. Histological analysis of AdalphaVEGFAb-treated mice demonstrated a reduction of edema fluid in the lung tissue that correlated with a reduction of lung wet-to-dry ratios and BALF total protein levels. Importantly, administration of AdalphaVEGFAb 48 hr after induction of pulmonary edema with AdVEGFA165 was effective in suppressing pulmonary edema. Administration of an adenoviral vector encoding an anti-VEGF antibody that is the equivalent of bevacizumab effectively suppresses VEGF-A(165)-induced high-permeability pulmonary edema, suggesting that anti-VEGF antibody therapy may represent a novel therapy for high-permeability pulmonary edema.

  3. Early Embolization for Ruptured Aneurysm in Acute Stage of Subarachnoid Hemorrhage with Neurogenic Pulmonary Edema

    PubMed Central

    Meguro, T.; Rada, K. TE; Hirotsune, N.; Nishino, S.; Asano, T.; Manabe, T.

    2007-01-01

    Summary Four cases of ruptured aneurysmal subarachnoid hemorrhage (SAH) presented with severe neurogenic pulmonary edema (NPE). On admission, two patients were grade IV and two were grade V according to Hunt and Hess grading. All patients needed respiratory management with the assistance of a ventilator. Three of them underwent endovascular treatment for the ruptured aneurysms within three days from onset after ensuring hemodynamic stability. Immediately after the endovascular treatment, lumbar spinal drainage was inserted in all the patients. The pulmonary edema findings disappeared rapidly after the respiratory management. The results were good recovery in two, and moderate disability in two. We concluded that early embolization of ruptured aneurysm and placement of spinal drainage is a satisfactory option for severe SAH with NPE. PMID:20566097

  4. Fatal pulmonary edema in white-tailed deer (Odocoileus virginianus) associated with adenovirus infection.

    PubMed

    Sorden, S D; Woods, L W; Lehmkuhl, H D

    2000-07-01

    Sporadic sudden deaths in adult white-tailed deer occurred from November 1997 through August 1998 on an Iowa game farm. Three of the 4 deer necropsied had severe pulmonary edema, widespread mild lymphocytic vasculitis, and amphophilic intranuclear inclusion bodies in scattered endothelial cells in blood vessels in the lung and abdominal viscera. Immunohistochemistry with bovine adenovirus 5 antisera and transmission electron microscopy demonstrated adenoviral antigen and nucleocapsids, respectively, within endothelial cells. Adenovirus was isolated in cell culture from 1 of the affected deer. The isolate was neutralized by California black-tailed deer adenovirus antiserum. These findings indicate that adenovirus should be considered in the differential diagnosis of both black-tailed and white-tailed deer with pulmonary edema and/or hemorrhagic enteropathy.

  5. Commercial double-indicator-dilution densitometer using heavy water: Evaluation in oleic-acid pulmonary edema

    SciTech Connect

    Leksell, L.G.; Schreiner, M.S.; Sylvestro, A.; Neufeld, G.R. )

    1990-04-01

    We evaluated a commercially available, double-indicator-dilution densitometric system for the estimation of pulmonary extravascular water volume in oleic acid-induced pulmonary edema. Indocyanine green and heavy water were used as the nondiffusible and diffusible tracers, respectively. Pulmonary extravascular water volume, measured with this system, was 67% of the gravimetric value (r = 0.91), which was consistent with values obtained from the radioisotope methods. The measured volume was not influenced by changes in cardiac index over a range of 1 to 4 L.min.m2. This system is less invasive than the thermal-dye technique and has potential for repeated clinical measurements of pulmonary extravascular lung water and cardiac output.

  6. High altitude pulmonary edema among “Amarnath Yatris”

    PubMed Central

    Koul, Parvaiz A.; Khan, Umar Hafiz; Hussain, Tajamul; Koul, Ajaz Nabi; Malik, Sajjad; Shah, Sanaullah; Bazaz, Sajjad Rajab; Rashid, Wasim; Jan, Rafi Ahmad

    2013-01-01

    Background: Annual pilgrimage (Yatra) to the cave shrine of Shri Amarnath Ji’ is a holy ritual among the Hindu devotees of Lord Shiva. Located in the Himalayan Mountain Range (altitude 13,000 ft) in south Kashmir, the shrine is visited by thousands of devotees and altitude sickness is reportedly common. Materials and Methods: More than 600,000 pilgrims visited the cave shrine in 2011 and 2012 with 239 recorded deaths. Thirty one patients with suspected altitude sickness were referred from medical centers en-route the cave to Sher-i-Kashmir Institute of Medical Sciences, a tertiary-care center in capital Srinagar (5,000 ft). The clinical features and the response to treatment were recorded. Results: Thirty-one patients (all lowlanders, 19 male; age 18-60 years, median 41) had presented with acute onset breathlessness of 1-4 days (median 1.9 d) starting within 12-24 h of a rapid ascent; accompanied by cough (68%), headache (8%), dizziness and nausea (65%). Sixteen patients had associated encephalopathy. Clinical features on admission included tachypnea (n = 31), tachycardia (n = 23), bilateral chest rales (n = 29), cyanosis (n = 22) and grade 2-4 encephalopathy. Hypoxemia was demonstrable in 24 cases and bilateral infiltrates on radiologic imaging in 29. Ten patients had evidence of high-altitude cerebral edema. All patients were managed with oxygen, steroids, nifedipine, sildenafil and other supportive measures including invasive ventilation (n = 3). Three patients died due to multiorgan dysfunction. Conclusions: Altitude sickness is common among Amaranath Yatris from the plains and appropriate educational strategies should be invoked for prevention and prompt treatment. PMID:24049253

  7. Genetic adaptation to extreme hypoxia: study of high-altitude pulmonary edema in a three-generation Han Chinese family.

    PubMed

    Lorenzo, V Felipe; Yang, Yingzhong; Simonson, Tatum S; Nussenzveig, Roberto; Jorde, Lynn B; Prchal, Josef T; Ge, Ri-Li

    2009-01-01

    Organismal response to hypoxia is essential for critical regulation of erythropoiesis, other physiological functions, and survival. There is evidence of individual variation in response to hypoxia as some but not all of the affected individuals develop polycythemia, and or pulmonary and cerebral edema. A significant population difference in response to hypoxia exist as many highland Tibetan, Ethiopian, and Andean natives developed adaptive mechanisms to extreme hypoxia. A proportion of non-adapted individuals exposed to high altitude develop pulmonary edema (HAPE), pulmonary hypertension, cerebral edema, and extreme polycythemia. The isolation of causative gene(s) responsible for HAPE and other extreme hypoxia complications would provide a rational basis for specific targeted therapy of HAPE, allow its targeted prevention for at-risk populations, and clarify the pathophysiology of other hypoxic maladaptations. The only suggested genetic linkage among unrelated individuals with HAPE has been with endothelial nitric oxide synthase (eNOS) gene. Here we describe a family with multiple members affected with HAPE in three generations. Families with multiple affected members with HAPE have not been described. We first ruled out linkage of HAPE with the eNOS gene. We then performed an analysis of the whole genome using high-density SNP arrays (Affymetrix v5.0) and, assuming a single gene causation of HAPE, ruled out linkage with 34 other candidate genes. Only the HIF2A haplotype was shared by individuals who exhibit the HAPE phenotype, and work on its possible causative role in HAPE is in progress. The small size of our family does not provide sufficient power for a conclusive analysis of linkage. We hope that collaboration with other investigators with access to more HAPE patients will lead to the identification of gene(s) responsible for HAPE and possibly other maladaptive hypoxic complications. PMID:19481479

  8. Morphometric analysis of oleic acid-induced permeability pulmonary edema: correlation with gravimetric lung water.

    PubMed

    Darien, B J; Saban, M R; Hart, A P; MacWilliams, P S; Clayton, M K; Kruse-Elliott, K T

    1997-07-01

    The technique used most commonly to quantitate pulmonary edema in in vivo animal models is postmortem gravimetric analysis (wet:dry) ratio. To determine whether lung water can be quantitated morphometrically, as accurately as by the commonly used gravimetric analysis, perivascular edema (cuff) area to vessel area ratio was correlated to wet:dry ratio. Anesthetized pigs were given either oleic acid (20 mg/kg/h, intravenously) or physiologic saline. At 4 h, lungs were excised and cuff:vessel and wet:dry ratio analysis was performed. The intermediate lobe was clamped across its main stem bronchus to maintain peak inspiratory inflation, excised, frozen in liquid nitrogen, and stored at -70 degrees C until cryostat sectioning and quantification of perivascular interstitial edema (cuff) area. Gravimetric analysis (wet:dry ratio) was performed on the remaining lung. Mean cuff:vessel and wet:dry analyzes showed that lung water increased significantly (p < .01) in the oleic-acid treated group (4.9 +/- .22 and 6.78 +/- .47, respectively), compared with the saline group (.03 +/- .02 and 2.55 +/- .27, respectively). The correlation coefficient between mean cuff:vessel and wet:dry ratios was .86 (p = .0016). This study demonstrates that cuff:vessel ratio analysis can be used to identify the distribution of edema fluid versus vessel diameter, and seems to be as effective a technique as gravimetric analysis to quantitate lung water changes in acute lung injury models. Moreover cuff:vessel ratio analysis can differentiate modest changes in pulmonary edema by direct quantitation, an important end-point not provided by wet:dry analysis. Therefore, it may be a more sensitive technique when investigating therapeutic interventions in in vivo models of acute lung injury.

  9. Case Report: Bilateral reexpansion pulmonary edema following treatment of a unilateral hemothorax

    PubMed Central

    de Wolf, Steven P; Deunk, Jaap; Cornet, Alexander D; Elbers, Paul WG

    2014-01-01

    Bilateral re-expansion pulmonary edema (RPE) is an extremely rare entity. We report the unique case of bilateral RPE following a traumatic, unilateral hemopneumothorax in a young healthy male. Bilateral RPE occurred only one hour after drainage of a unilateral hemopneumothorax. The patient was treated with diuretics and supplemental oxygen. Diagnosis was confirmed by excluding other causes, using laboratory findings, chest radiography, pulmonary and cardiac ultrasound and high resolution computed tomography. His recovery was uneventful. The pathophysiology of bilateral RPE is not well known. Treatment is mainly supportive and consists of diuretics, mechanical ventilation, inotropes and steroids. In case of a pulmonary deterioration after the drainage of a traumatic pneumothorax, bilateral RPE should be considered after exclusion of more common causes of dyspnea. PMID:25713699

  10. Reversible myocardial dysfunction and clinical outcome in scuba divers with immersion pulmonary edema.

    PubMed

    Gempp, Emmanuel; Louge, Pierre; Henckes, Anne; Demaistre, Sebastien; Heno, Phillipe; Blatteau, Jean-Eric

    2013-06-01

    Immersion pulmonary edema in scuba divers is a rare disorder that tends to recur and can be potentially fatal, even in the absence of underlying cardiac disease. Anecdotal cases of reversible myocardial dysfunction have been described in this setting, but little is known of its pathogenesis. The purpose of the present study was to determine the clinical outcomes and the determinants associated with this condition. The data from 54 consecutive divers admitted for acute immersion pulmonary edema during a 5.5-year period were retrospectively studied. A diagnosis of myocardial dysfunction was established by the presence of elevated cardiac troponin T levels, coupled with electrocardiographic changes and/or wall motion abnormalities on the echocardiogram. The demographic, clinical, biologic, and diving characteristics were tested as potential predictors of this disorder. All the patients had complete resolution of symptoms within 72 hours, but 3 required intensive ventilation or hemodynamic support at admission. Reversible myocardial dysfunction was observed in 28% and was associated more with age >50 years (odds ratio [OR] 5.5, 95% confidence interval [CI] 1.5 to 21, p = 0.013), hypertension (OR 8.2, 95% CI 2.1 to 32, p = 0.002), diabetes (OR 22.1, 95% CI 1.1 to 458; p = 0.002), and release of natriuretic peptides (OR 9.1, 95% CI 2.4 to 35, p = 0.001). Follow-up investigations at 1 month were obtained for 49 patients and revealed a significant number of patients with occult hypertension. In conclusion, reversible myocardial dysfunction is not uncommon in divers with immersion pulmonary edema. The short-term overall prognosis is not adversely altered, but severe heart failure with a fatal outcome is unpredictable. Close monitoring of older divers with latent cardiovascular risk factors is warranted.

  11. Hemorrhagic pulmonary edema associated with meat tenderizer treatment for esophageal meat impaction.

    PubMed

    Hall, M L; Huseby, J S

    1988-09-01

    We describe a case of acute hemorrhagic pulmonary edema caused by aspiration of Adolph's meat tenderizer, used in an attempt to relieve an esophageal meat impaction. We performed an animal experiment in which bronchial instillation of a similar solution reproduced the clinical findings in our patient. This is a previously unreported and potentially lethal complication of a therapy that has never been submitted to clinical trials. We recommend against the use of this therapy for patients with complete esophageal obstruction or in those otherwise at risk for aspiration. PMID:3409751

  12. Nicardipine-induced acute pulmonary edema: a rare but severe complication of tocolysis.

    PubMed

    Serena, Claire; Begot, Emmanuelle; Cros, Jérôme; Hodler, Charles; Fedou, Anne Laure; Nathan-Denizot, Nathalie; Clavel, Marc

    2014-01-01

    We report four cases of acute pulmonary edema that occurred during treatment by intravenous tocolysis using nicardipine in pregnancy patients with no previous heart problems. Clinical severity justified hospitalization in intensive care unit (ICU) each time. Acute dyspnea has begun at an average of 63 hours after initiation of treatment. For all patients, the first diagnosis suspected was pulmonary embolism. The patients' condition improved rapidly with appropriate diuretic treatment and by modifying the tocolysis. The use of intravenous nicardipine is widely used for tocolysis in France even if its prescription does not have a marketing authorization. The pathophysiological mechanisms of this complication remain unclear. The main reported risk factors are spontaneous preterm labor, multiple pregnancy, concomitant obstetrical disease, association with beta-agonists, and fetal lung maturation corticotherapy. A better knowledge of this rare but serious adverse event should improve the management of patients. Nifedipine or atosiban, the efficiency of which tocolysis was also studied, could be an alternative. PMID:25215245

  13. An Unusual Transudative Pleural Effusion Succeeded by Pulmonary and Brain Edema and Death

    PubMed Central

    Mortazavimoghaddam, Sayyed Gholam Reza; Riasi, H. R.

    2012-01-01

    Here we report a 22-year old woman with massive and bilateral transudative effusion succeeded by pulmonary edema and brain edema and death. Investigations for systemic disorders were negative. Exacerbation of dyspnea after intravenous fluid infusion was a main problem. As effusion was refractory to medical treatment, the patient was referred for surgical pleurodesis and bilateral surgical pleurodesis were done separately. Postsurgically, dyspnea exacerbation occurred after each common cold infection. Vertigo and high intracranial pressure were also a problem postsurgically. CSF pressure was 225 mm/H2O. Therapeutic lumbar puncture was done in two sequential weeks, and the patient was on acetazolamide 250 mg/trivise a day. Despite the medical treatment, progressive dyspnea, headache, and high intracranial pressure followed by death nine months after pleurodesis. As there is a gradient of pressure between pleura and CSF, after pleurodesis brain edema must be a consequence of inversing this gradient. In conclusion, when there are any abnormalities about fluid volume or pressure in any of these cavities, we have to study other cavities. PMID:22934227

  14. Lethal factor, but not edema factor, is required to cause fatal anthrax in cynomolgus macaques after pulmonary spore challenge.

    PubMed

    Hutt, Julie A; Lovchik, Julie A; Drysdale, Melissa; Sherwood, Robert L; Brasel, Trevor; Lipscomb, Mary F; Lyons, C Rick

    2014-12-01

    Inhalational anthrax is caused by inhalation of Bacillus anthracis spores. The ability of B. anthracis to cause anthrax is attributed to the plasmid-encoded A/B-type toxins, edema toxin (edema factor and protective antigen) and lethal toxin (lethal factor and protective antigen), and a poly-d-glutamic acid capsule. To better understand the contribution of these toxins to the disease pathophysiology in vivo, we used B. anthracis Ames strain and isogenic toxin deletion mutants derived from the Ames strain to examine the role of lethal toxin and edema toxin after pulmonary spore challenge of cynomolgus macaques. Lethal toxin, but not edema toxin, was required to induce sustained bacteremia and death after pulmonary challenge with spores delivered via bronchoscopy. After intravenous challenge with bacilli to model the systemic phase of infection, lethal toxin contributed to bacterial proliferation and subsequent host death to a greater extent than edema toxin. Deletion of protective antigen resulted in greater loss of virulence after intravenous challenge with bacilli than deletion of lethal toxin or edema toxin alone. These findings are consistent with the ability of anti-protective antigen antibodies to prevent anthrax and suggest that lethal factor is the dominant toxin that contributes to the escape of significant numbers of bacilli from the thoracic cavity to cause anthrax after inhalation challenge with spores.

  15. Acute pulmonary edema following liposuction due to heart failure and atypical pneumonia.

    PubMed

    Wollina, Uwe; Graf, Andreas; Hanisch, Volkmar

    2015-05-01

    Microcannular liposuction in tumescent anesthesia is the most effective treatment for painful lipedema. Tumescent anesthesia is an established and safe procedure in local analgesia when performed according to guidelines. Major adverse effects are rare. In patients with advanced lipedema, however, the commonly presented comorbidities bear additional risks.We report on post-surgical acute pulmonary edema after tumescent liposuction according to guidelines in a 52-year-old female patient with lipedema of the legs. We discuss in detail possible scenarios that might be involved in such emergency. In the present case the most likely was a retarded community acquired atypical pneumonia with aggravation of pre-existent comorbidities.A combined treatment with intravenous b-lactam antibiosis, positive pressure ventilation, and continuous venovenous hemodialysis and filtration resulted in complete remission in a couple of days. In conclusion, tumescent liposuction of advanced lipedema patients should only be performed in well-trained centers with sufficient infrastructure.

  16. Glycogen accumulation in alveolar type II cells in 3-methylindole--induced pulmonary edema in goats.

    PubMed Central

    Atwal, O. S.; Bray, T. M.

    1981-01-01

    The present study shows that intravenous infusion of 3-methylindole (3MI) induced acute pulmonary edema in goats. Edematous changes were seen in the alveoli and the interalveolar interstitium. At 72 hours after treatment, an accumulation of glycogen that had a pathognomonic appearance of alpha particles was observed in the alveolar Type II cells. A rich accumulation of glycogen particles and defective lamellar bodies containing triglycerides were the significant morphologic changes in the alveolar Type II cells. These findings suggest that massive glycogen deposition in the alveolar Type II cells is a defect that might interfere with surfactant production, further complicating the disease process. Images Figure 1 Figure 2 Figure 3 Figure 4 PMID:6274198

  17. Raised HIF1α during normoxia in high altitude pulmonary edema susceptible non-mountaineers

    PubMed Central

    Soree, Poonam; Gupta, Rajinder K.; Singh, Krishan; Desiraju, Koundinya; Agrawal, Anurag; Vats, Praveen; Bharadwaj, Abhishek; Baburaj, T. P.; Chaudhary, Pooja; Singh, Vijay K.; Verma, Saroj; Bajaj, Amir Chand; Singh, Shashi Bala

    2016-01-01

    High altitude pulmonary edema (HAPE) susceptibility is associated with EGLN1 polymorphisms, we hypothesized that HAPE-susceptible (HAPE-S, had HAPE episode in past) subjects may exhibit abnormal HIF1α levels in normoxic conditions. We measured HIF1α levels in HAPE-S and HAPE resistant (HAPE-R, no HAPE episode) individuals with similar pulmonary functions. Hemodynamic responses were also measured before and after normobaric hypoxia (Fi02 = 0.12 for 30 min duration at sea level) in both groups. . HIF1α was higher in HAPE-S (320.3 ± 267.5 vs 58.75 ± 33.88 pg/ml, P < 0.05) than HAPE-R, at baseline, despite no significant difference in baseline oxygen saturations (97.7 ± 1.7% and 98.8 ± 0.7). As expected, HAPE-S showed an exaggerated increase in pulmonary artery pressure (27.9 ± 6 vs 19.3 ± 3.7 mm Hg, P < 0.05) and a fall in peripheral oxygen saturation (66.9 ± 11.7 vs 78.7 ± 3.8%, P < 0.05), when exposed to hypoxia. HIF1α levels at baseline could accurately classify members of the two groups (AUC = 0.87). In a subset of the groups where hemoglobin fractions were additionally measured to understand the cause of elevated hypoxic response at baseline, two of four HAPE-S subjects showed reduced HbA. In conclusion, HIF 1 α levels during normoxia may represent an important marker for determination of HAPE susceptibility. PMID:27210110

  18. Elevated levels of plasminogen activator inhibitor-1 in pulmonary edema fluid are associated with mortality in acute lung injury.

    PubMed

    Prabhakaran, Priya; Ware, Lorraine B; White, Kimberly E; Cross, Michael T; Matthay, Michael A; Olman, Mitchell A

    2003-07-01

    The alveolar fibrinolytic system is altered in acute lung injury (ALI). Levels of the fibrinolytic protease inhibitor, plasminogen activator inhibitor-1 (PAI-1), are too low in bronchoalveolar lavage to address its prognostic significance. This study was performed to assess whether PAI-1 antigen in undiluted pulmonary edema fluid levels can identify patients with ALI and predict their outcome. PAI-1 antigen levels in both plasma and edema fluid were higher in ALI compared with hydrostatic edema, and edema fluid PAI-1 values identified those with ALI with high sensitivity and specificity. Both the high plasma and edema fluid PAI-1 antigen values were associated with a higher mortality rate and fewer days of unassisted ventilation in patients with ALI. Differences in PAI-1 activity were concordant with levels of PAI-1 antigen. Although the fibrin-derived alveolar D-dimer levels were strikingly similar in both groups, ALI patients had a higher relative proportion of D-monomer. In conclusion, PAI-1 levels in edema fluid and plasma identify those with ALI that have a poor prognosis. The data indicate that fibrin turnover in early ALI is a consequence of a rapid fibrinogen influx and fractional fibrinolytic inhibition.

  19. The lung at high altitude: bronchoalveolar lavage in acute mountain sickness and pulmonary edema.

    PubMed

    Schoene, R B; Swenson, E R; Pizzo, C J; Hackett, P H; Roach, R C; Mills, W J; Henderson, W R; Martin, T R

    1988-06-01

    High-altitude pulmonary edema (HAPE), a severe form of altitude illness that can occur in young healthy individuals, is a noncardiogenic form of edema that is associated with high concentrations of proteins and cells in bronchoalveolar lavage (BAL) fluid (Schoene et al., J. Am. Med. Assoc. 256: 63-69, 1986). We hypothesized that acute mountain sickness (AMS) in which gas exchange is impaired to a milder degree is a precursor to HAPE. We therefore performed BAL with 0.89% NaCl by fiberoptic bronchoscopy in eight subjects at 4,400 m (barometric pressure = 440 Torr) on Mt. McKinley to evaluate the cellular and biochemical responses of the lung at high altitude. The subjects included one healthy control (arterial O2 saturation = 83%), three climbers with HAPE (mean arterial O2 saturation = 55.0 +/- 5.0%), and four with AMS (arterial O2 saturation = 70.0 +/- 2.4%). Cell counts and differentials were done immediately on the BAL fluid, and the remainder was frozen for protein and biochemical analysis to be performed later. The results of this and of the earlier study mentioned above showed that the total leukocyte count (X10(5)/ml) in BAL fluid was 3.5 +/- 2.0 for HAPE, 0.9 +/- 4.0 for AMS, and 0.7 +/- 0.6 for controls, with predominantly alveolar macrophages in HAPE. The total protein concentration (mg/dl) was 616.0 +/- 3.3 for HAPE, 10.4 +/- 8.3 for AMS, and 12.0 +/- 3.4 for controls, with both large- (immunoglobulin M) and small- (albumin) molecular-weight proteins present in HAPE.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:3403445

  20. [Pulmonary edema in a child following laryngospasm triggered by a laryngeal mask airway during emergence from anesthesia].

    PubMed

    Nishikawa, M; Tajima, K; Hoshi, T; Mizutani, T; Toyooka, H

    2001-03-01

    A 9-year-old boy underwent biopsy of the tumor at the external auditory meatus under general anesthesia with a laryngeal mask airway(LMA). During emergence from anesthesia, laryngospasm with marked inspiratory effort and cyanosis occurred. The LMA was removed and the patient was orotracheally intubated following vecuronium administration. In spite of controlled ventilation with 100% oxygen, oxygen saturation remained at low 90s and pink frothy sputum appeared in the tracheal tube. We suspected negative pressure pulmonary edema and treated him with mechanical ventilation with positive end-expiratory pressure. Seventeen hours later the pink frothy sputum decreased and he was extubated. Laryngospasm during emergence from anesthesia with an LMA can induce negative pressure pulmonary edema, especially in pediatric patients.

  1. Effects of hyperoxia on ventilation and pulmonary hemodynamics during immersed prone exercise at 4.7 ATA: possible implications for immersion pulmonary edema

    PubMed Central

    Peacher, Dionne F.; Pecorella, Shelly R. H.; Freiberger, John J.; Natoli, Michael J.; Schinazi, Eric A.; Doar, P. Owen; Boso, Albert E.; Walker, Aaron J.; Gill, Matthew; Kernagis, Dawn; Uguccioni, Donna

    2010-01-01

    Immersion pulmonary edema (IPE) can occur in otherwise healthy swimmers and divers, likely because of stress failure of pulmonary capillaries secondary to increased pulmonary vascular pressures. Prior studies have revealed progressive increase in ventilation [minute ventilation (V̇e)] during prolonged immersed exercise. We hypothesized that this increase occurs because of development of metabolic acidosis with concomitant rise in mean pulmonary artery pressure (MPAP) and that hyperoxia attenuates this increase. Ten subjects were studied at rest and during 16 min of exercise submersed at 1 atm absolute (ATA) breathing air and at 4.7 ATA in normoxia and hyperoxia [inspired PO2 (PiO2) 1.75 ATA]. V̇e increased from early (E, 6th minute) to late (L, 16th minute) exercise at 1 ATA (64.1 ± 8.6 to 71.7 ± 10.9 l/min BTPS; P < 0.001), with no change in arterial pH or Pco2. MPAP decreased from E to L at 1 ATA (26.7 ± 5.8 to 22.7 ± 5.2 mmHg; P = 0.003). V̇e and MPAP did not change from E to L at 4.7 ATA. Hyperoxia reduced V̇e (62.6 ± 10.5 to 53.1 ± 6.1 l/min BTPS; P < 0.0001) and MPAP (29.7 ± 7.4 to 25.1 ± 5.7 mmHg, P = 0.002). Variability in MPAP among subjects was wide (range 14.1–42.1 mmHg during surface and depth exercise). Alveolar-arterial Po2 difference increased from E to L in normoxia, consistent with increased lung water. We conclude that increased V̇e at 1 ATA is not due to acidosis and is more consistent with respiratory muscle fatigue and that progressive pulmonary vascular hypertension does not occur during prolonged immersed exercise. Wide variation in MPAP among healthy subjects is consistent with variable individual susceptibility to IPE. PMID:20431020

  2. Bolus intravenous 0.9% saline, but not 4% albumin or 5% glucose, causes interstitial pulmonary edema in healthy subjects.

    PubMed

    Bihari, Shailesh; Wiersema, Ubbo F; Schembri, David; De Pasquale, Carmine G; Dixon, Dani-Louise; Prakash, Shivesh; Lawrence, Mark D; Bowden, Jeffrey J; Bersten, Andrew D

    2015-10-01

    Rapid intravenous (iv) infusion of 0.9% saline alters respiratory mechanics in healthy subjects. However, the relative cardiovascular and respiratory effects of bolus iv crystalloid vs. colloid are unknown. Six healthy male volunteers were given 30 ml/kg iv 0.9% saline, 4% albumin, and 5% glucose at a rate of 100 ml/min on 3 separate days in a double-blinded, randomized crossover study. Impulse oscillometry, spirometry, lung volumes, diffusing capacity (DLCO), and blood samples were measured before and after fluid administration. Lung ultrasound B-line score (indicating interstitial pulmonary edema) and Doppler echocardiography indices of cardiac preload were measured before, midway, immediately after, and 1 h after fluid administration. Infusion of 0.9% saline increased small airway resistance at 5 Hz (P = 0.04) and lung ultrasound B-line score (P = 0.01) without changes in Doppler echocardiography measures of preload. In contrast, 4% albumin increased DLCO, decreased lung volumes, and increased the Doppler echocardiography mitral E velocity (P = 0.001) and E-to-lateral/septal e' ratio, estimated blood volume, and N-terminal pro B-type natriuretic peptide (P = 0.01) but not lung ultrasound B-line score, consistent with increased pulmonary blood volume without interstitial pulmonary edema. There were no significant changes with 5% glucose. Plasma angiopoietin-2 concentration increased only after 0.9% saline (P = 0.001), suggesting an inflammatory mechanism associated with edema formation. In healthy subjects, 0.9% saline and 4% albumin have differential pulmonary effects not attributable to passive fluid filtration. This may reflect either different effects of these fluids on active signaling in the pulmonary circulation or a protective effect of albumin.

  3. All-transretinoic acid (ATRA) treatment-related pancarditis and severe pulmonary edema in a child with acute promyelocytic leukemia.

    PubMed

    Işık, Pamir; Çetin, Ilker; Tavil, Betul; Azik, Fatih; Kara, Abdurrahman; Yarali, Nese; Tunc, Bahattin

    2010-11-01

    Use of all-transretinoic acid (ATRA) with other chemotherapeutic agents in the treatment of acute promyelocytic leukemia (APL) has been shown to cause the differentiation of abnormally granulated specific blast cells into mature granulocytes by acting on the t(15; 17) fusion gene product. The complete remission rate is increased and survival time is prolonged in APL patients who receive chemotherapy plus ATRA, whereas ATRA syndrome and other ATRA-related adverse effects including pseudo tumor cerebri, headache, severe bone pain, mucosal and skin dryness, hypercholesterolemia, and cheilitis may be observed especially during induction phase of the treatment. In this paper, we report a 9-year-old girl with APL who developed pancarditis while receiving the APL-93 treatment protocol. In our patient, endocarditis and myocarditis were initially determined after ATRA treatment during the induction part of the protocol. All findings disappeared after ATRA was discontinued. When ATRA was readministered in the maintenance part of the treatment protocol, she developed pancarditis and severe pulmonary edema. As her symptoms decreased dramatically with the discontinuation of ATRA and the initiation of steroid treatment, the clinical picture strongly suggested the ATRA treatment as the causative factor. To the best of our knowledge, this clinical picture of pancarditis secondary to ATRA treatment has not been reported earlier in the English literature. PMID:20881874

  4. Genetic differences and aberrant methylation in the apelin system predict the risk of high-altitude pulmonary edema

    PubMed Central

    Mishra, Aastha; Kohli, Samantha; Dua, Sanchi; Thinlas, Tashi; Mohammad, Ghulam; Pasha, M. A. Qadar

    2015-01-01

    Hypoxia-inducible factor stimulates the expression of apelin, a potent vasodilator, in response to reduced blood arterial oxygen saturation. However, aberrations in the apelin system impair pulmonary vascular function, potentially resulting in the development of high-altitude (HA)-related disorders. This study aimed to elucidate the genetic and epigenetic regulation of apelin, apelin receptor (APLNR), and endothelial nitric oxide synthase (NOS3) in HA adaptation and HA pulmonary edema (HAPE). A genome-wide association study and sequencing identified variants of apelin, APLNR, and NOS3 that were validated in a larger sample size of HAPE-patients (HAPE-p), HAPE-free controls (HAPE-f), and healthy highland natives (HLs). Apelin-13 and nitrite levels and apelin and NOS3 expression were down-regulated in HAPE-p (P < 0.001). Among the several studied polymorphisms, apelin rs3761581, rs2235312, and rs3115757; APLNR rs11544374 and rs2282623; and NOS3 4b/4a, rs1799983, and rs7830 were associated with HAPE (P < 0.03). The risk allele rs3761581G was associated with a 58.6% reduction in gene expression (P = 0.017), and the risk alleles rs3761581G and rs2235312T were associated with low levels of apelin-13 and nitrite (P < 0.05). The latter two levels decreased further when both of these risk alleles were present in the patients (P < 0.05). Methylation of the apelin CpG island was significantly higher in HAPE-p at 11.92% than in HAPE-f and HLs at ≤7.1% (P < 0.05). Moreover, the methylation effect was 9% stronger in the 5′ UTR and was associated with decreased apelin expression and apelin-13 levels. The rs3761581 and rs2235312 polymorphisms and methylation of the CpG island influence the expression of apelin in HAPE. PMID:25918383

  5. Pulmonary edema following generalized tonic clonic seizures is directly associated with seizure duration

    PubMed Central

    Kennedy, Jeffrey D.; Hardin, Kimberly A.; Parikh, Palak; Li, Chin-Shang; Seyal, Masud

    2015-01-01

    Purpose Postictal pulmonary edema (PPE) is almost invariably present in human and animal cases of sudden unexpected death in epilepsy (SUDEP) coming to autopsy. PPE may be a contributing factor in SUDEP. The incidence of postictal PPE is unknown. We retrospectively investigated PPE following generalized tonic clonic seizures (GTCS) in the epilepsy monitoring unit. Methods Chest X-Rays (CXR) following each GTCS were obtained in 24 consecutive patients. Relationship of CXR abnormality to seizure duration, ictal/postictal oxygen desaturation (SpO2), apnea and presence of postictal generalized EEG suppression (PGES) was investigated using logistic regression. Results Eleven of 24 patients had CXR abnormalities following a GTCS. In these 11 patients, 22 CXR were obtained and abnormalities were present in 15 CXR. Abnormalities included PPE in 7 patients, of which 2 also had focal infiltrates. In 4 patients focal infiltrates were present without PPE. There was no significant difference in mean time to CXR (225 min) following GTCS in the abnormal CXR group versus the normal group of patients (196 min). Mean preceding seizure duration was longer (p=0.002) in GTCS with abnormal CXR (259.7 sec) versus GTCS with normal CXR (101.2 sec). Odds-ratio for CXR abnormality was 20.46 (p=0.006) with seizure duration greater than 100 sec versus less than 100 sec. On multivariable analysis, only the seizure duration was a significant predictor of CXR abnormality (p=0.015). Conclusions Radiographic abnormalities are not uncommon following GTCS. The presence of CXR abnormality is significantly associated with the duration of the preceding GTCS. Severe, untreated PPE may be relevant to the pathophysiology of SUDEP. PMID:25844030

  6. A neonate with hand, foot, and mouth disease complicated with brainstem encephalitis and pulmonary edema:A complete recovery.

    PubMed

    Guo, Shi-Jie; Wang, Dong-Xuan; Dai, Chun-Lai; Wu, Hui

    2014-07-01

    Hand, foot, and mouth disease (HFMD) with serious complications and fatal cases have been reported over the last decade worldwide. The authors report a rare case of HFMD in a neonate complicated with brainstem encephalitis and pulmonary edema. She had fever, lethargy, dyspnea. Physical examination revealed shock signs, fine rales on both lungs, absent Moro reflex. The patient had a rapidly progressive course with seizures, coma, no spontaneous breathing, chemosis. There were some vesicles on left sole and red maculopapular rashes on perianal skin. She had a history of exposure to HFMD. Fecal sample was positive for EV71 RNA by real-time PCR. Chest X-rays showed bilateral pulmonary infiltrates. MRI of the brain showed significant hypointensity in the brainstem on T1WI and hyperintensity on T2WI. She recovered well. This case highlights severe HFMD in neonates is rare. Medical history and physical examination are important in making diagnosis. PMID:25097545

  7. A neonate with hand, foot, and mouth disease complicated with brainstem encephalitis and pulmonary edema:A complete recovery.

    PubMed

    Guo, Shi-Jie; Wang, Dong-Xuan; Dai, Chun-Lai; Wu, Hui

    2014-07-01

    Hand, foot, and mouth disease (HFMD) with serious complications and fatal cases have been reported over the last decade worldwide. The authors report a rare case of HFMD in a neonate complicated with brainstem encephalitis and pulmonary edema. She had fever, lethargy, dyspnea. Physical examination revealed shock signs, fine rales on both lungs, absent Moro reflex. The patient had a rapidly progressive course with seizures, coma, no spontaneous breathing, chemosis. There were some vesicles on left sole and red maculopapular rashes on perianal skin. She had a history of exposure to HFMD. Fecal sample was positive for EV71 RNA by real-time PCR. Chest X-rays showed bilateral pulmonary infiltrates. MRI of the brain showed significant hypointensity in the brainstem on T1WI and hyperintensity on T2WI. She recovered well. This case highlights severe HFMD in neonates is rare. Medical history and physical examination are important in making diagnosis.

  8. [Anesthetic Management of a Parturient with Eclampsia, Posterior Reversible Encephalopathy Syndrome and Pulmonary Edema due to Pregnancy-induced Hypertension].

    PubMed

    Aida, Junko; Okutani, Hiroai; Oda, Yutaka; Okutani, Ryu

    2015-08-01

    A 27-year-old woman with mental retardation was admitted to a nearby hospital for an abrupt onset of seizure. Physical examination revealed remarkable hypertension and pregnancy with estimated gestational age of 28th week. Severe pulmonary edema and hypoxia led to a diagnosis of pregnancy-induced hypertension (PIH) accompanied by eclampsia. She was orotracheally intubated because of refractory seizure and hypoxemia, and transferred to our hospital for further treatment. Besides severe hypoxia and hypercapnea, an enhanced lesion was detected in the left posterior cerebrum by brain MRI. No abnormal findings were detected in the fetus, with heart rate of 150 beats x min. She was diagnosed with posterior reversible encephalopathy syndrome (PRES) caused by PIH and emergency cesarean section under general anesthesia was scheduled. A male newborn was delivered with Apgar score of 1/4 (1/5 min), followed by starting continuous infusion of nicardipine for controlling hypertension. Chest X-P on completion of surgery revealed remarkably alleviated pulmonary edema. She received intensive treatment and continued positive pressure ventilation for four days after delivery. She recovered with no neurological deficits and her child was well without any complications. PMID:26442424

  9. Management of three cardiogenic pulmonary edemas occurring in a patient scheduled for left ventricular assist device implantation: indicators for determining left ventricular assist device pump speed.

    PubMed

    Toyama, Hiroaki; Takei, Yusuke; Saito, Kazutomo; Ota, Takahisa; Kurotaki, Kenji; Ejima, Yutaka; Matsuura, Takeshi; Akiyama, Masatoshi; Saiki, Yoshikatsu; Yamauchi, Masanori

    2016-08-01

    A male patient with Marfan syndrome underwent aortic root replacement and developed left ventricular (LV) failure. Four years later, he underwent aortic arch and aortic valve replacement. Thereafter, his LV failure progressed, and cardiogenic pulmonary edema (CPE) appeared, which we treated with extracorporeal LV assist device (LVAD) placement. Three months later, the patient developed aspiration pneumonia, which caused hyperdynamic right ventricle (RV) and CPE. We treated by changing his pneumatic LVAD to a high-flow centrifugal pump. A month later, he underwent thoracoabdominal aortic replacement. After four weeks, he developed septic thrombosis and LVAD failure, which caused CPE. We treated with LVAD circuit replacement and an additional membrane oxygenator. Four months later, he underwent DuraHeart(®) implantation. During this course, pulmonary artery wedge pressure (PAWP) varied markedly. Additionally, systolic pulmonary artery pressure (sPAP), left atrial diameter (LAD), RV end-diastolic diameter (RVEDD) and estimated RV systolic pressure (esRVP) changed with PAWP changes. In this patient, LV failure and hyperdynamic RV caused the CPEs, which we treated by adjusting the LVAD output to the RV output. Determining LVAD output, RV function and LV end-diastolic diameter are typically referred, and PAWP, LAD, RVEDD, and sPAP could be also referred.

  10. Salmonella myocarditis in a young adult patient presenting with acute pulmonary edema, rhabdomyolysis, and multi-organ failure.

    PubMed

    Al-aqeedi, Rafid Fayadh; Kamha, Ahmed; Al-aani, Fuad K; Al-ani, Ahmed A

    2009-12-01

    The mortality and morbidity of salmonella infections is seriously underestimated. Salmonella myocarditis is an unusual complication of salmonella sepsis in adults. Cases that do occur may be associated with high morbidity and mortality. We present a rare case of salmonella myocarditis with multi-organ failure in a previously healthy young adult man who was brought to the emergency room with fever, diarrhea, shortness of breath, and altered sensorium, discovered to have acute pulmonary edema and respiratory compromise for which he was assisted with mechanical ventilation for 8 days. Blood culture grew Salmonella typhi. Biochemically he exhibited myocardial, hepatic, and muscular enzymatic surge with renal failure, features of rhabdomyolysis, and disseminated intravascular coagulation. The patient showed a progressive improvement on treatment with ceftriaxone for 2 weeks in addition to decongestive therapy. He was discharged in good condition afterward. PMID:19944325

  11. Role of PiCCO monitoring for the integrated management of neurogenic pulmonary edema following traumatic brain injury: A case report and literature review

    PubMed Central

    Lin, Xiaoping; Xu, Zhijun; Wang, Pengfei; Xu, Yan; Zhang, Gensheng

    2016-01-01

    Neurogenic pulmonary edema (NPE) is occasionally observed in patients with traumatic brain injury (TBI); however, this condition is often underappreciated. NPE is frequently misdiagnosed due to its atypical clinical performance, thus delaying appropriate treatment. A comprehensive management protocol of NPE in patients with TBI has yet to be established. The current study reported the case of a 67-year-old man with severe TBI who was transferred to our intensive care unit (ICU). On day 7 after hospitalization, the patient suddenly suffered tachypnea, tachycardia, systemic hypertension and hypoxemia during lumbar cistern drainage. Intravenous diuretics, tranquilizer and glucocorticoid were administered due to suspected left heart failure attack. Chest radiography examination supported the diagnosis of pulmonary edema; however, hypotension and hypovolemia were subsequently observed. Pulse index continuous cardiac output (PiCCO) hemodynamic monitoring and bedside echocardiography were performed, which excluded the diagnosis of cardiac pulmonary edema, and thus the diagnosis of NPE was confirmed. Goal-directed therapy by dynamic PiCCO monitoring was then implemented. In addition, levosimendan, an inotropic agent, was introduced to improve cardiac output. The patient had complete recovered from pulmonary edema and regained consciousness on day 11 of hospitalization. The current case demonstrated that PiCCO monitoring may serve a central role in the integrated management of NPE in patients with TBI. Levosimendan may be a potential medicine in treating cardiac dysfunction, along with its benefit from improving neurological function in NPE patients. PMID:27698733

  12. Role of PiCCO monitoring for the integrated management of neurogenic pulmonary edema following traumatic brain injury: A case report and literature review

    PubMed Central

    Lin, Xiaoping; Xu, Zhijun; Wang, Pengfei; Xu, Yan; Zhang, Gensheng

    2016-01-01

    Neurogenic pulmonary edema (NPE) is occasionally observed in patients with traumatic brain injury (TBI); however, this condition is often underappreciated. NPE is frequently misdiagnosed due to its atypical clinical performance, thus delaying appropriate treatment. A comprehensive management protocol of NPE in patients with TBI has yet to be established. The current study reported the case of a 67-year-old man with severe TBI who was transferred to our intensive care unit (ICU). On day 7 after hospitalization, the patient suddenly suffered tachypnea, tachycardia, systemic hypertension and hypoxemia during lumbar cistern drainage. Intravenous diuretics, tranquilizer and glucocorticoid were administered due to suspected left heart failure attack. Chest radiography examination supported the diagnosis of pulmonary edema; however, hypotension and hypovolemia were subsequently observed. Pulse index continuous cardiac output (PiCCO) hemodynamic monitoring and bedside echocardiography were performed, which excluded the diagnosis of cardiac pulmonary edema, and thus the diagnosis of NPE was confirmed. Goal-directed therapy by dynamic PiCCO monitoring was then implemented. In addition, levosimendan, an inotropic agent, was introduced to improve cardiac output. The patient had complete recovered from pulmonary edema and regained consciousness on day 11 of hospitalization. The current case demonstrated that PiCCO monitoring may serve a central role in the integrated management of NPE in patients with TBI. Levosimendan may be a potential medicine in treating cardiac dysfunction, along with its benefit from improving neurological function in NPE patients.

  13. Anti-asthmatic agents alleviate pulmonary edema by upregulating AQP1 and AQP5 expression in the lungs of mice with OVA-induced asthma.

    PubMed

    Dong, Chunling; Wang, Guifang; Li, Bo; Xiao, Kui; Ma, Zhongsen; Huang, Hua; Wang, Xiangdong; Bai, Chunxue

    2012-04-15

    Ovalbumin (OVA)-induced asthma in mouse lungs causes changes in the mRNA and protein levels of aquaporins (AQPs). AQP expression was examined in the presence of various anti-asthmatic agents, including dexamethasone, ambroxol, and terbutaline. The influence of these agents on OVA-induced airway inflammation was also evaluated. The mRNA expression levels of AQP1, 4, and 5 were significantly reduced and that of AQP3 was significantly increased 24h after the last OVA exposure. The protein levels of AQP1, 3, and 5 mirrored the mRNA expression profiles, but AQP4 did not exhibit any changes. Only the mRNA and protein expression levels of AQP1 and AQP5 were significantly increased by these three anti-asthmatic agents. Dexamethasone and ambroxol improved the eosinophil infiltration, mucus secretion, and pulmonary edema caused by OVA, but terbutaline only alleviated pulmonary edema. These results indicate that AQP1 and AQP5 are closely related to pulmonary edema but not to eosinophil infiltration or mucus secretion during asthma. Anti-asthmatic agents could alleviate pulmonary edema through upregulating the expression of AQP1 and AQP5 in mouse lungs that have OVA-induced asthma. PMID:22226856

  14. Acute ozone-induced lung injury in rats: Structural-functional relationships of developing alveolar edema

    SciTech Connect

    Paterson, J.F.; Hammond, M.D.; Montgomery, M.R.; Sharp, J.T.; Farrier, S.E.; Balis, J.U. )

    1992-11-01

    As part of a study on the effects of acute ozone stress on the lung surfactant system, we correlated morphometric, biochemical, and functional indices of lung injury using male rats exposed to 3 ppm ozone for 1, 2, 4, and 8 hr. Evaluation of lung mechanics, using the Pulmonary Evaluation and Diagnostic Laboratory System, revealed a significant decrease in dynamic lung compliance (ml/cmH[sub 2]O/kg) from a control value of 0.84 [plus minus] 0.02 (SEM) to 0.72 [plus minus] 0.04 and 0.57 [plus minus] 0.06 at 4 and 8 hr, respectively. At 2 hr there was a transient increase in PaO[sub 2] to 116 torr (control = 92 torr) followed by a decrease at 4 hr (65 torr) and 8 hr (55 torr). Morphometry of lung tissue, fixed by perfusion of fixative via the pulmonary artery at 12 cm H[sub 2]O airway distending pressure, demonstrated an increase in the area of the intravascular compartment at 8 hr, in association with a 65 and 39% replacement of the alveolar area by fluid in ventral and dorsal lung regions, respectively. There was a positive correlation (r = 0.966) between alveolar edema and transudated proteins in lavage fluid. A stepwise multiple regression model, with edema as the dependent variable, suggested that pulmonary vasodilatation, hypoxemia, and depletion of surfactant tubular myelin in lavage fluid were indices for predicting alveolar edema. In a second model, with lavage protein concentration as the dependent variable, decreasing dynamic compliance and hypoxemia were predictors of progressive, intraalveolar transudation of plasma proteins. The above structural-functional relationships support the concept that ozone-induced high-protein alveolar edema is pathogenetically linked to pulmonary hyperemia, deficiency of surfactant tubular myelin, and associated lung dysfunctions.

  15. Positive end-expiratory pressure (PEEP) does not depress left ventricular function in patients with pulmonary edema

    SciTech Connect

    Calvin, J.E.; Driedger, A.A.; Sibbald, W.J.

    1981-08-01

    Researchers evaluated the effects of positive end-expiratory pressure (PEEP) on left ventricular function in 15 patients with acute respiratory insufficiency secondary to pulmonary edema with invasive (pressure; flow) measurements and radionuclide angiography (RA). Using RNA allowed a definition of the left ventricular ejection fraction (LVEF), and then calculation of the left ventricular end-diastolic volume (LVEDV), both before and after PEEP. With a mean PEEP of 14.2 +/- 1.8 cm H2O (mean +/- SD) (range, 10 to 15), a fall in the cardiac index (4.34 +/- 1.5 to 3.84 +/- 1.4 L/min/M2; p less than 0.001) was accompanied by a significant decrease in the stroke volume index (42 +/- 13 to 39 +/- 12 ml/beat M2; p less than 0.01) and pulse rate (103.4 +/- 14.3 to 98 +/- 13.5 beats/min; p less than 0.01). The decrease in the stroke volume index was primarily due to a significant decrease in left ventricular preload (LVEDV) from 85.9 +/- 19 to 71.4 +/- 21.4 ml/m2 (p less than 0.01). Simultaneously, the mean LVEF increased from 0.47 +/- 0.10 to 0.53 +/- 0.08 (p less than 0.05), despite a significant increase in the systemic vascular resistance (1,619 +/- 575 to 1,864 +/- 617 dynes . s. cm-5/M2; p less than 0.01). Researchers concluded that the use of PEEP in patients with acute pulmonary edema, to the degree used in this study, may depress cardiac output by simply decreasing left ventricular preload. Researchers were unable to produce any evidence that would support a change in the contractile state of the left ventricle as a cause of depressed forward flow with the use of PEEP.

  16. Soluble Urokinase-Type Plasminogen Activator Receptor Plasma Concentration May Predict Susceptibility to High Altitude Pulmonary Edema.

    PubMed

    Hilty, Matthias Peter; Zügel, Stefanie; Schoeb, Michele; Auinger, Katja; Dehnert, Christoph; Maggiorini, Marco

    2016-01-01

    Introduction. Acute exposure to high altitude induces inflammation. However, the relationship between inflammation and high altitude related illness such as high altitude pulmonary edema (HAPE) and acute mountain sickness (AMS) is poorly understood. We tested if soluble urokinase-type plasminogen activator receptor (suPAR) plasma concentration, a prognostic factor for cardiovascular disease and marker for low grade activation of leukocytes, will predict susceptibility to HAPE and AMS. Methods. 41 healthy mountaineers were examined at sea level (SL, 446 m) and 24 h after rapid ascent to 4559 m (HA). 24/41 subjects had a history of HAPE and were thus considered HAPE-susceptible (HAPE-s). Out of the latter, 10/24 HAPE-s subjects were randomly chosen to suppress the inflammatory cascade with dexamethasone 8 mg bid 24 h prior to ascent. Results. Acute hypoxic exposure led to an acute inflammatory reaction represented by an increase in suPAR (1.9 ± 0.4 at SL versus 2.3 ± 0.5 at HA, p < 0.01), CRP (0.7 ± 0.5 at SL versus 3.6 ± 4.6 at HA, p < 0.01), and IL-6 (0.8 ± 0.4 at SL versus 3.3 ± 4.9 at HA, p < 0.01) in all subjects except those receiving dexamethasone. The ascent associated decrease in PaO2 correlated with the increase in IL-6 (r = 0.46, p < 0.001), but not suPAR (r = 0.27, p = 0.08); the increase in IL-6 was not correlated with suPAR (r = 0.16, p = 0.24). Baseline suPAR plasma concentration was higher in the HAPE-s group (2.0 ± 0.4 versus 1.8 ± 0.4, p = 0.04); no difference was found for CRP and IL-6 and for subjects developing AMS. Conclusion. High altitude exposure leads to an increase in suPAR plasma concentration, with the missing correlation between suPAR and IL-6 suggesting a cytokine independent, leukocyte mediated mechanism of low grade inflammation. The correlation between IL-6 and PaO2 suggests a direct effect of hypoxia, which is not the case for suPAR. However, suPAR plasma concentration measured before hypoxic exposure may predict

  17. Soluble Urokinase-Type Plasminogen Activator Receptor Plasma Concentration May Predict Susceptibility to High Altitude Pulmonary Edema

    PubMed Central

    Zügel, Stefanie; Schoeb, Michele; Auinger, Katja; Dehnert, Christoph; Maggiorini, Marco

    2016-01-01

    Introduction. Acute exposure to high altitude induces inflammation. However, the relationship between inflammation and high altitude related illness such as high altitude pulmonary edema (HAPE) and acute mountain sickness (AMS) is poorly understood. We tested if soluble urokinase-type plasminogen activator receptor (suPAR) plasma concentration, a prognostic factor for cardiovascular disease and marker for low grade activation of leukocytes, will predict susceptibility to HAPE and AMS. Methods. 41 healthy mountaineers were examined at sea level (SL, 446 m) and 24 h after rapid ascent to 4559 m (HA). 24/41 subjects had a history of HAPE and were thus considered HAPE-susceptible (HAPE-s). Out of the latter, 10/24 HAPE-s subjects were randomly chosen to suppress the inflammatory cascade with dexamethasone 8 mg bid 24 h prior to ascent. Results. Acute hypoxic exposure led to an acute inflammatory reaction represented by an increase in suPAR (1.9 ± 0.4 at SL versus 2.3 ± 0.5 at HA, p < 0.01), CRP (0.7 ± 0.5 at SL versus 3.6 ± 4.6 at HA, p < 0.01), and IL-6 (0.8 ± 0.4 at SL versus 3.3 ± 4.9 at HA, p < 0.01) in all subjects except those receiving dexamethasone. The ascent associated decrease in PaO2 correlated with the increase in IL-6 (r = 0.46, p < 0.001), but not suPAR (r = 0.27, p = 0.08); the increase in IL-6 was not correlated with suPAR (r = 0.16, p = 0.24). Baseline suPAR plasma concentration was higher in the HAPE-s group (2.0 ± 0.4 versus 1.8 ± 0.4, p = 0.04); no difference was found for CRP and IL-6 and for subjects developing AMS. Conclusion. High altitude exposure leads to an increase in suPAR plasma concentration, with the missing correlation between suPAR and IL-6 suggesting a cytokine independent, leukocyte mediated mechanism of low grade inflammation. The correlation between IL-6 and PaO2 suggests a direct effect of hypoxia, which is not the case for suPAR. However, suPAR plasma concentration measured before hypoxic exposure may predict

  18. [Maternal pulmonary edema as an anesthesia complication after intravenous tocolysis and stimulating of lung maturation].

    PubMed

    Beer, P; Passweg, D

    1992-01-01

    Maternal lung edema due to the use of beta-mimetic tocolytic agents is a well-documented complication. The risk increases if several other factors are present: infectious diseases, the use of inhaled anesthetics, EPH gestosis, hydramnios, twin gestation and preexisting cardiovascular disease. The complications induced by beta-mimetic tocolytic agents can be reduced by remembering their side effects and contraindications and restricting fluid intake. During obstetric general anesthesia in patients undergoing tocolysis, the infusion of large amounts of saline, as is widely practised today, is strictly contraindicated. PMID:1356538

  19. [Experimental study on different concentration alcohol humidifying oxygen supply improving hypoxia caused by pulmonary edema].

    PubMed

    Jiang, X W; Gao, M Z; Liang, J H

    1996-07-01

    In order to research the best alcoholic concentration in the humidifying bottle when pneumonedema oxygen inhalation, 32 rabbits, divided into 4 groups, are replicated into pneumonedema models using method of rapid transfusion, and given oxygen inhalation with 20%, 50%, 70%, and 90% alcohol as humidifying agent (shortly called alcoholic oxygen). The results are as follows: using 20% alcohol as humidifying agent, the increasing amplitude of blood PaO2 is 147.30% (P < 0.001), the injury to the pulmonary bronchial mucosa and the wall of pulmonary alveoli is slight; using 50% alcohol, the increasing amplitude of blood PaO2 is 39.46% (P < 0.001), the injury to the parts mentioned above exacerbates and bronchiole cavity mucosa has moderate bleeding; using 70% alcohol, the increasing amplitude of blood PaO2 is 21.97% (P < 0.05), pneumorrhagia occurs; using 90% alcohol, the increasing amplitude of blood PaO2 is 94.46% (P < 0.01), a great number of blood cells aggregate inside the pulmonary alveoli and the bronchiole. This study proves that choosing 20% alcohol as humidifying agent has the best result, and as well, the explanation of the mechanism of alcohol suppressing foam, meaning being able to decrease only the surface tension of the foam inside the pulmonary alveoli, is incomprehensive, and the nature of the material itself forming foam has decisive function.

  20. [Acute pulmonary edema from inhalation of the bite-block after anesthesia with a laryngeal mask].

    PubMed

    Banchereau, F; Marié, S; Pez, H; Boully-Balihaut, A; Tueux, O

    2001-12-01

    We report a case of acute pulmonary oedema, consecutive to upper airway obstruction due to the inhalation of the laryngeal mask airway (LMA) bite block during recovery. The LMA was used for general anaesthesia with the bite-block provided in France. No trouble occurred during LMA insertion and anaesthesia. Symptomatic treatment provided complete resolution within a few days. PMID:11803848

  1. Using a Caesalpinia echinata Lam. protease inhibitor as a tool for studying the roles of neutrophil elastase, cathepsin G and proteinase 3 in pulmonary edema.

    PubMed

    Cruz-Silva, Ilana; Neuhof, Christiane; Gozzo, Andrezza Justino; Nunes, Viviane Abreu; Hirata, Izaura Yoshico; Sampaio, Misako Uemura; Figueiredo-Ribeiro, Rita de Cássia; Neuhof, Heinz; Araújo, Mariana da Silva

    2013-12-01

    Acute lung injury (ALI) is characterized by neutrophil infiltration and the release of proteases, mainly elastase (NE), cathepsin G (Cat G) and proteinase 3 (PR3), which can be controlled by specific endogenous inhibitors. However, inhibitors of these proteases have been isolated from different sources, including plants. For this study, CeEI, or Caesalpinia echinata elastase inhibitor, was purified from C. echinata (Brazil-wood) seeds after acetone fractionation, followed by ion exchange and reversed phase chromatographic steps. Characterization with SDS-PAGE, stability assays, amino acid sequencing and alignment with other protein sequences confirmed that CeEI is a member of the soybean Kunitz trypsin inhibitor family. Like other members of this family, CeEI is a 20 kDa monomeric protein; it is stable within a large pH and temperature range, with four cysteine residues forming two disulfide bridges, conserved amino acid residues and leucine-isoleucine residues in the reactive site. CeEI was able to inhibit NE and Cat G at a nanomolar range (with K(i)s of 1.9 and 3.6 nM, respectively) and inhibited PR3 within a micromolar range (K(i) 3.7 μM), leading to hydrolysis of specific synthetic substrates. In a lung edema model, CeEI reduced the lung weight and pulmonary artery pressure until 180 min after the injection of zymosan-activated polymorphonuclear neutrophils. In experiments performed in the presence of a Cat G and PR3, but not an NE inhibitor, lung edema was reduced only until 150 min and pulmonary artery pressure was similar to that of the control. These results confirm that NE action is crucial to edema establishment and progression. Additionally, CeEI appears to be a useful tool for studying the physiology of pulmonary edema and provides a template for molecular engineering and drug design for ALI therapy.

  2. Correlation between single nucleotide polymorphisms in hypoxia-related genes and susceptibility to acute high-altitude pulmonary edema.

    PubMed

    Wu, A L; Xiong, Y S; Li, Z Q; Liu, Y G; Quan, Q; Wu, L J

    2015-01-01

    This study aimed to explore the relationship between genetic changes and high-altitude pulmonary edema (HAPE) susceptibility, and to screen for the key single nucleotide polymorphism (SNP) loci in the HAPE-susceptibility gene, by investigating the SNPs occurring in hypoxia-related genes in HAPE-susceptible and control (non-susceptible) populations. This research was conducted on Han recruits, who travelled to the Lhasa plateau (altitude, 3658 m). Ten loci located on ten genes extracted from the HAPE and healthy populations were amplified by polymerase chain reaction, and subsequently sequenced. The investigated genes included those coding for aldosterone synthase 2 (CYP11B2), angiotensin-converting enzyme (ACE), heat-shock protein 70 (HSP70), nuclear factor kappa B (NF-κB), surfactant protein A2 (SP-A2), plasminogen activator inhibitor-1 (PAI-1), nitric oxide synthetase (NOS), vascular endothelial growth factor (VEGF), prolyl hydroxylase (EGLN1), and zinc finger protein A20. The gene distribution of each SNP loci and its correlation with HAPE was analyzed. Statistical analyses of the genotype frequencies of the SNPs revealed significant differences in the ACE (rs4309), EGLN1 (rs480902), SP-A2 (rs1965708), HSP70 (rs1008438), PAI-1 (rs1799889), and NOS (rs199983) expressions between the HAPE and healthy control groups (P < 0.05); therefore, these SNP loci were believed to indicate HAPE susceptibility. HAPE is correlated with multiple- SNP loci. A correlation analysis between genetic polymorphism and HAPE susceptibility revealed that 6 hypoxia-related genes were key sites accounting for HAPE. These findings could help assess the risk of HAPE in populations expressing different genotypes, in order to reduce the occurrence of HAPE. PMID:26436397

  3. Physiological mechanisms of pulmonary hypertension.

    PubMed

    MacIver, David H; Adeniran, Ismail; MacIver, Iain R; Revell, Alistair; Zhang, Henggui

    2016-10-01

    Pulmonary hypertension is usually related to obstruction of pulmonary blood flow at the level of the pulmonary arteries (eg, pulmonary embolus), pulmonary arterioles (idiopathic pulmonary hypertension), pulmonary veins (pulmonary venoocclusive disease) or mitral valve (mitral stenosis and regurgitation). Pulmonary hypertension is also observed in heart failure due to left ventricle myocardial diseases regardless of the ejection fraction. Pulmonary hypertension is often regarded as a passive response to the obstruction to pulmonary flow. We review established fluid dynamics and physiology and discuss the mechanisms underlying pulmonary hypertension. The important role that the right ventricle plays in the development and maintenance of pulmonary hypertension is discussed. We use principles of thermodynamics and discuss a potential common mechanism for a number of disease states, including pulmonary edema, through adding pressure energy to the pulmonary circulation. PMID:27659877

  4. Severe Tumor Lysis Syndrome and Acute Pulmonary Edema Requiring Extracorporeal Membrane Oxygenation Following Initiation of Chemotherapy for Metastatic Alveolar Rhabdomyosarcoma.

    PubMed

    Sanford, Ethan; Wolbrink, Traci; Mack, Jennifer; Rowe, R Grant

    2016-05-01

    We present an 8-year-old male with metastatic alveolar rhabdomyosarcoma (ARMS) who developed precipitous cardiopulmonary collapse with severe tumor lysis syndrome (TLS) 48 hr after initiation of chemotherapy. Despite no detectable pulmonary metastases, acute hypoxemic respiratory failure developed, requiring extracorporeal membrane oxygenation (ECMO). Although TLS has been reported in disseminated ARMS, this singular case of life-threatening respiratory deterioration developing after initiation of chemotherapy presented unique therapeutic dilemmas. We review the clinical aspects of this case, including possible mechanisms of respiratory failure, and discuss the role of ECMO utilization in pediatric oncology. PMID:26713672

  5. Interactions among Vascular-Tone Modulators Contribute to High Altitude Pulmonary Edema and Augmented Vasoreactivity in Highlanders

    PubMed Central

    Ali, Zahara; Mishra, Aastha; Kumar, Rahul; Alam, Perwez; Pandey, Priyanka; Ram, Rekhbala; Thinlas, Tashi; Mohammad, Ghulam; Pasha, M. A. Qadar

    2012-01-01

    Background The interactions among various biomarkers remained unexplored under the stressful environment of high-altitude. Present study evaluated interactions among biomarkers to study susceptibility for high altitude pulmonary edema (HAPE) in HAPE-patients (HAPE-p) and adaptation in highland natives (HLs); both in comparison to HAPE-free sojourners (HAPE-f). Methodology/Principal Findings All the subjects were recruited at 3500 m. We measured clinical parameters, biochemical levels in plasma and gene expression using RNA from blood; analyzed various correlations between and among the clinical parameters, especially arterial oxygen saturation (SaO2) and mean arterial pressure (MAP) and biochemical parameters like, asymmetric dimethylarginine (ADMA), serotonin (5-HT), 8-iso-prostaglandin F2α (8-isoPGF2α), endothelin-1 (ET-1), plasma renin activity (PRA), plasma aldosterone concentration (PAC), superoxide dismutase (SOD) and nitric oxide (NO) in HAPE-p, HAPE-f and HLs. ADMA, 5-HT, 8-isoPGF2α, ET-1 levels, and PAC were significantly higher (p<0.0001, each), whereas SOD activity and NO level were significantly lower in HAPE-p than HAPE-f (p≤0.001). Furthermore, ADMA, 5-HT, 8-isoPGF2α, NO levels and PAC were significantly higher (p<0.0001), whereas ET-1 level significantly (p<0.0001) and SOD activity non-significantly (p>0.05) lower in HLs than HAPE-f. The expression of respective genes differed in the three groups. In the correlations, SaO2 inversely correlated with ADMA, 5-HT and 8-isoPGF2α and positively with SOD in HAPE-p (p≤0.009). MAP correlated positively with 5-HT and 8-isoPGF2α in HAPE-p and HLs (p≤0.004). A strong positive correlation was observed between ADMA and 5-HT, 5-HT and 8-isoPGF2α (p≤0.001), whereas inverse correlation of SOD with ET-1 in HAPE-p and HLs (p≤0.004), with 5-HT and 8-isoPGF2α in HAPE-p (p = 0.01) and with 5-HT in HLs (p = 0.05). Conclusions/Significance The interactions among these markers confer enhanced

  6. ROCK2 and MYLK variants under hypobaric hypoxic environment of high altitude associate with high altitude pulmonary edema and adaptation

    PubMed Central

    Pandey, Priyanka; Mohammad, Ghulam; Singh, Yogendra; Qadar Pasha, MA

    2015-01-01

    Objective To date, a major class of kinases, serine–threonine kinase, has been scantly investigated in stress-induced rare, fatal (if not treated early), and morbid disorder, high altitude pulmonary edema (HAPE). This study examined three major serine–threonine kinases, ROCK2, MYLK, and JNK1, along with six other genes, tyrosine hydroxylase, G-protein subunits GNA11 and GNB3, and alpha1 adrenergic receptor isoforms 1A, 1B, and 1D as candidate gene markers of HAPE and adaptation. Methods For this, 57 variants across these nine genes were genotyped in HAPE patients (n=225), HAPE controls (n=210), and highlanders (n=259) by Sequenom MS (TOF)-based MassARRAY® platform using iPLEX™ Gold technology. In addition, to study the gene expression, quantitative real-time polymerase chain reaction was performed in human peripheral blood mononuclear cells of the three study groups. Results A significant association was observed for C allele (ROCK2 single-nucleotide polymorphism, rs10929728) with HAPE (P=0.03) and C, T, and A alleles (MYLK single-nucleotide polymorphisms, rs11717814, rs40305, and rs820336) with both HAPE and adaptation (P=0.001, P=0.006, and P=0.02, respectively). ROCK2 88 kb GGGTTGGT haplotype was associated with lower risk of HAPE (P=0.0009). MYLK 7 kb haplotype CTA, composed of variant alleles, was associated with higher risk of HAPE (P=0.0006) and lower association with adaptation (P=1E–06), whereas haplotype GCG, composed of wild-type alleles, was associated with lower risk of HAPE (P=0.001) and higher association with adaptation (P=1E–06). Haplotype–haplotype and gene–gene interactions demonstrated a correlation in working of ROCK2 and MYLK. Conclusion The data suggest the association of ROCK2 with HAPE and MYLK with HAPE and adaptation in Indian population. The outcome has provided new insights into the physiology of HAPE and adaptation. PMID:26586960

  7. The clinical usefulness of extravascular lung water and pulmonary vascular permeability index to diagnose and characterize pulmonary edema: a prospective multicenter study on the quantitative differential diagnostic definition for acute lung injury/acute respiratory distress syndrome

    PubMed Central

    2012-01-01

    Introduction Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is characterized by features other than increased pulmonary vascular permeability. Pulmonary vascular permeability combined with increased extravascular lung water content has been considered a quantitative diagnostic criterion of ALI/ARDS. This prospective, multi-institutional, observational study aimed to clarify the clinical pathophysiological features of ALI/ARDS and establish its quantitative diagnostic criteria. Methods The extravascular lung water index (EVLWI) and the pulmonary vascular permeability index (PVPI) were measured using the transpulmonary thermodilution method in 266 patients with PaO2/FiO2 ratio ≤ 300 mmHg and bilateral infiltration on chest radiography, in 23 ICUs of academic tertiary referral hospitals. Pulmonary edema was defined as EVLWI ≥ 10 ml/kg. Three experts retrospectively determined the pathophysiological features of respiratory insufficiency by considering the patients' history, clinical presentation, chest computed tomography and radiography, echocardiography, EVLWI and brain natriuretic peptide level, and the time course of all preceding findings under systemic and respiratory therapy. Results Patients were divided into the following three categories on the basis of the pathophysiological diagnostic differentiation of respiratory insufficiency: ALI/ARDS, cardiogenic edema, and pleural effusion with atelectasis, which were noted in 207 patients, 26 patients, and 33 patients, respectively. EVLWI was greater in ALI/ARDS and cardiogenic edema patients than in patients with pleural effusion with atelectasis (18.5 ± 6.8, 14.4 ± 4.0, and 8.3 ± 2.1, respectively; P < 0.01). PVPI was higher in ALI/ARDS patients than in cardiogenic edema or pleural effusion with atelectasis patients (3.2 ± 1.4, 2.0 ± 0.8, and 1.6 ± 0.5; P < 0.01). In ALI/ARDS patients, EVLWI increased with increasing pulmonary vascular permeability (r = 0.729, P < 0.01) and was weakly

  8. Airway surface liquid volume expansion induces rapid changes in amiloride-sensitive Na+ transport across upper airway epithelium-Implications concerning the resolution of pulmonary edema.

    PubMed

    Azizi, Fouad; Arredouani, Abdelilah; Mohammad, Ramzi M

    2015-09-01

    During airway inflammation, airway surface liquid volume (ASLV) expansion may result from the movement of plasma proteins and excess liquid into the airway lumen due to extravasation and elevation of subepithelial hydrostatic pressure. We previously demonstrated that elevation of submucosal hydrostatic pressure increases airway epithelium permeability resulting in ASLV expansion by 500 μL cm(-2) h(-1). Liquid reabsorption by healthy airway epithelium is regulated by active Na(+) transport at a rate of 5 μL cm(-2) h(-1). Thus, during inflammation the airway epithelium may be submerged by a large volume of luminal liquid. Here, we have investigated the mechanism by which ASLV expansion alters active epithelial Na(+) transport, and we have characterized the time course of the change. We used primary cultures of tracheal airway epithelium maintained under air interface (basal ASLV, depth is 7 ± 0.5 μm). To mimic airway flooding, ASLV was expanded to a depth of 5 mm. On switching from basal to expanded ASLV conditions, short-circuit current (Isc, a measure of total transepithelial active ion transport) declined by 90% with a half-time (t1/2) of 1 h. 24 h after the switch, there was no significant change in ATP concentration nor in the number of functional sodium pumps as revealed by [(3)H]-ouabain binding. However, amiloride-sensitive uptake of (22)Na(+) was reduced by 70% upon ASLV expansion. This process is reversible since after returning cells back to air interface, Isc recovered with a t1/2 of 5-10 h. These results may have important clinical implications concerning the development of Na(+) channels activators and resolution of pulmonary edema.

  9. Atrial natriuretic peptide attenuates agonist-induced pulmonary edema in mice with targeted disruption of the gene for natriuretic peptide receptor-A

    PubMed Central

    Tsai, Shu-Whei; Green, Sabrina; Grinnell, Katie L.; Machan, Jason T.; Harrington, Elizabeth O.

    2013-01-01

    Atrial natriuretic peptide (ANP) inhibits agonist-induced pulmonary edema formation, but the signaling pathway responsible is not well defined. To investigate the role of the particulate guanylate cyclase-linked receptor, natriuretic peptide receptor-A (NPR-A), we measured acute lung injury responses in intact mice and pulmonary microvascular endothelial cells (PMVEC) with normal and disrupted expression of NPR-A. NPR-A wild-type (NPR-A+/+), heterozygous (NPR-A+/−), and knockout (NPR-A−/−) mice were anesthetized and treated with thrombin receptor agonist peptide (TRAP) or lipopolysaccharide (LPS). Lung injury was assessed by lung wet-to-dry (W/D) weight and by protein and cell concentration of bronchoalveolar lavage (BAL) fluid. No difference in pulmonary edema formation was seen between NPR-A genotypes under baseline conditions. TRAP and LPS increased lung W/D weight and BAL fluid cell counts more in NPR-A−/− mice than in NPR-A+/− or NPR-A+/+ mice, but no genotype-related differences were seen in TRAP-induced increases in bloodless lung W/D weight or LPS-induced increases in BAL protein concentration. Pretreatment with ANP infusion completely blocked TRAP-induced increases in lung W/D weight and blunted LPS-induced increases in BAL cell counts and protein concentration in both NPR-A−/− and NPR-A+/+ mice. Thrombin decreased transmembrane electrical resistance in monolayers of PMVECs in vitro, and this effect was attenuated by ANP in PMVECs isolated from both genotypes. Administration of the NPR-C-specific ligand, cANF, also blocked TRAP-induced increases in lung W/D weight and LPS-induced increases in BAL cell count and protein concentration in NPR-A+/+ and NPR-A−/− mice. We conclude that ANP is capable of attenuating agonist-induced lung edema in the absence of NPR-A. The protective effect of ANP on agonist-induced lung injury and pulmonary barrier function may be mediated by NPR-C. PMID:23195629

  10. Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness

    PubMed Central

    Louge, Pierre; Coulange, Mathieu; Beneton, Frederic; Gempp, Emmanuel; Le Pennetier, Olivier; Algoud, Maxime; Dubourg, Lorene; Naibo, Pierre; Marlinge, Marion; Michelet, Pierre; Vairo, Donato; Kipson, Nathalie; Kerbaul, François; Jammes, Yves; Jones, Ian M.; Steinberg, Jean-Guillaume; Ruf, Jean; Guieu, Régis; Boussuges, Alain; Fenouillet, Emmanuel

    2016-01-01

    Abstract Immersion pulmonary edema (IPE) is a misdiagnosed environmental illness caused by water immersion, cold, and exertion. IPE occurs typically during SCUBA diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury and/or loss of consciousness in water, which may be fatal. IPE is thought to involve hemodynamic and cardiovascular disturbances, but its pathophysiology remains largely unclear, which makes IPE prevention difficult. This observational study aimed to document IPE pathogenesis and improve diagnostic reliability, including distinguishing in some conditions IPE from decompression sickness (DCS), another diving-related disorder. Thirty-one patients (19 IPE, 12 DCS) treated at the Hyperbaric Medicine Department (Ste-Anne hospital, Toulon, France; July 2013–June 2014) were recruited into the study. Ten healthy divers were recruited as controls. We tested: (i) copeptin, a surrogate marker for antidiuretic hormone and a stress marker; (ii) ischemia-modified albumin, an ischemia/hypoxia marker; (iii) brain-natriuretic peptide (BNP), a marker of heart failure, and (iv) ultrasensitive-cardiac troponin-I (cTnI), a marker of myocardial ischemia. We found that copeptin and cardiac biomarkers were higher in IPE versus DCS and controls: (i) copeptin: 68% of IPE patients had a high level versus 25% of DCS patients (P < 0.05) (mean ± standard-deviation: IPE: 53 ± 61 pmol/L; DCS: 15 ± 17; controls: 6 ± 3; IPE versus DCS or controls: P < 0.05); (ii) ischemia-modified albumin: 68% of IPE patients had a high level versus 16% of DCS patients (P < 0.05) (IPE: 123 ± 25 arbitrary-units; DCS: 84 ± 25; controls: 94 ± 7; IPE versus DCS or controls: P < 0.05); (iii) BNP: 53% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 383 ± 394 ng/L; DCS: 37 ± 28; controls: 19 ± 15; IPE versus DCS or controls: P < 0.01); (iv) cTnI: 63% of IPE

  11. Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness.

    PubMed

    Louge, Pierre; Coulange, Mathieu; Beneton, Frederic; Gempp, Emmanuel; Le Pennetier, Olivier; Algoud, Maxime; Dubourg, Lorene; Naibo, Pierre; Marlinge, Marion; Michelet, Pierre; Vairo, Donato; Kipson, Nathalie; Kerbaul, François; Jammes, Yves; Jones, Ian M; Steinberg, Jean-Guillaume; Ruf, Jean; Guieu, Régis; Boussuges, Alain; Fenouillet, Emmanuel

    2016-06-01

    Immersion pulmonary edema (IPE) is a misdiagnosed environmental illness caused by water immersion, cold, and exertion. IPE occurs typically during SCUBA diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury and/or loss of consciousness in water, which may be fatal. IPE is thought to involve hemodynamic and cardiovascular disturbances, but its pathophysiology remains largely unclear, which makes IPE prevention difficult. This observational study aimed to document IPE pathogenesis and improve diagnostic reliability, including distinguishing in some conditions IPE from decompression sickness (DCS), another diving-related disorder.Thirty-one patients (19 IPE, 12 DCS) treated at the Hyperbaric Medicine Department (Ste-Anne hospital, Toulon, France; July 2013-June 2014) were recruited into the study. Ten healthy divers were recruited as controls. We tested: (i) copeptin, a surrogate marker for antidiuretic hormone and a stress marker; (ii) ischemia-modified albumin, an ischemia/hypoxia marker; (iii) brain-natriuretic peptide (BNP), a marker of heart failure, and (iv) ultrasensitive-cardiac troponin-I (cTnI), a marker of myocardial ischemia.We found that copeptin and cardiac biomarkers were higher in IPE versus DCS and controls: (i) copeptin: 68% of IPE patients had a high level versus 25% of DCS patients (P < 0.05) (mean ± standard-deviation: IPE: 53 ± 61 pmol/L; DCS: 15 ± 17; controls: 6 ± 3; IPE versus DCS or controls: P < 0.05); (ii) ischemia-modified albumin: 68% of IPE patients had a high level versus 16% of DCS patients (P < 0.05) (IPE: 123 ± 25 arbitrary-units; DCS: 84 ± 25; controls: 94 ± 7; IPE versus DCS or controls: P < 0.05); (iii) BNP: 53% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 383 ± 394 ng/L; DCS: 37 ± 28; controls: 19 ± 15; IPE versus DCS or controls: P < 0.01); (iv) cTnI: 63% of IPE patients had a high

  12. Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness.

    PubMed

    Louge, Pierre; Coulange, Mathieu; Beneton, Frederic; Gempp, Emmanuel; Le Pennetier, Olivier; Algoud, Maxime; Dubourg, Lorene; Naibo, Pierre; Marlinge, Marion; Michelet, Pierre; Vairo, Donato; Kipson, Nathalie; Kerbaul, François; Jammes, Yves; Jones, Ian M; Steinberg, Jean-Guillaume; Ruf, Jean; Guieu, Régis; Boussuges, Alain; Fenouillet, Emmanuel

    2016-06-01

    Immersion pulmonary edema (IPE) is a misdiagnosed environmental illness caused by water immersion, cold, and exertion. IPE occurs typically during SCUBA diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury and/or loss of consciousness in water, which may be fatal. IPE is thought to involve hemodynamic and cardiovascular disturbances, but its pathophysiology remains largely unclear, which makes IPE prevention difficult. This observational study aimed to document IPE pathogenesis and improve diagnostic reliability, including distinguishing in some conditions IPE from decompression sickness (DCS), another diving-related disorder.Thirty-one patients (19 IPE, 12 DCS) treated at the Hyperbaric Medicine Department (Ste-Anne hospital, Toulon, France; July 2013-June 2014) were recruited into the study. Ten healthy divers were recruited as controls. We tested: (i) copeptin, a surrogate marker for antidiuretic hormone and a stress marker; (ii) ischemia-modified albumin, an ischemia/hypoxia marker; (iii) brain-natriuretic peptide (BNP), a marker of heart failure, and (iv) ultrasensitive-cardiac troponin-I (cTnI), a marker of myocardial ischemia.We found that copeptin and cardiac biomarkers were higher in IPE versus DCS and controls: (i) copeptin: 68% of IPE patients had a high level versus 25% of DCS patients (P < 0.05) (mean ± standard-deviation: IPE: 53 ± 61 pmol/L; DCS: 15 ± 17; controls: 6 ± 3; IPE versus DCS or controls: P < 0.05); (ii) ischemia-modified albumin: 68% of IPE patients had a high level versus 16% of DCS patients (P < 0.05) (IPE: 123 ± 25 arbitrary-units; DCS: 84 ± 25; controls: 94 ± 7; IPE versus DCS or controls: P < 0.05); (iii) BNP: 53% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 383 ± 394 ng/L; DCS: 37 ± 28; controls: 19 ± 15; IPE versus DCS or controls: P < 0.01); (iv) cTnI: 63% of IPE patients had a high

  13. Comparison of quantitative computed tomography analysis and single-indicator thermodilution to measure pulmonary edema in patients with acute respiratory distress syndrome

    PubMed Central

    2014-01-01

    Objective To compare quantitative computed tomography (CT) analysis and single-indicator thermodilution to measure pulmonary edema in patients with acute respiratory distress syndrome (ARDS). Method Ten patients with ARDS were included. All underwent spiral CT of the thorax for estimating gas content of lung (GVCT), tissue volume of lung (TVCT), tissue volume index (TVI), mean radiographic attenuation (CTmean) for the whole lung and gas-to-tissue ratio (g/t). Pulmonary thermal volume (PTV) and extravascular lung water index (ELWI) were determined by the PiCCO plus system. CT or single-indicator thermodilution variables were correlated with respiratory system compliance (Crs), PaO2/FiO2, and Acute Physiology And Chronic Health EvaluationII (APACHE II) and Sequential Organ Failure Assessment (SOFA) scores. Results 1) TVCT and PTV were positively correlated (r =0.8878; P = 0.0006; equation of regression line: PTV = 1.0793 × TVCT + 179.8) as were TVI and ELWI (r =0.9459; P < 0.0001; equation of regression line: ELWI = 1.4506 × TVI-8.7792). The bias between TVCT and PTV as well as TVI and ELWI was -277 ± 217 and 0.62 ± 4.56, respectively. 2) ELWI and CT distribution of lung-tissue compartments were not correlated. 3) CT or single-indicator thermodilution variables were not correlated with Crs, PaO2/FiO2 or APACHE II or SOFA score. Conclusion Quantitative CT analysis and single-indicator thermodilution showed good agreement in measuring pulmonary edema. PMID:24625023

  14. Peri-partum cardiomyopathy in a pregnant woman at term revealed by acute pulmonary edema: what to do in front this catastrophic situation?

    PubMed Central

    Abdedaim, Hatim El ghadbane; Benali, Zine el abidine; Omari, Driss; Mohammed, Drissi; Hicham, Balkhi; Charki, Haimeur

    2014-01-01

    Peripartum Cardiomyopathy is insufficient congestive heart occurring in the last month of pregnancy and 5 months after delivery, in the absence of preexisting heart disease and identified etiology. This heart disease is associated with echocardiography systolic dysfunction and left ventricular dilatation. Its incidence ranges from 1/3000 to 1/15000, depending on the region, including much higher in some African countries, it particularly concern women over 30 years, multiparous and multiple pregnancies. The pathogenesis remains unclear, the prognosis is closely related to the complete recovery of cardiac function. We report through the clinical case of a woman aged 33 years admitted to the ICU for acute pulmonary edema of sudden onset of a term pregnancy and what to do before this critical situation PMID:25368718

  15. [Edema and the tropics].

    PubMed

    Holzer, B R

    2004-11-01

    People visiting or living in tropical or subtropical regions are exposed to various factors, which can lead to edema. Tourists staying for only a short time in the tropics are exposed to different risks, with other disease patterns, than people living in the tropics or immigrants from tropical regions. The differential diagnosis of edema and swelling is extensive and it can sometimes be difficult to distinguish classical edema with fluid retention in the extravascular interstitial space, from lymphedema or swelling due to other aetiologies. The patients often connect the edema to their stay in the tropics although it may have been pre-existing with no obvious relation to their travels. Already the long trip in the plane can lead to an "economy class syndrome" due to deep venous thrombosis. Contacts with animal or plant toxins, parasites or parasitic larvae can produce peripheral edema. The diagnosis can often only be made by taking a meticulous history, checking for eosinophilia and with the help of serological investigations. Chronic lymphedema or elephantiasis of the limbs is often due to blocked lymph vessels by filarial worms. It has to be distinguished from other forms as e.g. podoconiosis due to blockage by mineral particles in barefoot walking people. The trend to book adventure and trekking holidays at high altitude leads to high altitude peripheral edema or non-freezing cold injuries such as frostbites and trench foot. Edema can be an unwanted side effect of a range of drugs e.g. nifedipine, which is used to prevent and treat high altitude pulmonary edema. Protein malnutrition, (Kwashiorkor), and vitamin B6 deficiency, (Beri-Beri) are very rarely observed in immigrants and almost never in tourists. A very painful swelling of fingers and hands in children and young adults of African origin can be observed during a sickle cell crisis. Many protein loosing nephropathies connected with plant and animal toxins but also bacterial, viral or parasitic agents, can

  16. TRPV4 inhibition counteracts edema and inflammation and improves pulmonary function and oxygen saturation in chemically induced acute lung injury

    PubMed Central

    Balakrishna, Shrilatha; Song, Weifeng; Achanta, Satyanarayana; Doran, Stephen F.; Liu, Boyi; Kaelberer, Melanie M.; Yu, Zhihong; Sui, Aiwei; Cheung, Mui; Leishman, Emma; Eidam, Hilary S.; Ye, Guosen; Willette, Robert N.; Thorneloe, Kevin S.; Bradshaw, Heather B.; Matalon, Sadis

    2014-01-01

    The treatment of acute lung injury caused by exposure to reactive chemicals remains challenging because of the lack of mechanism-based therapeutic approaches. Recent studies have shown that transient receptor potential vanilloid 4 (TRPV4), an ion channel expressed in pulmonary tissues, is a crucial mediator of pressure-induced damage associated with ventilator-induced lung injury, heart failure, and infarction. Here, we examined the effects of two novel TRPV4 inhibitors in mice exposed to hydrochloric acid, mimicking acid exposure and acid aspiration injury, and to chlorine gas, a severe chemical threat with frequent exposures in domestic and occupational environments and in transportation accidents. Postexposure treatment with a TRPV4 inhibitor suppressed acid-induced pulmonary inflammation by diminishing neutrophils, macrophages, and associated chemokines and cytokines, while improving tissue pathology. These effects were recapitulated in TRPV4-deficient mice. TRPV4 inhibitors had similar anti-inflammatory effects in chlorine-exposed mice and inhibited vascular leakage, airway hyperreactivity, and increase in elastance, while improving blood oxygen saturation. In both models of lung injury we detected increased concentrations of N-acylamides, a class of endogenous TRP channel agonists. Taken together, we demonstrate that TRPV4 inhibitors are potent and efficacious countermeasures against severe chemical exposures, acting against exaggerated inflammatory responses, and protecting tissue barriers and cardiovascular function. PMID:24838754

  17. TRPV4 inhibition counteracts edema and inflammation and improves pulmonary function and oxygen saturation in chemically induced acute lung injury.

    PubMed

    Balakrishna, Shrilatha; Song, Weifeng; Achanta, Satyanarayana; Doran, Stephen F; Liu, Boyi; Kaelberer, Melanie M; Yu, Zhihong; Sui, Aiwei; Cheung, Mui; Leishman, Emma; Eidam, Hilary S; Ye, Guosen; Willette, Robert N; Thorneloe, Kevin S; Bradshaw, Heather B; Matalon, Sadis; Jordt, Sven-Eric

    2014-07-15

    The treatment of acute lung injury caused by exposure to reactive chemicals remains challenging because of the lack of mechanism-based therapeutic approaches. Recent studies have shown that transient receptor potential vanilloid 4 (TRPV4), an ion channel expressed in pulmonary tissues, is a crucial mediator of pressure-induced damage associated with ventilator-induced lung injury, heart failure, and infarction. Here, we examined the effects of two novel TRPV4 inhibitors in mice exposed to hydrochloric acid, mimicking acid exposure and acid aspiration injury, and to chlorine gas, a severe chemical threat with frequent exposures in domestic and occupational environments and in transportation accidents. Postexposure treatment with a TRPV4 inhibitor suppressed acid-induced pulmonary inflammation by diminishing neutrophils, macrophages, and associated chemokines and cytokines, while improving tissue pathology. These effects were recapitulated in TRPV4-deficient mice. TRPV4 inhibitors had similar anti-inflammatory effects in chlorine-exposed mice and inhibited vascular leakage, airway hyperreactivity, and increase in elastance, while improving blood oxygen saturation. In both models of lung injury we detected increased concentrations of N-acylamides, a class of endogenous TRP channel agonists. Taken together, we demonstrate that TRPV4 inhibitors are potent and efficacious countermeasures against severe chemical exposures, acting against exaggerated inflammatory responses, and protecting tissue barriers and cardiovascular function. PMID:24838754

  18. Disrupted pulmonary vascular development and pulmonary hypertension in transgenic mice overexpressing transforming growth factor-alpha.

    PubMed

    Le Cras, Timothy D; Hardie, William D; Fagan, Karen; Whitsett, Jeffrey A; Korfhagen, Thomas R

    2003-11-01

    Pulmonary vascular disease plays a major role in morbidity and mortality in infant and adult lung diseases in which increased levels of transforming growth factor (TGF)-alpha and its receptor EGFR have been associated. The aim of this study was to determine whether overexpression of TGF-alpha disrupts pulmonary vascular development and causes pulmonary hypertension. Lung-specific expression of TGF-alpha in transgenic mice was driven with the human surfactant protein (SP)-C promoter. Pulmonary arteriograms and arterial counts show that pulmonary vascular development was severely disrupted in TGF-alpha mice. TGF-alpha mice developed severe pulmonary hypertension and vascular remodeling characterized by abnormally extensive muscularization of small pulmonary arteries. Pulmonary vascular development was significantly improved and pulmonary hypertension and vascular remodeling were prevented in bi-transgenic mice expressing both TGF-alpha and a dominant-negative mutant EGF receptor under the control of the SP-C promoter. Vascular endothelial growth factor (VEGF-A), an important angiogenic factor produced by the distal epithelium, was decreased in the lungs of TGF-alpha adults and in the lungs of infant TGF-alpha mice before detectable abnormalities in pulmonary vascular development. Hence, overexpression of TGF-alpha caused severe pulmonary vascular disease, which was mediated through EGFR signaling in distal epithelial cells. Reductions in VEGF may contribute to the pathogenesis of pulmonary vascular disease in TGF-alpha mice.

  19. Regression of pulmonary artery hypertension due to development of a pulmonary arteriovenous malformation

    PubMed Central

    Hasan, Ashfaq; Sastry, B.K.S.; Aleem, M.A.; Reddy, Gokul; Mahmood, Syed

    2014-01-01

    Idiopathic Pulmonary Hypertension (IPAH) is characterized by elevated pulmonary arterial pressure in the absence of an identifiable underlying cause. The condition is usually relentlessly progressive with a short survival in the absence of treatment.1 We describe a patient of IPAH in whom the pulmonary artery pressures significantly abated with complete disappearance of symptoms, following spontaneous development of a pulmonary arterio-venous malformation (PAVM). PMID:25443608

  20. Regional pulmonary distribution of iodine-125-labeled oleic acid. Its relationship to the pattern of oleic acid edema and pulmonary blood flow

    SciTech Connect

    Tarver, R.D.; Tsai, J.; Hedlund, L.W.; Sullivan, D.C.; Lischko, M.M.; Harris, C.C.; Effmann, E.L.; Putman, C.E.

    1986-02-01

    Oleic acid infusion in dogs produces a patchy, predominantly peripheral lesion on CT scans. This study correlates the pattern of oleic acid injury with the distribution of infused oleic acid and pulmonary blood flow. Radiolabeled oleic acid (I-125, 0.05 ml/kg) and radiolabeled 15-micron microspheres (Co-57) were infused into the right atria of 11 dogs. Oleic acid was given after the microspheres in six dogs and before microspheres in five dogs. Ten minutes after infusion, the lungs were removed. Four transverse slices (0.5 cm thick) of the lower lobes were taken from each dog and cubed. Samples were grouped into three regions of the transverse slice: outer, middle, and inner concentric rings. In both groups, I-125 (oleic acid) activity was greater in the outer than the middle and inner concentric layers (P less than 0.001). When Cobalt-57 microspheres were given before oleic acid, Cobalt-57 activity was marginally lower in the outer layer compared with the middle and inner layers. However, when oleic acid was given first, microsphere activity in the outer layer was significantly lower (P less than 0.001) than the middle layer. Thus, oleic acid was preferentially distributed to the peripheral regions of the lung, similar to the regions of injury on CT. This distribution did not correspond to the pattern of pulmonary blood flow as indicated by the microspheres. Immediately after oleic acid infusion, pulmonary blood flow to the periphery was reduced, reflecting a response to the predominantly peripheral injury by oleic acid.

  1. Familial Thoracic Aortic Aneurysm with Dissection Presenting as Flash Pulmonary Edema in a 26-Year-Old Man

    PubMed Central

    Omar, Sabry; Moore, Tyler; Payne, Drew; Momeni, Parastoo; Mulkey, Zachary; Nugent, Kenneth

    2014-01-01

    We are reporting a case of familial thoracic aortic aneurysm and dissection in a 26-year-old man with no significant past medical history and a family history of dissecting aortic aneurysm in his mother at the age of 40. The patient presented with cough, shortness of breath, and chest pain. Chest X-ray showed bilateral pulmonary infiltrates. CT scan of the chest showed a dissection of the ascending aorta. The patient underwent aortic dissection repair and three months later he returned to our hospital with new complaints of back pain. CT angiography showed a new aortic dissection extending from the left carotid artery through the bifurcation and into the iliac arteries. The patient underwent replacement of the aortic root, ascending aorta, total aortic arch, and aortic valve. The patient recovered well postoperatively. Genetic studies of the patient and his children revealed no mutations in ACTA2, TGFBR1, TGFBR2, TGFB2, MYH11, MYLK, SMAD3, or FBN1. This case report focuses on a patient with familial TAAD and discusses the associated genetic loci and available screening methods. It is important to recognize potential cases of familial TAAD and understand the available screening methods since early diagnosis allows appropriate management of risk factors and treatment when necessary. PMID:25104961

  2. Iron chelation inhibits the development of pulmonary vascular remodeling.

    PubMed

    Wong, Chi-Ming; Preston, Ioana R; Hill, Nicholas S; Suzuki, Yuichiro J

    2012-11-01

    Reactive oxygen species (ROS) have been implicated in the pathogenesis of pulmonary hypertension. Because iron is an important regulator of ROS biology, this study examined the effects of iron chelation on the development of pulmonary vascular remodeling. The administration of an iron chelator, deferoxamine, to rats prevented chronic hypoxia-induced pulmonary hypertension and pulmonary vascular remodeling. Various iron chelators inhibited the growth of cultured pulmonary artery smooth muscle cells. Protein carbonylation, an important iron-dependent biological event, was promoted in association with pulmonary vascular remodeling and cell growth. A proteomic approach identified that Rho GDP-dissociation inhibitor (a negative regulator of RhoA) is carbonylated. In human plasma, the protein carbonyl content was significantly higher in patients with idiopathic pulmonary arterial hypertension than in healthy controls. These results suggest that iron plays an important role in the ROS-dependent mechanism underlying the development of pulmonary hypertension.

  3. Iron chelation inhibits the development of pulmonary vascular remodeling

    PubMed Central

    Wong, Chi-Ming; Preston, Ioana R.; Hill, Nicholas S.; Suzuki, Yuichiro J.

    2012-01-01

    Reactive oxygen species (ROS) have been implicated in the pathogenesis of pulmonary hypertension. Since iron is an important regulator of ROS biology, the present study examined the effect of iron chelation on the development of pulmonary vascular remodeling. The administration of an iron chelator, deferoxamine, to rats prevented chronic hypoxia-induced pulmonary hypertension and pulmonary vascular remodeling. Various iron chelators inhibited growth of cultured pulmonary artery smooth muscle cells. Protein carbonylation, an important iron-dependent biological event, was promoted in association with pulmonary vascular remodeling and cell growth. A proteomic approach identified that Rho GDP-dissociation inhibitor (a negative regulator of RhoA) is carbonylated. In human plasma, the protein carbonyl content was significantly higher in patients with idiopathic pulmonary arterial hypertension than in healthy controls. These results suggest that iron plays an important role in the ROS-dependent mechanism underlying the development of pulmonary hypertension. PMID:22974762

  4. Two Functional Variants of IRF5 Influence the Development of Macular Edema in Patients with Non-Anterior Uveitis

    PubMed Central

    Cordero-Coma, Miguel; Ortego-Centeno, Norberto; Adán, Alfredo; Fonollosa, Alejandro; Díaz Valle, David; Pato, Esperanza; Blanco, Ricardo; Cañal, Joaquín; Díaz-Llopis, Manuel; de Ramón, Enrique; del Rio, María José; García Serrano, José Luis; Artaraz, Joseba; Martín-Villa, José Manuel; Llorenç, Víctor; Gorroño-Echebarría, Marina Begoña; Martín, Javier

    2013-01-01

    Objective Interferon (IFN) signaling plays a crucial role in autoimmunity. Genetic variation in interferon regulatory factor 5 (IRF5), a major regulator of the type I interferon induction, has been associated with risk of developing several autoimmune diseases. In the current study we aimed to evaluate whether three sets of correlated IRF5 genetic variants, independently associated with SLE and with different functional roles, are involved in uveitis susceptibility and its clinical subphenotypes. Methods Three IRF5 polymorphisms, rs2004640, rs2070197 and rs10954213, representative of each group, were genotyped using TaqMan® allelic discrimination assays in a total of 263 non-anterior uveitis patients and 724 healthy controls of Spanish origin. Results A clear association between two of the three analyzed genetic variants, rs2004640 and rs10954213, and the absence of macular edema was observed in the case/control analysis (PFDR=5.07E-03, OR=1.48, CI 95%=1.14-1.92 and PFDR=3.37E-03, OR=1.54, CI 95%=1.19-2.01, respectively). Consistently, the subphenotype analysis accordingly with the presence/absence of this clinical condition also reached statistical significance (rs2004640: P=0.037, OR=0.69, CI 95%=0.48-0.98; rs10954213: P=0.030, OR=0.67, CI 95%=0.47-0.96), thus suggesting that both IRF5 genetic variants are specifically associated with the lack of macular edema in uveitis patients. Conclusion Our results clearly showed for the first time that two functional genetic variants of IRF5 may play a role in the development of macular edema in non-anterior uveitis patients. Identifying genetic markers for macular edema could lead to the possibility of developing novel treatments or preventive therapies. PMID:24116155

  5. [Pathopshysiological mechanisms in macular edema].

    PubMed

    Turlea, Cristian; Zolog, Ileana; Blăjan, Codruta; Roşca, C; Turlea, Magdalena; Munteanu, Mihnea; Boruga, Ovidiu

    2014-01-01

    The treatment of diabetic macular edema has known a fast development in the last 5 years where the transition from laser monotherapy to intravitreal pharmacotherapy is becoming standard practice. Intravitreal injections therapy is in a continuous development with promising positive results. The use of intratvitreal devices in the treatment of macular edema of vascular cause has become a viable alternative also in treating diabetic macular edema. Several clinical studies have revealed the superiority of intravitreal treatment versus laser monotherapy. This article is evaluating and reviewing present and future treatments used to combat diabetic macular edema. [corrected].

  6. Effect of a Dynamic Air Cushion on the Development of Leg Edema during Wheelchair Sitting.

    PubMed

    Murata, Jun; Murata, Shin; Ohyama, Michie; Kogo, Haruki; Matsubara, Shohzo

    2014-06-01

    [Purpose] To clarify how a novel dynamic cushion affects the leg edema evoked by wheelchair sitting, we measured the changes in leg volume induced during wheelchair sitting with the dynamic air cushion or a static cushion. [Subjects and Methods] Nine healthy male subjects participated in this study. Leg edema during wheelchair sitting was evaluated with strain gauge plethysmography (the gauge was placed around the middle portion of the lower thigh). Following a period of rest, each subject was asked to sit on a wheelchair containing the dynamic cushion for 15 min. Then, the protocol was repeated with a static cushion. The angles of the knee and ankle joints were set to 90 degrees, and no footrests were used. [Results] The change in leg volume observed during sitting on the dynamic cushion (0.00 ± 0.03 mL/100 mL) was smaller than that observed during sitting on the static cushion (0.02 ± 0.02 mL/100 mL). [Conclusion] These results suggested that the dynamic cushion relieved leg edema during wheelchair sitting.

  7. Elevated blood plasma levels of epinephrine, norepinephrine, tyrosine hydroxylase, TGFβ1, and TNFα associated with high-altitude pulmonary edema in an Indian population.

    PubMed

    Pandey, Priyanka; Ali, Zahara; Mohammad, Ghulam; Pasha, M A Qadar

    2016-01-01

    Biomarkers are essential to unravel the locked pathophysiology of any disease. This study investigated the role of biomarkers and their interactions with each other and with the clinical parameters to study the physiology of high-altitude pulmonary edema (HAPE) in HAPE-patients (HAPE-p) against adapted highlanders (HLs) and healthy sojourners, HAPE-controls (HAPE-c). For this, seven circulatory biomarkers, namely, epinephrine, norepinephrine, tyrosine hydroxylase, transforming growth factor beta 1, tumor necrosis factor alpha (TNFα), platelet-derived growth factor beta beta, and C-reactive protein (CRP), were measured in blood plasma of the three study groups. All the subjects were recruited at ~3,500 m, and clinical features such as arterial oxygen saturation (SaO2), body mass index, and mean arterial pressure were measured. Increased levels of epinephrine, norepinephrine, tyrosine hydroxylase, transforming growth factor-beta 1, and TNFα were observed in HAPE-p against the healthy groups, HAPE-c, and HLs (P<0.0001). CRP levels were decreased in HAPE-p against HAPE-c and HLs (P<0.0001). There was no significant difference or very marginal difference in the levels of these biomarkers in HAPE-c and HLs (P>0.01). Correlation analysis revealed a negative correlation between epinephrine and norepinephrine (P=4.6E-06) in HAPE-p and positive correlation in HAPE-c (P=0.004) and HLs (P=9.78E-07). A positive correlation was observed between TNFα and CRP (P=0.004) in HAPE-p and a negative correlation in HAPE-c (P=4.6E-06). SaO2 correlated negatively with platelet-derived growth factor beta beta (HAPE-p; P=0.05), norepinephrine (P=0.01), and TNFα (P=0.005) and positively with CRP (HAPE-c; P=0.02) and norepinephrine (HLs; P=0.04). Body mass index correlated negatively with epinephrine (HAPE-p; P=0.001) and positively with norepinephrine and tyrosine hydroxylase in HAPE-c (P<0.05). Mean arterial pressure correlated positively with TNFα in HAPE-p and norepinephrine in HLs (P

  8. Elevated blood plasma levels of epinephrine, norepinephrine, tyrosine hydroxylase, TGFβ1, and TNFα associated with high-altitude pulmonary edema in an Indian population

    PubMed Central

    Pandey, Priyanka; Ali, Zahara; Mohammad, Ghulam; Pasha, M A Qadar

    2016-01-01

    Biomarkers are essential to unravel the locked pathophysiology of any disease. This study investigated the role of biomarkers and their interactions with each other and with the clinical parameters to study the physiology of high-altitude pulmonary edema (HAPE) in HAPE-patients (HAPE-p) against adapted highlanders (HLs) and healthy sojourners, HAPE-controls (HAPE-c). For this, seven circulatory biomarkers, namely, epinephrine, norepinephrine, tyrosine hydroxylase, transforming growth factor beta 1, tumor necrosis factor alpha (TNFα), platelet-derived growth factor beta beta, and C-reactive protein (CRP), were measured in blood plasma of the three study groups. All the subjects were recruited at ~3,500 m, and clinical features such as arterial oxygen saturation (SaO2), body mass index, and mean arterial pressure were measured. Increased levels of epinephrine, norepinephrine, tyrosine hydroxylase, transforming growth factor-beta 1, and TNFα were observed in HAPE-p against the healthy groups, HAPE-c, and HLs (P<0.0001). CRP levels were decreased in HAPE-p against HAPE-c and HLs (P<0.0001). There was no significant difference or very marginal difference in the levels of these biomarkers in HAPE-c and HLs (P>0.01). Correlation analysis revealed a negative correlation between epinephrine and norepinephrine (P=4.6E−06) in HAPE-p and positive correlation in HAPE-c (P=0.004) and HLs (P=9.78E−07). A positive correlation was observed between TNFα and CRP (P=0.004) in HAPE-p and a negative correlation in HAPE-c (P=4.6E−06). SaO2 correlated negatively with platelet-derived growth factor beta beta (HAPE-p; P=0.05), norepinephrine (P=0.01), and TNFα (P=0.005) and positively with CRP (HAPE-c; P=0.02) and norepinephrine (HLs; P=0.04). Body mass index correlated negatively with epinephrine (HAPE-p; P=0.001) and positively with norepinephrine and tyrosine hydroxylase in HAPE-c (P<0.05). Mean arterial pressure correlated positively with TNFα in HAPE-p and norepinephrine in

  9. Recapitulation of developing artery muscularization in pulmonary hypertension.

    PubMed

    Sheikh, Abdul Q; Lighthouse, Janet K; Greif, Daniel M

    2014-03-13

    Excess smooth muscle accumulation is a key component of many vascular disorders, including atherosclerosis, restenosis, and pulmonary artery hypertension, but the underlying cell biological processes are not well defined. In pulmonary artery hypertension, reduced pulmonary artery compliance is a strong independent predictor of mortality, and pathological distal arteriole muscularization contributes to this reduced compliance. We recently demonstrated that embryonic pulmonary artery wall morphogenesis consists of discrete developmentally regulated steps. In contrast, poor understanding of distal arteriole muscularization in pulmonary artery hypertension severely limits existing therapies that aim to dilate the pulmonary vasculature but have modest clinical benefit and do not prevent hypermuscularization. Here, we show that most pathological distal arteriole smooth muscle cells, but not alveolar myofibroblasts, derive from pre-existing smooth muscle. Furthermore, the program of distal arteriole muscularization encompasses smooth muscle cell dedifferentiation, distal migration, proliferation, and then redifferentiation, thereby recapitulating many facets of arterial wall development. PMID:24582963

  10. Pulmonary vascular development goes awry in congenital lung abnormalities.

    PubMed

    Kool, Heleen; Mous, Daphne; Tibboel, Dick; de Klein, Annelies; Rottier, Robbert J

    2014-12-01

    Pulmonary vascular diseases of the newborn comprise a wide range of pathological conditions with developmental abnormalities in the pulmonary vasculature. Clinically, pulmonary arterial hypertension (PH) is characterized by persistent increased resistance of the vasculature and abnormal vascular response. The classification of PH is primarily based on clinical parameters instead of morphology and distinguishes five groups of PH. Congenital lung anomalies, such as alveolar capillary dysplasia (ACD) and PH associated with congenital diaphragmatic hernia (CDH), but also bronchopulmonary dysplasia (BPD), are classified in group three. Clearly, tight and correct regulation of pulmonary vascular development is crucial for normal lung development. Human and animal model systems have increased our knowledge and make it possible to identify and characterize affected pathways and study pivotal genes. Understanding of the normal development of the pulmonary vasculature will give new insights in the origin of the spectrum of rare diseases, such as CDH, ACD, and BPD, which render a significant clinical problem in neonatal intensive care units around the world. In this review, we describe normal pulmonary vascular development, and focus on four diseases of the newborn in which abnormal pulmonary vascular development play a critical role in morbidity and mortality. In the future perspective, we indicate the lines of research that seem to be very promising for elucidating the molecular pathways involved in the origin of congenital pulmonary vascular disease. PMID:25424472

  11. Pulmonary Function in Children with Development Coordination Disorder

    ERIC Educational Resources Information Center

    Wu, Sheng K.; Cairney, John; Lin, Hsiao-Hui; Li, Yao-Chuen; Song, Tai-Fen

    2011-01-01

    The purpose of this study was to compare pulmonary function in children with developmental coordination disorder (DCD) with children who are typically developing (TD), and also analyze possible gender differences in pulmonary function between these groups. The Movement ABC test was used to identify the movement coordination ability of children.…

  12. Lung edema due to hydrogen peroxide is independent of cyclooxygenase products

    SciTech Connect

    Burghuber, O.; Mathias, M.M.; McMurtry, I.F.; Reeves, J.T.; Voelkel, N.F.

    1984-01-01

    Active oxygen species can cause lung injury. Although a direct action on endothelial cells is proposed, the possibility exists that they might cause injury via mediators. We considered that active oxygen species would stimulate the generation of cyclooxygenase metabolites, which then alter pulmonary vasoreactivity and cause edema. We chemically produced hydrogen peroxide by adding glucose oxidase to a plasma- and cell-free, but ..beta..-D-glucose-containing, solution, which perfused isolated rat lungs. Addition of glucose oxidase to the perfusate caused a marked decrease in pulmonary vasoreactivity, accompanied by an increase in the concentrations of prostacyclin, thromboxane A/sub 2/, and prostaglandin F/sub 2..cap alpha../. Pretreatment with catalase, a specific scavenger of hydrogen peroxide, preserved pulomonary vasoreactivity, inhibited the increase of the concentration of the measured prostaglandins, and prevented edema formation. Indomethacin effectively blocked lung prostaglandin production but neither prevented the decrease in vasoreactivity nor inhibited edema formation. From these data we conclude the hydrogen peroxide impaired pulmonary vasoreactivity and subsequently caused edema. Depsite the fact that hydrogen peroxide stimulated lung prostaglandin production, cyclooxygenase-derived products neither caused the decrease in vasoreactivity nor the development of edema.

  13. Notch3 signaling promotes the development of pulmonary arterial hypertension.

    PubMed

    Li, Xiaodong; Zhang, Xiaoxue; Leathers, Robin; Makino, Ayako; Huang, Chengqun; Parsa, Pouria; Macias, Jesus; Yuan, Jason X-J; Jamieson, Stuart W; Thistlethwaite, Patricia A

    2009-11-01

    Notch receptor signaling is implicated in controlling smooth muscle cell proliferation and in maintaining smooth muscle cells in an undifferentiated state. Pulmonary arterial hypertension is characterized by excessive vascular resistance, smooth muscle cell proliferation in small pulmonary arteries, leading to elevation of pulmonary vascular resistance, right ventricular failure and death. Here we show that human pulmonary hypertension is characterized by overexpression of NOTCH3 in small pulmonary artery smooth muscle cells and that the severity of disease in humans and rodents correlates with the amount of NOTCH3 protein in the lung. We further show that mice with homozygous deletion of Notch3 do not develop pulmonary hypertension in response to hypoxic stimulation and that pulmonary hypertension can be successfully treated in mice by administration of N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT), a gamma-secretase inhibitor that blocks activation of Notch3 in smooth muscle cells. We show a mechanistic link from NOTCH3 receptor signaling through the Hairy and enhancer of Split-5 (HES-5) protein to smooth muscle cell proliferation and a shift to an undifferentiated smooth muscle cell phenotype. These results suggest that the NOTCH3-HES-5 signaling pathway is crucial for the development of pulmonary arterial hypertension and provide a target pathway for therapeutic intervention. PMID:19855400

  14. Polymorphisms of the Tissue Inhibitor of Metalloproteinase 3 Gene Are Associated with Resistance to High-Altitude Pulmonary Edema (HAPE) in a Japanese Population: A Case Control Study Using Polymorphic Microsatellite Markers

    PubMed Central

    Kobayashi, Nobumitsu; Hanaoka, Masayuki; Droma, Yunden; Ito, Michiko; Katsuyama, Yoshihiko; Kubo, Keishi; Ota, Masao

    2013-01-01

    Introduction High-altitude pulmonary edema (HAPE) is a hypoxia-induced, life-threatening, high permeability type of edema attributable to pulmonary capillary stress failure. Genome-wide association analysis is necessary to better understand how genetics influence the outcome of HAPE. Materials and Methods DNA samples were collected from 53 subjects susceptible to HAPE (HAPE-s) and 67 elite Alpinists resistant to HAPE (HAPE-r). The genome scan was carried out using 400 polymorphic microsatellite markers throughout the whole genome in all subjects. In addition, six single nucleotide polymorphisms (SNPs) of the gene encoding the tissue inhibitor of metalloproteinase 3 (TIMP3) were genotyped by Taqman® SNP Genotyping Assays. Results The results were analyzed using case-control comparisons. Whole genome scanning revealed that allele frequencies in nine markers were statistically different between HAPE-s and HAPE-r subjects. The SNP genotyping of the TIMP3 gene revealed that the derived allele C of rs130293 was associated with resistance to HAPE [odds ratio (OR) = 0.21, P = 0.0012) and recessive inheritance of the phenotype of HAPE-s (P = 0.0012). A haplotype CAC carrying allele C of rs130293 was associated with resistance to HAPE. Discussion This genome-wide association study revealed several novel candidate genes associated with susceptibility or resistance to HAPE in a Japanese population. Among those, the minor allele C of rs130293 (C/T) in the TIMP3 gene was linked to resistance to HAPE; while, the ancestral allele T was associated with susceptibility to HAPE. PMID:23991023

  15. Pulmonary stenosis development and reduction of pulmonary arterial hypertension in atrioventricular septal defect: a case report

    PubMed Central

    Barth, Emeline; Bouvaist, Hélène; Marlière, Stéphanie; Ninet, Gérard; Vanzetto, Gérald

    2009-01-01

    A 24-year-old patient was admitted for dyspnoea and syncope. He had a previous history of complete atrio-ventricular septal defect and trisomy 21. At the age of 6 months, in 1984, cardiac catheterization revealed a quasi-systemic pulmonary arterial hypertension with a bidirectional shunt corresponding to an Eisenmenger syndrome. Corrective cardiac surgery was not performed at this time because surgical risk was considered too high. Until the age of 20 years old, he showed few symptoms while under medical treatment. But since 2006, his functional status became worse with an increased dyspnoea, syncopes, and severe cyanosis. In these conditions, haemodynamic parameters have been re-evaluated in 2006 and 2008. They highlighted a late and progressive development of a valvular and infundibular pulmonary stenosis leading to a normalisation of pulmonary arterial pressures. At the age of 24 , the patient underwent corrective cardiac surgery which was successful. Late development of both infundibular and valvular pulmonary stenosis have not been described before in non operated congenital ventricular septal defects, but development of one or the other abnormality would be found in 8% of patients. The physiopathological mechanism of this obstruction is unclear. Nevertheless, in unoperated congenital cardiac shunt lesions, reversibility of severe pulmonary arterial hypertension should be reconidered and re-assessed during follow up. PMID:19758423

  16. Development of pulmonary vascular response to oxygen

    SciTech Connect

    Morin, F.C. III, Egan, E.A.; Ferguson, W.; Lundgren, C.E. )

    1988-03-01

    The ability of the pulmonary circulation of the fetal lamb to respond to a rise in oxygen tension was studied from 94 to 146 days of gestation. The unanesthetized ewe breathed room air at normal atmospheric pressure, followed by 100% oxygen at three atmospheres absolute pressure in a hyperbaric chamber. In eleven near-term lambs, fetal arterial oxygen tension (Pa{sub O{sub 2}}) increased from 25 to 55 Torr, which increased the proportion or right ventricular output distributed to the fetal lungs from 8 to 59%. In five very immature lambs fetal Pa{sub O{sub 2}} increased from 27 to 174 Torr, but the proportion of right ventricular output distributed to the lung did not change. In five of the near-term lambs, pulmonary blood flow was measured. For each measurement of the distribution of blood flow, approximately 8 {times} 10{sup 5} spheres of 15-{mu}m diameter, labeled with either {sup 153}Gd, {sup 113}Sn, {sup 103}Ru, {sup 95}Nb, or {sup 46}Sc were injected. It increased from 34 to 298 ml {center dot} kg fetal wt{sup {minus}1} {center dot} min{sup {minus}1}, an 8.8-fold increase. The authors conclude that the pulmonary circulation of the fetal lamb does not respond to an increase in oxygen tension before 101 days of gestation; however, near term an increase in oxygen tension alone can induce the entire increase in pulmonary blood flow that normally occurs after the onset of breathing at birth.

  17. Notch Activation of Ca2+ Signaling in the Development of Hypoxic Pulmonary Vasoconstriction and Pulmonary Hypertension

    PubMed Central

    Smith, Kimberly A.; Voiriot, Guillaume; Tang, Haiyang; Fraidenburg, Dustin R.; Song, Shanshan; Yamamura, Hisao; Yamamura, Aya; Guo, Qiang; Wan, Jun; Pohl, Nicole M.; Tauseef, Mohammad; Bodmer, Rolf; Ocorr, Karen; Thistlethwaite, Patricia A.; Haddad, Gabriel G.; Powell, Frank L.; Makino, Ayako; Mehta, Dolly

    2015-01-01

    Hypoxic pulmonary vasoconstriction (HPV) is an important physiological response that optimizes the ventilation/perfusion ratio. Chronic hypoxia causes vascular remodeling, which is central to the pathogenesis of hypoxia-induced pulmonary hypertension (HPH). We have previously shown that Notch3 is up-regulated in HPH and that activation of Notch signaling enhances store-operated Ca2+ entry (SOCE), an important mechanism that contributes to pulmonary arterial smooth muscle cell (PASMC) proliferation and contraction. Here, we investigate the role of Notch signaling in HPV and hypoxia-induced enhancement of SOCE. We examined SOCE in human PASMCs exposed to hypoxia and pulmonary arterial pressure in mice using the isolated perfused/ventilated lung method. Wild-type and canonical transient receptor potential (TRPC) 6−/− mice were exposed to chronic hypoxia to induce HPH. Inhibition of Notch signaling with a γ-secretase inhibitor attenuates hypoxia-enhanced SOCE in PASMCs and hypoxia-induced increase in pulmonary arterial pressure. Our results demonstrate that hypoxia activates Notch signaling and up-regulates TRPC6 channels. Additionally, treatment with a Notch ligand can mimic hypoxic responses. Finally, inhibition of TRPC6, either pharmacologically or genetically, attenuates HPV, hypoxia-enhanced SOCE, and the development of HPH. These results demonstrate that hypoxia-induced activation of Notch signaling mediates HPV and the development of HPH via functional activation and up-regulation of TRPC6 channels. Understanding the molecular mechanisms that regulate cytosolic free Ca2+ concentration and PASMC proliferation is critical to elucidation of the pathogenesis of HPH. Targeting Notch regulation of TRPC6 will be beneficial in the development of novel therapies for pulmonary hypertension associated with hypoxia. PMID:25569851

  18. Cardiovascular Magnetic Resonance Imaging of Scar Development Following Pulmonary Vein Isolation: A Prospective Study

    PubMed Central

    Knowles, Benjamin R.; Manning, Warren J.; Josephson, Mark E.

    2014-01-01

    Aims Cardiovascular magnetic resonance (MR) provides non-invasive assessment of early (24-hour) edema and injury following pulmonary vein isolation (by ablation) and subsequent scar formation. We hypothesize that 24-hours after ablation, cardiovascular MR would demonstrate a pattern of edema and injury due to ablation and the severity would correlate with subsequent scar. Methods Fifteen atrial fibrillation patients underwent cardiovascular MR prior to pulmonary vein isolation, 24-hours post (N = 11) and 30-days post (N = 7) ablation, with T2-weighted (T2W) and late gadolinium enhancement (LGE) imaging. Left atrial wall thickness, edema enhancement ratio and LGE enhancement were assessed at each time point. Volumes of LGE and edema enhancement were measured, and the circumferential presence of injury was assessed at 24-hours, including comparison with LGE enhancement at 30 days. Results Left atrial wall thickness was increased 24-hours post-ablation (10.7±4.1 mm vs. 7.0±1.8 mm pre-PVI, p<0.05). T2W enhancement at 24-hours showed increased edema enhancement ratio (1.5±0.4 for post-ablation, vs. 0.9±0.2 pre-ablation, p<0.001). Edema and LGE volumes at 24-hours were correlated with 30-day LGE volume (R = 0.76, p = 0.04, and R = 0.74, p = 0.09, respectively). Using a 16 segment model for assessment, 24-hour T2W had sensitivity, specificity, and accuracy of 82%, 63%, and 79% respectively, for predicting 30-day LGE. 24-hour LGE had sensitivity, specificity, and accuracy of 91%, 47%, and 84%. Conclusions Increased left atrial wall thickening and edema were characterized on cardiovascular MR early post-ablation, and found to correlate with 30-day LGE scar. PMID:25251403

  19. High-altitude cerebral edema with absence of headache.

    PubMed

    Thomassen, Oyvind; Skaiaa, Sven Chr

    2007-01-01

    Headache is the cardinal symptom of acute mountain sickness (AMS). The headache normally worsens, with increased cerebral affection and the development of high-altitude cerebral edema (HACE). A Norwegian expedition aimed to climb Baruntse (7129 m) in Nepal in 2003. At 5400 m a 35-year-old man felt exhausted. The next day he aborted his attempt at further climbing as a result of extreme fatigue. Over the next 24 hours he developed cough, dyspnea, and severe hypoxia before progressing to ataxia and blurred vision. At no point did he experience headache or nausea. The patient was evacuated by helicopter. He improved immediately after descent and recovered completely within a week. The speed of progression from AMS to HACE varies. Abrupt onset of HACE is occasionally reported. High-altitude pulmonary edema (HAPE) may induce severe hypoxia that can lead to rapid development of HACE. High-altitude cerebral edema in the setting of HAPE was the most likely diagnosis despite the unusual lack of headache. Rapid onset of HAPE with subsequent severe desaturation should raise awareness of the development of HACE, even in the absence of headache. PMID:17447714

  20. Preadult Stage Parasites and Multiple Timed Exposure to Infective Larvae Are Involved in Development of Limb Edema in Brugia malayi-Infected Indian Leaf Monkeys (Presbytis entellus)†

    PubMed Central

    Murthy, P. K.; Khan, M. A.; Rajani, H. B.; Srivastava, V. M. L.

    2002-01-01

    The pathogenesis of filarial limb edema is not known. The role of parasitological variables and parasite-mediated phenomena in the development of limb edema was investigated in the Presbytis entellus-Brugia malayi model. Infection was initiated with subcutaneous inoculation of infective third-stage larvae (L3), and the animals were reexposed to different doses of L3 at the prepatent, patent, and diminishing microfilaremia (0 to 5% of peak microfilaremia count) stages of infection. A large L3 inoculum size and repeated inoculation in the ankle region during the prepatent, patent, and diminishing microfilaremia stages of infection were found to be necessary for reproducible induction of limb edema. The preadult stage of the parasite was found to be the most potent inducer of limb edema, followed by L5 and L4. The presence of the proinflammatory cytokines tumor necrosis factor alpha, interleukin-1β, and interleukin-6 in edema fluid in the leg receiving the parasite challenge indicated that the limb edema development was due to parasite-mediated cytokine responses. The absence of bacterial infection or anti-streptolysin O titer in the edema fluid and blood indicated that bacterial infection is not necessary for the development of limb edema. PMID:12093695

  1. Estrogens and development of pulmonary hypertension - Interaction of estradiol metabolism and pulmonary vascular disease

    PubMed Central

    Tofovic, Stevan P.

    2010-01-01

    endothelial remodeling in PAH and this may be even more significant if the E2’s effects on injured endothelium are not opposed by 2ME (e.g., in the event of reduced E2 conversion to 2ME due to hypoxia, inflammation, drugs, environmental factors, or genetic polymorphism of metabolizing enzymes). This review focuses on the effects of estrogens and their metabolites on pulmonary vascular pathobiology and the development of experimental PAH, and offers potential explanation for the estrogen paradox in PAH. Furthermore, we propose that unbalanced estradiol metabolism may lead to the development of PAH. Recent animal data and studies in patients with PAH support this concept. PMID:20881610

  2. Transient Corneal Edema is a Predictive Factor for Pseudophakic Cystoid Macular Edema after Uncomplicated Cataract Surgery

    PubMed Central

    Do, Jae Rock; Oh, Jong-Hyun; Chuck, Roy S.

    2015-01-01

    Purpose To report transient corneal edema after phacoemulsification as a predictive factor for the development of pseudophakic cystoid macular edema (PCME). Methods A total of 150 eyes from 150 patients (59 men and 91 women; mean age, 68.0 ± 10.15 years) were analyzed using spectral domain optical coherence tomography 1 week and 5 weeks after routine phacoemulsification cataract surgery. Transient corneal edema detected 1 week after surgery was analyzed to reveal any significant relationship with the development of PCME 5 weeks after surgery. Results Transient corneal edema developed in 17 (11.3%) of 150 eyes 1 week after surgery. A history of diabetes mellitus was significantly associated with development of transient corneal edema (odds ratio [OR], 4.04; 95% confidence interval [CI], 1.41 to 11.54; p = 0.011). Both diabetes mellitus and transient corneal edema were significantly associated with PCME development 5 weeks after surgery (OR, 4.58; 95% CI, 1.56 to 13.43; p = 0.007; and OR, 6.71; CI, 2.05 to 21.95; p = 0.003, respectively). In the 8 eyes with both diabetes mellitus and transient corneal edema, 4 (50%) developed PCME 5 weeks after surgery. Conclusions Transient corneal edema detected 1 week after routine cataract surgery is a predictive factor for development of PCME. Close postoperative observation and intervention is recommended in patients with transient corneal edema. PMID:25646056

  3. [Vulvar edema in pregnancy].

    PubMed

    Radomański, T; Sikorski, R; Baszak, E

    1998-12-01

    Reported is a case of massive vulvar edema complicating pregnancy probably as a result of mycotic vulvovaginitis or chemical vulvitis associated with drugs being used in the medication. Medical therapy failed to relieve the edema while the mechanical drainage showed to be an effective method of treatment. PMID:10224778

  4. Interferon-Stimulated Gene 15 Upregulation Precedes the Development of Blood–Brain Barrier Disruption and Cerebral Edema after Traumatic Brain Injury in Young Mice

    PubMed Central

    Todd, Tracey; Daniels, Zachary; Bazan, Nicolas G.; Belayev, Ludmila

    2015-01-01

    Abstract Recent studies show that myosin light chain kinase (MLCK) plays a pivotal role in development of cerebral edema, a known complication following traumatic brain injury (TBI) in children and a contributing factor to worsened neurologic recovery. Interferon-stimulated gene 15 (ISG15) is upregulated after cerebral ischemia and is neuroprotective. The significant role of ISG15 after TBI has not been studied. Postnatal Day (PND) 21 and PND24 mice were subjected to lateral closed-skull injury with impact depth of 2.0 or 2.25 mm. Behavior was examined at 7 d using two-object novel recognition and Wire Hang tests. Mice were sacrificed at 6 h, 12 h, 24 h, 48 h, 72 h, and 7 d. ISG15 and MLCK were analyzed by Western blot and immunohistochemistry, blood–brain barrier (BBB) disruption with Evans Blue (EB), and cerebral edema with wet/dry weights. EB extravasation and edema peaked at 72 h in both ages. PND21 mice had more severe neurological deficits, compared with PND24 mice. PND24 mice showed peak ISG15 expression at 6 h, and PND21 mice at 72 h. MLCK peaked in both age groups at 12 h and co-localized with ISG15 on immunohistochemistry and co-immunoprecipitation. These studies provide evidence, ISG15 is elevated following TBI in mice, preceding MLCK elevation, development of BBB disruption, and cerebral edema. PMID:25669448

  5. Development of a patient needs assessment model for pulmonary rehabilitation.

    PubMed

    Sully, Jennie-Laure; Baltzan, Marcel A; Wolkove, Norman; Demers, Louise

    2012-01-01

    Patients with chronic obstructive pulmonary disease are often referred to pulmonary rehabilitation programs to manage their symptoms and the consequences of the disease on their lives. Finding ways to target programs to a specific patient's needs could help improve individual response to the program. The purpose of this study was to develop a conceptual model for the assessment of patients' rehabilitation needs by using a grounded theory approach. Focus groups, consultations of medical charts, and a literature review helped us develop a conceptual model characterized by the following categories: need recognition, knowledge, motivation, expectations, goals, ability to fulfill needs, and the ability for personal adjustment. Based on a content matrix reflecting the conceptual model and disease consequences, items to be included in a prototype instrument were formulated and a preliminary validation phase was conducted.

  6. Pulmonary atresia

    MedlinePlus

    ... disease - pulmonary atresia; Cyanotic heart disease - pulmonary atresia; Valve - disorder pulmonary atresia ... septum may also have a poorly developed tricuspid valve. They may also have an underdeveloped right ventricle ...

  7. Roles of changes in active glutamine transport in brain edema development during hepatic encephalopathy: an emerging concept.

    PubMed

    Zielińska, Magdalena; Popek, Mariusz; Albrecht, Jan

    2014-01-01

    Excessive glutamine (Gln) synthesis in ammonia-overloaded astrocytes contributes to astrocytic swelling and brain edema, the major complication of hepatic encephalopathy (HE). Much of the newly formed Gln is believed to enter mitochondria, where it is recycled to ammonia, which causes mitochondrial dysfunction (a "Trojan horse" mode of action). A portion of Gln may increase osmotic pressure in astrocytes and the interstitial space, directly and independently contributing to brain tissue swelling. Here we discuss the possibility that altered functioning of Gln transport proteins located in the cellular or mitochondrial membranes, modulates the effects of increased Gln synthesis. Accumulation of excess Gln in mitochondria involves a carrier-mediated transport which is activated by ammonia. Studies on the expression of the cell membrane N-system transporters SN1 (SNAT3) and SN2 (SNAT5), which mediate Gln efflux from astrocytes rendered HE model-dependent effects. HE lowered the expression of SN1 at the RNA and protein level in the cerebral cortex (cc) in the thioacetamide (TAA) model of HE and the effect paralleled induction of cerebral cortical edema. Neither SN1 nor SN2 expression was affected by simple hyperammonemia, which produces no cc edema. TAA-induced HE is also associated with decreased expression of mRNA coding for the system A carriers SAT1 and SAT2, which stimulate Gln influx to neurons. Taken together, changes in the expression of Gln transporters during HE appear to favor retention of Gln in astrocytes and/or the interstitial space of the brain. HE may also affect arginine (Arg)/Gln exchange across the astrocytic cell membrane due to changes in the expression of the hybrid Arg/Gln transporter y(+)LAT2. Gln export from brain across the blood-brain barrier may be stimulated by HE via its increased exchange with peripheral tryptophan. PMID:24072671

  8. Incidence and recognition of interstitial pulmonary fibrosis in developing countries.

    PubMed

    Jindal, S K; Gupta, D

    1997-09-01

    Interstitial pulmonary fibrosis in developing countries is now diagnosed with an increased frequency. Increased awareness and more frequent availability of computed tomography and fiberoptic bronchoendoscopy have helped in making the diagnosis more often. The spectrum of diseases causing pulmonary fibrosis is broadly similar to that seen in the West. Connective tissue disorders such as systemic sclerosis and rheumatoid arthritis and sarcoidosis are more common causes. Idiopathic fibrosis is seen in approximately half the patients. Pneumoconiosis such as silicosis are also important. Diagnosis is often established on the basis of clinical features and radiologic findings alone. Transbronchial lung biopsy is used as a frequent method to make histologic diagnosis. Some of the causes described from India are rather rare. One of the interesting examples included a patient in whom pulmonary fibrosis was related to his ascent to very high altitude. Extreme cold, solar radiation, and other factors complicating low atmospheric oxygen pressure were implicated as causative factors. Lung fibrosis, secondary to exposure to toxic gas (methyl isocyanate), is reported in survivors of the Bhopal gas leakage tragedy of 1984. Serial bronchoalveolar studies have show elevated fibronectin levels and the presence of macrophage-neutrophilic exudate in the lavage fluid.

  9. Alcohol exposure leads to unrecoverable cardiovascular defects along with edema and motor function changes in developing zebrafish larvae

    PubMed Central

    Li, Xu; Gao, Aiai; Wang, Yanan; Chen, Man; Peng, Jun; Yan, Huaying; Zhao, Xin; Feng, Xizeng

    2016-01-01

    ABSTRACT Maternal alcohol consumption during pregnancy can cause a series of developmental disorders in the fetus called FAS (fetal alcohol syndrome). In the present study we exposed zebrafish embryos to 1% and 2% alcohol and observed the morphology of heart and blood vessels during and after exposure to investigate motor function alterations, and damage and recovery to the cardiovascular system. The results showed that alcohol exposure could induce heart deformation, slower heart rate, and incomplete blood vessels and pericardium. After stopping exposure, larvae exposed to 1% alcohol could recover only in heart morphology, but larvae in 2% alcohol could not recover either morphology or function of cardiovascular system. The edema-like characteristics in the 2% alcohol group became more conspicuous afterwards, with destruction in the dorsal aorta, coarctation in segmental arteries and a decrease in motor function, implying more serious unrecoverable cardiovascular defects in the 2% group. The damaged blood vessels in the 2% alcohol group resulted in an alteration in permeability and a decrease of blood volume, which were the causes of edema in pathology. These findings contribute towards a better understanding of ethanol-induced cardiovascular abnormalities and co-syndrome in patients with FAS, and warns against excessive maternal alcohol consumption during pregnancy. PMID:27422904

  10. Alcohol exposure leads to unrecoverable cardiovascular defects along with edema and motor function changes in developing zebrafish larvae.

    PubMed

    Li, Xu; Gao, Aiai; Wang, Yanan; Chen, Man; Peng, Jun; Yan, Huaying; Zhao, Xin; Feng, Xizeng; Chen, Dongyan

    2016-01-01

    Maternal alcohol consumption during pregnancy can cause a series of developmental disorders in the fetus called FAS (fetal alcohol syndrome). In the present study we exposed zebrafish embryos to 1% and 2% alcohol and observed the morphology of heart and blood vessels during and after exposure to investigate motor function alterations, and damage and recovery to the cardiovascular system. The results showed that alcohol exposure could induce heart deformation, slower heart rate, and incomplete blood vessels and pericardium. After stopping exposure, larvae exposed to 1% alcohol could recover only in heart morphology, but larvae in 2% alcohol could not recover either morphology or function of cardiovascular system. The edema-like characteristics in the 2% alcohol group became more conspicuous afterwards, with destruction in the dorsal aorta, coarctation in segmental arteries and a decrease in motor function, implying more serious unrecoverable cardiovascular defects in the 2% group. The damaged blood vessels in the 2% alcohol group resulted in an alteration in permeability and a decrease of blood volume, which were the causes of edema in pathology. These findings contribute towards a better understanding of ethanol-induced cardiovascular abnormalities and co-syndrome in patients with FAS, and warns against excessive maternal alcohol consumption during pregnancy. PMID:27422904

  11. Developments in pulmonary arterial hypertension-targeted therapy for chronic thromboembolic pulmonary hypertension.

    PubMed

    Hadinnapola, Charaka; Pepke-Zaba, Joanna

    2015-10-01

    Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare disease characterised by the presence of organised chronic thromboembolic material occluding the proximal pulmonary arteries and a vasculopathy in the distal pulmonary arterial tree. Pulmonary endarterectomy (PEA) is a potential cure for many patients with CTEPH. However, PEA is not suitable for patients with a significant distal distribution of chronic thromboembolic material or with significant comorbidities. Also, a proportion of patients are left with residual CTEPH post PEA. Until recently, pulmonary arterial hypertension-targeted therapies have been used off licence to treat patients with inoperable or residual CTEPH. The CHEST1 study investigated the use of riociguat and was the first randomised controlled trial to show efficacy in inoperable or residual CTEPH. In this review, we explore the pathophysiology of CTEPH and review the current trial evidence for pulmonary arterial hypertension-targeted therapies. We also include a discussion of physiological considerations that require further investigation.

  12. Aquaporin-4 and traumatic brain edema.

    PubMed

    Xu, Miao; Su, Wei; Xu, Qiu-ping

    2010-04-01

    Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Classically, two major types of traumatic brain edema exist: "vasogenic" and "cytotoxic/cellular". However, the cellular and molecular mechanisms contributing to the development/resolution of traumatic brain edema are poorly understood and no effective drugs can be used now. Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 has been proposed as a novel drug target in brain edema. These findings suggest that modulation of AQP4 expression or function may be beneficial in traumatic brain edema.

  13. Laparoscopic Surgery Can Reduce Postoperative Edema Compared with Open Surgery

    PubMed Central

    Guo, Dong; Gong, Jianfeng; Cao, Lei; Wei, Yao; Guo, Zhen

    2016-01-01

    Aim. The study aimed to investigate the impact of laparoscopic surgery and open surgery on postoperative edema in Crohn's disease. Methods. Patients who required enterectomy were divided into open group (Group O) and laparoscopic group (Group L). Edema was measured using bioelectrical impedance analysis preoperatively (PRE) and on postoperative day 3 (POD3) and postoperative day 5 (POD5). The postoperative edema was divided into slight edema and edema by an edema index, defined as the ratio of total extracellular water to total body water. Results. Patients who underwent laparoscopic surgery had better clinical outcomes and lower levels of inflammatory and stress markers. A total of 31 patients (26.05%) developed slight edema and 53 patients (44.54%) developed edema on POD3. More patients developed postoperative edema in Group O than in Group L on POD3 (p = 0.006). The value of the edema index of Group O was higher than that of Group L on POD3 and POD5 (0.402 ± 0.010 versus 0.397 ± 0.008, p = 0.001; 0.401 ± 0.009 versus 0.395 ± 0.007, p = 0.039, resp.). Conclusions. Compared with open surgery, laparoscopic surgery can reduce postoperative edema, which may contribute to the better outcomes of laparoscopic surgery over open surgery. PMID:27777583

  14. Perspectives on edema in childhood nephrotic syndrome.

    PubMed

    Teoh, Chia Wei; Robinson, Lisa A; Noone, Damien

    2015-10-01

    There have been two major theories surrounding the development of edema in nephrotic syndrome (NS), namely, the under- and overfill hypotheses. Edema is one of the cardinal features of NS and remains one of the principal reasons for admission of children to the hospital. Recently, the discovery that proteases in the glomerular filtrate of patients with NS are activating the epithelial sodium channel (ENaC), resulting in intrarenal salt retention and thereby contributing to edema, might suggest that targeting ENaC with amiloride might be a suitable strategy to manage the edema of NS. Other potential agents, particularly urearetics and aquaretics, might also prove useful in NS. Recent evidence also suggests that there may be other areas involved in salt storage, especially the skin, and it will be intriguing to study the implications of this in NS.

  15. Latest advances in edema

    NASA Technical Reports Server (NTRS)

    Villavicencio, J. L.; Hargens, A. R.; Pikoulicz, E.

    1996-01-01

    Basic concepts in the physiopathology of edema are reviewed. The mechanisms of fluid exchange across the capillary endothelium are explained. Interstitial flow and lymph formation are examined. Clinical disorders of tissue and lymphatic transport, microcirculatory derangements in venous disorders, protein disorders, and lymphatic system disorders are explored. Techniques for investigational imaging of the lymphatic system are explained.

  16. Studying the pulmonary circulation with positron emission tomography

    SciTech Connect

    Schuster, D.P.; Mintun, M.A.

    1988-01-01

    Positron emission tomography and appropriately labeled, short-lived radiopharmaceuticals can be used to study a variety of physiologic processes within the lung. Recently, methods have been developed to measure regional pulmonary blood flow and pulmonary vascular permeability to protein macromolecules. The advantages of these techniques include accurate quantitation, regional data available in an image format, noninvasiveness, and repeatability. These methods have recently been applied to studies of hypoxic vasoconstriction, pulmonary edema, and chronic obstructive lung disease in man and large experimental animals. Although the technology is complex and requires the integration of people from a variety of disciplines, these methods offer a unique opportunity to study in vivo lung physiology.

  17. 78 FR 66744 - Draft Guidance for Industry on Pulmonary Tuberculosis: Developing Drugs for Treatment; Availability

    Federal Register 2010, 2011, 2012, 2013, 2014

    2013-11-06

    ... HUMAN SERVICES Food and Drug Administration Draft Guidance for Industry on Pulmonary Tuberculosis... industry entitled ``Pulmonary Tuberculosis: Developing Drugs for Treatment.'' The purpose of the draft... tuberculosis. This guidance applies to the development of a single investigational drug as well as...

  18. WNTLESS IS REQUIRED FOR PERIPHERAL LUNG DIFFERENTIATION AND PULMONARY VASCULAR DEVELOPMENT

    PubMed Central

    Cornett, Bridget; Snowball, John; Varisco, Brian M.; Lang, Richard; Whitsett, Jeffrey; Sinner, Debora

    2013-01-01

    Wntless (Wls), a gene highly conserved across the animal kingdom, encodes for a transmembrane protein that mediates Wnt ligand secretion. Wls is expressed in developing lung, wherein Wnt signaling is necessary for pulmonary morphogenesis. We hypothesize that Wls plays a critical role in modulating Wnt signaling during lung development and therefore affects processes critical for pulmonary morphogenesis. We generated conditional Wls mutant mice utilizing Shh-Cre and Dermo1-Cre mice to delete Wls in the embryonic respiratory epithelium and mesenchyme, respectively. Epithelial deletion of Wls disrupted lung branching morphogenesis, peripheral lung development and pulmonary endothelial differentiation. Epithelial Wls mutant mice died at birth due to respiratory failure caused by lung hypoplasia and pulmonary hemorrhage. In the lungs of these mice, VEGF and Tie2-angiopoietin signaling pathways, which mediate vascular development, were downregulated from early stages of development. In contrast, deletion of Wls in mesenchymal cells of the developing lung did not alter branching morphogenesis or early mesenchymal differentiation. In vitro assays support the concept that Wls acts in part via Wnt5a to regulate pulmonary vascular development. We conclude that epithelial Wls modulates Wnt ligand activities critical for pulmonary vascular differentiation and peripheral lung morphogenesis. These studies provide a new framework for understanding the molecular mechanisms underlying normal pulmonary vasculature formation and the dysmorphic pulmonary vasculature development associated with congenital lung disease. PMID:23523683

  19. [Pulmonary thromboembolism that developed during an airplane flight "economy-class syndrome"].

    PubMed

    Satoh, A; Daimaru, O; Magaki, K; Morishita, M; Katoh, H; Kawajiri, T; Miyara, H; Sakurai, E; Tutui, S; Oguri, T

    1998-06-01

    The occurrence of thromboembolic phenomena during long-duration airplane flights is called "economy-class syndrome". Recently it has become more popular for Japanese to go abroad by airplane, and an increase in the prevalence of pulmonary thromboembolism should be expected. However, there are few reports of the economy-class syndrome in Japan. A 52-year-old woman was admitted to our hospital because of chest discomfort and dyspnea that developed during an airplane flight. We suspected pulmonary thromboembolism, on the basis of a chest X-ray film and on electrocardiogram. A ventilation-perfusion lung scan disclosed mismatching between ventilation and perfusion in the right upper lung field. Pulmonary thromboembolism was confirmed by pulmonary arteriography. The patient was treated with heparin and urokinase. A phlebogram of the legs showed no significant findings. There was no history of thromboembolic disease or of consumption of oral contraceptives. We conclude that the pulmonary thromboembolism might have been caused by stasis of blood in the lower limb veins during the airplane flight. We emphasize the importance of including pulmonary thromboembolism in the differential diagnosis of patients with chest discomfort and dyspnea that develop during airplane flights. No noninvasive test can lead to a definitive diagnosis of pulmonary thromboembolism. Early pulmonary angiography should be recommended when pulmonary thromboembolism is suspected.

  20. QUANTITATIVE PCR ANALYSIS OF FUNGI IN DUST FROM HOMES OF INFANTS WHO DEVELOPED IDIOPATHIC PULMONARY HEMORRHAGING

    EPA Science Inventory

    Fungal concentrations were measured in the dust of six homes in Cleveland, OH, where a child developed pulmonary hemorrhage (pulmonary hemorrhage homes, i.e. PHH), and 26 reference homes (RH) with no known fungal contamination. QPCR assays for 82 species (or assay groups) were u...

  1. Loss of osteoclasts contributes to development of osteosarcoma pulmonary metastases.

    PubMed

    Endo-Munoz, Liliana; Cumming, Andrew; Rickwood, Danny; Wilson, Danielle; Cueva, Claudia; Ng, Charlotte; Strutton, Geoffrey; Cassady, A Ian; Evdokiou, Andreas; Sommerville, Scott; Dickinson, Ian; Guminski, Alexander; Saunders, Nicholas A

    2010-09-15

    We conducted a transcriptomic screen of osteosarcoma (OS) biopsies and found that expression of osteoclast-specific tartrate-resistant acid phosphatase 5 (ACP5/TRAP) is significantly downregulated in OS compared with nonmalignant bone (P < 0.0001). Moreover, lesions from OS patients with pulmonary metastases had 2-fold less ACP5/TRAP expression (P < 0.018) than lesions from patients without metastases. In addition, we found a direct correlation (P = 0.0166) between ACP5/TRAP expression and time to metastasis. Therefore, we examined whether metastasis-competent (MC) OS cells could induce loss of ACP5(+) osteoclasts and contribute to metastasis. We found that MC OS cell lines can inhibit osteoclastogenesis in vitro and in vivo. In addition, osteoclasts can inhibit the migration of MC OS cells in vitro. Finally, ablation of osteoclasts with zoledronic acid increases the number of metastatic lung lesions in an orthotopic OS model, whereas fulvestrant treatment increases osteoclast numbers and reduces metastatic lesions. These data indicate that the metastatic potential of OS is determined early in tumor development and that loss of osteoclasts in the primary lesion enhances OS metastasis.

  2. Diabetic Macular Edema

    NASA Astrophysics Data System (ADS)

    Lobo, Conceição; Pires, Isabel; Cunha-Vaz, José

    The optical coherence tomography (OCT), a noninvasive and noncontact diagnostic method, was introduced in 1995 for imaging macular diseases. In diabetic macular edema (DME), OCT scans show hyporeflectivity, due to intraretinal and/or subretinal fluid accumulation, related to inner and/or outer blood-retinal barrier breakdown. OCT tomograms may also reveal the presence of hard exudates, as hyperreflective spots with a shadow, in the outer retinal layers, among others. In conclusion, OCT is a particularly valuable diagnostic tool in DME, helpful both in the diagnosis and follow-up procedure.

  3. Mechanics of the left ventricular myocardial interstitium: effects of acute and chronic myocardial edema.

    PubMed

    Desai, Ketaki V; Laine, Glen A; Stewart, Randolph H; Cox, Charles S; Quick, Christopher M; Allen, Steven J; Fischer, Uwe M

    2008-06-01

    Myocardial interstitial edema forms as a result of several disease states and clinical interventions. Acute myocardial interstitial edema is associated with compromised systolic and diastolic cardiac function and increased stiffness of the left ventricular chamber. Formation of chronic myocardial interstitial edema results in deposition of interstitial collagen, which causes interstitial fibrosis. To assess the effect of myocardial interstitial edema on the mechanical properties of the left ventricle and the myocardial interstitium, we induced acute and chronic interstitial edema in dogs. Acute myocardial edema was generated by coronary sinus pressure elevation, while chronic myocardial edema was generated by chronic pulmonary artery banding. The pressure-volume relationships of the left ventricular myocardial interstitium and left ventricular chamber for control animals were compared with acutely and chronically edematous animals. Collagen content of nonedematous and chronically edematous animals was also compared. Generating acute myocardial interstitial edema resulted in decreased left ventricular chamber compliance compared with nonedematous animals. With chronic edema, the primary form of collagen changed from type I to III. Left ventricular chamber compliance in animals made chronically edematous was significantly higher than nonedematous animals. The change in primary collagen type secondary to chronic left ventricular myocardial interstitial edema provides direct evidence for structural remodeling. The resulting functional adaptation allows the chronically edematous heart to maintain left ventricular chamber compliance when challenged with acute edema, thus preserving cardiac function over a wide range of interstitial fluid pressures. PMID:18375722

  4. Fetal pulmonary development: the role of respiratory movements.

    PubMed

    Harding, R

    1997-06-01

    The lung develops before birth as a collapsible, liquid-filled, organ. Throughout the later stages of gestation the fetal lungs are maintained at a level of expansion that is considerably greater than the level achieved as a result of passive equilibration between lung recoil and the chest wall. Fetal breathing movements (FBM) are a feature of normal fetal life and, as such, are used clinically in the assessment of fetal wellbeing. By opposing lung recoil, FBM help to maintain the high level of lung expansion that is now known to be essential for normal growth and structural maturation of the fetal lungs. During 'apnoeic' periods between successive episodes of FBM, active laryngeal constriction has the effect of opposing lung recoil by resisting the escape of lung liquid via the trachea. The prolonged absence or impairment of FBM is likely to result in a reduced mean level of lung expansion which can lead to hypoplasia of the lungs. There is clinical evidence, disputed by some, that the absence of FBM exacerbates the effects of other factors that are associated with lung hypoplasia, such as premature rupture of fetal membranes and oligohydramnios. Even in the absence of such factors, prolonged or repeated reductions or abolition of FBM may contribute to impairments of fetal lung development; FBM can be inhibited by fetal hypoxaemia, hypoglycaemia, maternal alcohol consumption, maternal smoking, intra-amniotic infection and maternal consumption of sedatives or narcotic drugs. Abnormal growth of the fetal lungs has relevance for postnatal respiratory health as it is now recognised that there may be only a limited capacity after birth for the restoration of normal pulmonary architecture following impaired intra-uterine lung development. PMID:9355800

  5. Bilateral leg edema in an older woman.

    PubMed

    Thaler, H W; Pienaar, S; Wirnsberger, G; Roller-Wirnsberger, R E

    2015-01-01

    Bilateral leg edema is a frequent symptom in older people and an important concern in geriatric medicine. Further evaluation is frequently not performed and simple therapy with diuretics is prescribed. Particularly in older patients, long-term use of diuretics can lead to severe electrolyte imbalances, volume depletion, and falls. In this case report we want to focus the physicians' attention on the necessity to determine the cause and show a correspondingly effective treatment for bilateral leg edema in older people. A thorough approach is required to recognize diseases and to avoid adverse drug events as geriatric patients often show an atypical presentation or minor symptoms. The cause of swollen legs is often multifactorial; therefore, the patient's individual history and an appropriate physical examination are important. Depending on the clinical symptoms, evaluation including basic laboratory tests, urinalysis, chest radiography, and echocardiogram may be indicated. The most probable cause of bilateral edema in older patients is chronic venous insufficiency. Heart failure is also a common cause. Other systemic causes such as renal disease or liver disease are much rarer. Antihypertensive and anti-inflammatory drugs can frequently cause leg edema, but the incidence of drug-induced leg swelling is unknown. With the help of this special case we tried to develop an approach to the diagnosis of symmetric leg edema in older patients, a problem frequently neglected in geriatric medicine.

  6. Androctonus australis hector venom contributes to the interaction between neuropeptides and mast cells in pulmonary hyperresponsiveness.

    PubMed

    Chaïr-Yousfi, Imène; Laraba-Djebari, Fatima; Hammoudi-Triki, Djelila

    2015-03-01

    Lung injury and respiratory distress syndrome are frequent symptoms observed in the most severe cases of scorpion envenomation. The uncontrolled transmigration of leukocyte cells into the lung interstitium and alveolar space and pulmonary edema may be the cause of death. Mast cells can release various inflammatory mediators known to be involved in the development of lung edema following scorpion venom injection. The present study was designed to determine the evidence of neurokinin 1 (NK1) receptor and the involvement of mast cell activation to induce pulmonary edema and to increase vascular permeability after Androctonus australis hector (Aah) venom administration. To this end, mast cells were depleted using compound 48/80 (C48/80). Furthermore, the involvement of tachykinin NK1 receptors expressed on mast cell membranes was elucidated by their blocking with an antagonist. On the other hand, the ability of Aah venom to increase vascular permeability and to induce edema was also assessed by measuring the amount of Evans blue dye (EBD) extravasation in bronchoalveolar lavage (BAL) fluid and in the lungs of mice. Pulmonary edema, as assessed by the levels of EBD extravasation, was completely inhibited in compound 48/80-treated animals. Depletion by stimuli non-immunological C48/80 component markedly reduced induced inflammatory response following the venom administration. The mast cells seem to play an important role in the development of lung injury and the increase of vascular permeability in mice following the subcutaneous administration of Aah scorpion venom through the NK1 receptor. PMID:25601496

  7. Small changes in lung function in runners with marathon‐induced interstitial lung edema

    PubMed Central

    Zavorsky, Gerald S.; Milne, Eric N.C.; Lavorini, Federico; Rienzi, Joseph P.; Cutrufello, Paul T.; Kumar, Sridhar S.; Pistolesi, Massimo

    2014-01-01

    Abstract The purpose of this study was to assess lung function in runners with marathon‐induced lung edema. Thirty‐six (24 males) healthy subjects, 34 (SD 9) years old, body mass index 23.7 (2.6) kg/m2 had posterior/anterior (PA) radiographs taken 1 day before and 21 (6) minutes post marathon finish. Pulmonary function was performed 1–3 weeks before and 73 (27) minutes post finish. The PA radiographs were viewed together, as a set, and evaluated by two experienced readers separately who were blinded as to time the images were obtained. Radiographs were scored for edema based on four different radiological characteristics such that the summed scores for any runner could range from 0 (no edema) to a maximum of 8 (severe interstitial edema). Overall, the mean edema score increased significantly from 0.2 to 1.0 units (P <0.01), and from 0.0 to 2.9 units post exercise in the six subjects that were edema positive (P = 0.03). Despite a 2% decrease in forced vital capacity (FVC, P =0.024) and a 12% decrease in alveolar‐membrane diffusing capacity for carbon monoxide (DmCO, P =0.01), there was no relation between the change in the edema score and the change in DmCO or FVC. In conclusion, (1) mild pulmonary edema occurs in at least 17% of subjects and that changes in pulmonary function cannot predict the occurrence or severity of edema, (2) lung edema is of minimal physiological significance as marathon performance is unaffected, exercise‐induced arterial hypoxemia is unlikely, and postexercise pulmonary function changes are mild. PMID:24973330

  8. An improved gravimetric measure of cerebral edema.

    PubMed

    Marmarou, A; Tanaka, K; Shulman, K

    1982-02-01

    Significant errors are introduced into the measurement of brain tissue water by the specific gravity technique when the edema fluid contains protein. Protein adds to the tissue solids, increasing the density of the tissue, and masks the proportional increase of brain water. Existing equations relating measured specific gravity and tissue water are not applicable, and a new formula was developed that compensates for the protein component of edema and reduces the experimental error. The new method was applied to the measurement of tissue water in cat brain made edematous by direct infusion of fluids of known composition and volume to test the theory. This technique for improving the gravimetric assessment of brain edema is presented.

  9. Molecular pathophysiology of cerebral edema.

    PubMed

    Stokum, Jesse A; Gerzanich, Volodymyr; Simard, J Marc

    2016-03-01

    Advancements in molecular biology have led to a greater understanding of the individual proteins responsible for generating cerebral edema. In large part, the study of cerebral edema is the study of maladaptive ion transport. Following acute CNS injury, cells of the neurovascular unit, particularly brain endothelial cells and astrocytes, undergo a program of pre- and post-transcriptional changes in the activity of ion channels and transporters. These changes can result in maladaptive ion transport and the generation of abnormal osmotic forces that, ultimately, manifest as cerebral edema. This review discusses past models and current knowledge regarding the molecular and cellular pathophysiology of cerebral edema. PMID:26661240

  10. Molecular pathophysiology of cerebral edema

    PubMed Central

    Gerzanich, Volodymyr; Simard, J Marc

    2015-01-01

    Advancements in molecular biology have led to a greater understanding of the individual proteins responsible for generating cerebral edema. In large part, the study of cerebral edema is the study of maladaptive ion transport. Following acute CNS injury, cells of the neurovascular unit, particularly brain endothelial cells and astrocytes, undergo a program of pre- and post-transcriptional changes in the activity of ion channels and transporters. These changes can result in maladaptive ion transport and the generation of abnormal osmotic forces that, ultimately, manifest as cerebral edema. This review discusses past models and current knowledge regarding the molecular and cellular pathophysiology of cerebral edema. PMID:26661240

  11. Pulmonary drug delivery systems: recent developments and prospects.

    PubMed

    Courrier, H M; Butz, N; Vandamme, Th F

    2002-01-01

    Targeting drug delivery into the lungs has become one of the most important aspects of systemic or local drug delivery systems. Consequently, in the last few years, techniques and new drug delivery devices intended to deliver drugs into the lungs have been widely developed. Currently, the main drug targeting regimens include direct application of a drug into the lungs, mostly by inhalation therapy using either pressurized metered dose inhalers (pMDI) or dry powder inhalers (DPI). Intratracheal administration is commonly used as a first approach in lung drug delivery in vivo. To convey a sufficient dose of drug to the lungs, suitable drug carriers are required. These can be either solid, liquid, or gaseous excipients. Liposomes, nano- and microparticles, cyclodextrins, microemulsions, micelles, suspensions, or solutions are all examples of this type of pharmaceutical carrier that have been successfully used to target drugs into the lungs. The use of microreservoir-type systems offers clear advantages, such as high loading capacity and the possibility of controlling size and permeability, and thus of controlling the release kinetics of the drugs from the carrier systems. These systems make it possible to use relatively small numbers of vector molecules to deliver substantial amounts of a drug to the target. This review discusses the drug carriers administered or intended to be administered into the lungs. The transition to CFC-free inhalers and drug delivery systems formulated with new propellants are also discussed. Finally, in addition to the various advances made in the field of pulmonary-route administration, we describe new systems based on perfluorooctyl bromide, which guarantee oxygen delivery in the event of respiratory distress and drug delivery into the lungs.

  12. Cold-induced pulmonary oedema in scuba divers and swimmers and subsequent development of hypertension.

    PubMed

    Wilmshurst, P T; Nuri, M; Crowther, A; Webb-Peploe, M M

    1989-01-14

    The effect of cold and/or a raised partial pressure of oxygen was examined in eleven people with no demonstrable cardiac abnormality but who had pulmonary oedema when scuba diving or surface swimming, and in ten normal divers. These stimuli induced pathological vasoconstriction in the pulmonary oedema group, nine of whom also showed signs of cardiac decompensation when so stimulated. The pulmonary oedema patients have been followed-up for an average of 8 years. Seven have become hypertensive. Except for the onset of lone atrial fibrillation in one normotensive female diver and development of Raynaud's phenomenon in a normotensive man, there have been no cardiovascular events and no deaths.

  13. Massive vulvar edema in 2 prepartum dairy cows.

    PubMed

    Cheong, Soon Hon; Gilbert, Robert O

    2014-05-01

    Two late gestation Holstein cows about to begin the third lactation developed massive vulvar edema. These were the only affected animals in the herd of 500 milking cows. The vulvar edema spontaneously regressed postpartum for both cows. Massive vulvar swelling is seldom observed in dairy cows in advanced pregnancy and is not described in the literature.

  14. Alpha-syntrophin deletion removes the perivascular but not endothelial pool of aquaporin-4 at the blood-brain barrier and delays the development of brain edema in an experimental model of acute hyponatremia.

    PubMed

    Amiry-Moghaddam, Mahmood; Xue, Rong; Haug, Finn-Mogens; Neely, John D; Bhardwaj, Anish; Agre, Peter; Adams, Marvin E; Froehner, Stanley C; Mori, Susumu; Ottersen, Ole P

    2004-03-01

    The formation of brain edema, commonly occurring as a potentially lethal complication of acute hyponatremia, is delayed following knockout of the water channel aquaporin-4 (AQP4). Here we show by high-resolution immunogold analysis of the blood-brain-barrier that AQP4 is expressed in brain endothelial cells as well as in the perivascular membranes of astrocyte endfeet. A selective removal of perivascular AQP4 by alpha-syntrophin deletion delays the buildup of brain edema (assessed by Diffusion-weighted MRI) following water intoxication, despite the presence of a normal complement of endothelial AQP4. This indicates that the perivascular membrane domain, which is peripheral to the endothelial blood-brain barrier, may control the rate of osmotically driven water entry. This study is also the first to demonstrate that the time course of edema development differs among brain regions, probably reflecting differences in aquaporin-4 distribution. The resolution of the molecular basis and subcellular site of osmotically driven brain water uptake should help design new therapies for acute brain edema.

  15. Pulmonary artery stump thrombosis developed during the late postoperative period

    PubMed Central

    Kaya, Seyda Ors; Samancilar, Ozgur; Ceylan, Kenan Can

    2016-01-01

    A 73-year-old man underwent left pneumonectomy for squamous cell lung carcinoma 3 years ago. The postoperative and follow-up periods were uneventful. A thrombus was detected in the left pulmonary artery stump during the last chest computed tomography (CT) scan. Anticoagulant treatment was applied: intravenous heparin for 3 days followed by oral warfarin. The follow-up chest CT examination revealed regression in the size of the thrombus.

  16. Rapid culture-based diagnosis of pulmonary tuberculosis in developed and developing countries.

    PubMed

    Asmar, Shady; Drancourt, Michel

    2015-01-01

    Culturing Mycobacterium tuberculosis remains the gold standard for the laboratory diagnosis of pulmonary tuberculosis, with 9 million new cases and 1.5 million deaths mainly in developing countries. Reviewing data reported over 20 years yields a state-of-the-art procedure for the routine culture of M. tuberculosis in both developed and developing countries. Useful specimens include sputum, induced sputum, and stools collected in quaternary ammonium preservative-containing sterile cans. The usefulness of other non-invasive specimens remains to be evaluated. Specimens can be collected in a diagnosis kit also containing sampling materials, instructions, laboratory requests, and informed consent. Automated direct LED fluorescence microscopy after auramine staining precedes inoculation of an egg-lecithin-containing culture solid medium under microaerophilic atmosphere, inverted microscope reading or scanning video-imaging detection of colonies and colonies identification by recent molecular methods. This procedure should result in a diagnosis of pulmonary tuberculosis as fast as 5 days. It may be implemented in both developed and developing countries with automated steps replaceable by manual steps depending on local resources. PMID:26579092

  17. Rapid culture-based diagnosis of pulmonary tuberculosis in developed and developing countries

    PubMed Central

    Asmar, Shady; Drancourt, Michel

    2015-01-01

    Culturing Mycobacterium tuberculosis remains the gold standard for the laboratory diagnosis of pulmonary tuberculosis, with 9 million new cases and 1.5 million deaths mainly in developing countries. Reviewing data reported over 20 years yields a state-of-the-art procedure for the routine culture of M. tuberculosis in both developed and developing countries. Useful specimens include sputum, induced sputum, and stools collected in quaternary ammonium preservative-containing sterile cans. The usefulness of other non-invasive specimens remains to be evaluated. Specimens can be collected in a diagnosis kit also containing sampling materials, instructions, laboratory requests, and informed consent. Automated direct LED fluorescence microscopy after auramine staining precedes inoculation of an egg-lecithin-containing culture solid medium under microaerophilic atmosphere, inverted microscope reading or scanning video-imaging detection of colonies and colonies identification by recent molecular methods. This procedure should result in a diagnosis of pulmonary tuberculosis as fast as 5 days. It may be implemented in both developed and developing countries with automated steps replaceable by manual steps depending on local resources. PMID:26579092

  18. Pulmonary Aspects of Exercise and Sports.

    PubMed

    Bove, Alfred A

    2016-01-01

    Although the lungs are a critical component of exercise performance, their response to exercise and other environmental stresses is often overlooked when evaluating pulmonary performance during high workloads. Exercise can produce capillary leakage, particularly when left atrial pressure increases related to left ventricular (LV) systolic or diastolic failure. Diastolic LV dysfunction that results in elevated left atrial pressure during exercise is particularly likely to result in pulmonary edema and capillary hemorrhage. Data from race horses, endurance athletes, and triathletes support the concept that the lungs can react to exercise and immersion stress with pulmonary edema and pulmonary hemorrhage. Immersion in water by swimmers and divers can also increase stress on pulmonary capillaries and result in pulmonary edema. Swimming-induced pulmonary edema and immersion pulmonary edema in scuba divers are well-documented events caused by the fluid shifts that occur with immersion, elevated pulmonary venous pressure during extreme exercise, and negative alveolar pressure due to inhalation resistance. Prevention strategies include avoiding extreme exercise, avoiding over hydration, and assuring that inspiratory resistance is minimized. PMID:27486491

  19. Pulmonary Aspects of Exercise and Sports

    PubMed Central

    Bove, Alfred A.

    2016-01-01

    Although the lungs are a critical component of exercise performance, their response to exercise and other environmental stresses is often overlooked when evaluating pulmonary performance during high workloads. Exercise can produce capillary leakage, particularly when left atrial pressure increases related to left ventricular (LV) systolic or diastolic failure. Diastolic LV dysfunction that results in elevated left atrial pressure during exercise is particularly likely to result in pulmonary edema and capillary hemorrhage. Data from race horses, endurance athletes, and triathletes support the concept that the lungs can react to exercise and immersion stress with pulmonary edema and pulmonary hemorrhage. Immersion in water by swimmers and divers can also increase stress on pulmonary capillaries and result in pulmonary edema. Swimming-induced pulmonary edema and immersion pulmonary edema in scuba divers are well-documented events caused by the fluid shifts that occur with immersion, elevated pulmonary venous pressure during extreme exercise, and negative alveolar pressure due to inhalation resistance. Prevention strategies include avoiding extreme exercise, avoiding over hydration, and assuring that inspiratory resistance is minimized. PMID:27486491

  20. Protection by oestradiol against the development of cardiovascular changes associated with monocrotaline pulmonary hypertension in rats.

    PubMed Central

    Farhat, M. Y.; Chen, M. F.; Bhatti, T.; Iqbal, A.; Cathapermal, S.; Ramwell, P. W.

    1993-01-01

    1. We studied the effects of oestradiol 17 beta on the development of pulmonary vascular changes and right ventricular (RV) hypertrophy in response to monocrotaline in male Sprague-Dawley rats. 2. Rats were treated with either placebo or oestradiol 17 beta (10 mg) in the form of slow release pellets implanted subcutaneously 48 h before monocrotaline administration. Rats were injected with either saline or a single dose of monocrotaline (60 mg kg-1, i.m.). Pulmonary vascular changes and RV hypertrophy were studied at 4 weeks following monocrotaline administration. 3. Monocrotaline induced a significant increase in the ratio of right ventricle (RV) to left ventricle-plus-septum (LV + S) weights. Monocrotaline-treated rats also showed significant myointimal proliferation in small pulmonary arteries, decrease of arterial numbers and increase in the number of abnormal alveolar macrophages. 4. Oestradiol 17 beta attenuated myointimal hyperplasia in pulmonary vessels, decreased the RV/(LV + S) ratio in monocrotaline-treated rats. Oestradiol 17 beta had no significant effect on control animals. 5. Oestradiol treatment prevented the increase in lung wet to dry weight ratio, observed 7 days post monocrotaline administration. 6. These results suggest that oestradiol 17 beta protects against the pulmonary vascular remodelling and RV hypertrophy associated with monocrotaline-induced pulmonary hypertension in the rat. Oestradiol also protects against microvascular leak observed in the early days of lesion. Images Figure 2 PMID:8242243

  1. Bridging Lung Development with Chronic Obstructive Pulmonary Disease. Relevance of Developmental Pathways in Chronic Obstructive Pulmonary Disease Pathogenesis.

    PubMed

    Boucherat, Olivier; Morissette, Mathieu C; Provencher, Steeve; Bonnet, Sébastien; Maltais, François

    2016-02-15

    Chronic obstructive pulmonary disease (COPD) is characterized by chronic airflow limitation. This generic term encompasses emphysema and chronic bronchitis, two common conditions, each having distinct but also overlapping features. Recent epidemiological and experimental studies have challenged the traditional view that COPD is exclusively an adult disease occurring after years of inhalational insults to the lungs, pinpointing abnormalities or disruption of the pathways that control lung development as an important susceptibility factor for adult COPD. In addition, there is growing evidence that emphysema is not solely a destructive process because it is also characterized by a failure in cell and molecular maintenance programs necessary for proper lung development. This leads to the concept that tissue regeneration required stimulation of signaling pathways that normally operate during development. We undertook a review of the literature to outline the contribution of developmental insults and genes in the occurrence and pathogenesis of COPD, respectively.

  2. Prothymosin α overexpression contributes to the development of pulmonary emphysema.

    PubMed

    Su, Bing-Hua; Tseng, Yau-Lin; Shieh, Gia-Shing; Chen, Yi-Cheng; Shiang, Ya-Chieh; Wu, Pensee; Li, Kuo-Jung; Yen, Te-Hsin; Shiau, Ai-Li; Wu, Chao-Liang

    2013-01-01

    Emphysema is one of the disease conditions that comprise chronic obstructive pulmonary disease. Prothymosin α transgenic mice exhibit an emphysema phenotype, but the pathophysiological role of prothymosin α in emphysema remains unclear. Here we show that prothymosin α contributes to the pathogenesis of emphysema by increasing acetylation of histones and nuclear factor-kappaB, particularly upon cigarette smoke exposure. We find a positive correlation between prothymosin α levels and the severity of emphysema in prothymosin α transgenic mice and emphysema patients. Prothymosin α overexpression increases susceptibility to cigarette smoke-induced emphysema, and cigarette smoke exposure further enhances prothymosin α expression. We show that prothymosin α inhibits the association of histone deacetylases with histones and nuclear factor-kappaB, and that prothymosin α overexpression increases expression of nuclear factor-kappaB-dependent matrix metalloproteinase 2 and matrix metalloproteinase 9, which are found in the lungs of patients with chronic obstructive pulmonary disease. These results demonstrate the clinical relevance of prothymosin α in regulating acetylation events during the pathogenesis of emphysema.

  3. Diagnostic Evaluation of Chronic Thromboembolic Pulmonary Hypertension.

    PubMed

    Gopalan, Deepa; Blanchard, Daniel; Auger, William R

    2016-07-01

    Pulmonary hypertension is defined by a mean pulmonary artery pressure greater than 25 mm Hg. Chronic thromboembolic pulmonary hypertension (CTEPH) is defined as pulmonary hypertension in the presence of an organized thrombus within the pulmonary vascular bed that persists at least 3 months after the onset of anticoagulant therapy. Because CTEPH is potentially curable by surgical endarterectomy, correct identification of patients with this form of pulmonary hypertension and an accurate assessment of surgical candidacy are essential to provide optimal care. Patients most commonly present with symptoms of exertional dyspnea and otherwise unexplained decline in exercise capacity. Atypical chest pain, a nonproductive cough, and episodic hemoptysis are observed less frequently. With more advanced disease, patients often develop symptoms suggestive of right ventricular compromise. Physical examination findings are minimal early in the course of this disease, but as pulmonary hypertension progresses, may include nonspecific finding of right ventricular failure, such as a tricuspid regurgitation murmur, pedal edema, and jugular venous distention. Chest radiographs may suggest pulmonary hypertension, but are neither sensitive nor specific for the diagnosis. Radioisotopic ventilation-perfusion scanning is sensitive for detecting CTEPH, making it a valuable screening study. Conventional catheter-based pulmonary angiography retains an important role in establishing the presence and extent of chronic thromboembolic disease. However, computed tomographic and magnetic resonance imaging are playing a growing diagnostic role. Innovative technologies such as dual-energy computed tomography, dynamic contrast-enhanced magnetic resonance imaging, and optical coherence tomography show promise for contributing diagnostic information and assisting in the preoperative characterization of patients with CTEPH. PMID:27571004

  4. Aquaporin-4 and brain edema.

    PubMed

    Papadopoulos, Marios C; Verkman, Alan S

    2007-06-01

    Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid (CSF) and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. Experiments using AQP4-null mice provide strong evidence for AQP4 involvement in cerebral water balance. AQP4-null mice are protected from cellular (cytotoxic) brain edema produced by water intoxication, brain ischemia, or meningitis. However, AQP4 deletion aggravates vasogenic (fluid leak) brain edema produced by tumor, cortical freeze, intraparenchymal fluid infusion, or brain abscess. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 deletion also worsens obstructive hydrocephalus. Recently, AQP4 was also found to play a major role in processes unrelated to brain edema, including astrocyte migration and neuronal excitability. These findings suggest that modulation of AQP4 expression or function may be beneficial in several cerebral disorders, including hyponatremic brain edema, hydrocephalus, stroke, tumor, infection, epilepsy, and traumatic brain injury.

  5. Letter to the Editor Reply to commentary by G. Sikri and S. Dua on the article "Correlation between single nucleotide polymorphisms in hypoxia-related genes and susceptibility to acute high-altitude pulmonary edema" published in Genetics and Molecular Research 14 (3): 11562-11572 to the letter published in Genet. Mol. Res. 14 (4): 15904-15905.

    PubMed

    Wu, L J

    2016-03-24

    The object in this study was a Han Chinese population in Lhasa, with 3658 m in altitude from Chengdu, which has 505 m in altitude by air. Within 24 to 48 h before the subjects arrived in the plateau, they completed a basic situation questionnaire, under the guidance of medical staff. Within 24 to 48 h after they reached the plateau, the subjects completed an acute plateau disease questionnaire. The diagnostic standard of HAPE and the diagnosis of acute plateau disease were adopted by the Lake Louise diagnostic standards in 1991 and the Chinese Medical Association promulgated the domestic diagnostic criteria on the Third National Plateau Medical Academic Seminar. Other diseases that cause acute symptoms of altitude sickness, such as plateau pulmonary edema, plateau cerebral edema, acute respiratory infections and neurosis, were excluded. According to the Lake Louise standard, questionnaire and symptom score values >3 points were diagnosed as HAPE. According to the national standard, the questionnaire and symptom score values >5 points were diagnosed as HAPE. At the present, morbidity of HAPE remains relatively high in China. The research shows that usually in the case of not taking preventive measures, according to the factors such as altitude, speed, and time of arrival, the incidence of HAPE is 30% to 90%. Epidemiological survey shows that HAPE happens at an altitude of 2500 m above the plateau. And an altitude of 3000 m above the plateau of China is occupied 1/6 of the total land area, the population of permanent residents is more than sixty million. We detected the 200 cases who adapted to plateau and the 106 cases of patients with HAPE susceptibility genes SNP locus, and got the key SNP loci of HAPE susceptibility genes. We maked the corresponding gene chip diagnostic kits.

  6. Letter to the Editor Reply to commentary by G. Sikri and S. Dua on the article "Correlation between single nucleotide polymorphisms in hypoxia-related genes and susceptibility to acute high-altitude pulmonary edema" published in Genetics and Molecular Research 14 (3): 11562-11572 to the letter published in Genet. Mol. Res. 14 (4): 15904-15905.

    PubMed

    Wu, L J

    2016-01-01

    The object in this study was a Han Chinese population in Lhasa, with 3658 m in altitude from Chengdu, which has 505 m in altitude by air. Within 24 to 48 h before the subjects arrived in the plateau, they completed a basic situation questionnaire, under the guidance of medical staff. Within 24 to 48 h after they reached the plateau, the subjects completed an acute plateau disease questionnaire. The diagnostic standard of HAPE and the diagnosis of acute plateau disease were adopted by the Lake Louise diagnostic standards in 1991 and the Chinese Medical Association promulgated the domestic diagnostic criteria on the Third National Plateau Medical Academic Seminar. Other diseases that cause acute symptoms of altitude sickness, such as plateau pulmonary edema, plateau cerebral edema, acute respiratory infections and neurosis, were excluded. According to the Lake Louise standard, questionnaire and symptom score values >3 points were diagnosed as HAPE. According to the national standard, the questionnaire and symptom score values >5 points were diagnosed as HAPE. At the present, morbidity of HAPE remains relatively high in China. The research shows that usually in the case of not taking preventive measures, according to the factors such as altitude, speed, and time of arrival, the incidence of HAPE is 30% to 90%. Epidemiological survey shows that HAPE happens at an altitude of 2500 m above the plateau. And an altitude of 3000 m above the plateau of China is occupied 1/6 of the total land area, the population of permanent residents is more than sixty million. We detected the 200 cases who adapted to plateau and the 106 cases of patients with HAPE susceptibility genes SNP locus, and got the key SNP loci of HAPE susceptibility genes. We maked the corresponding gene chip diagnostic kits. PMID:27050977

  7. PULMONARY CIRCULATION AT EXERCISE

    PubMed Central

    NAEIJE, R; CHESLER, N

    2012-01-01

    The pulmonary circulation is a high flow and low pressure circuit, with an average resistance of 1 mmHg.min.L−1 in young adults, increasing to 2.5 mmHg.min.L−1 over 4–6 decades of life. Pulmonary vascular mechanics at exercise are best described by distensible models. Exercise does not appear to affect the time constant of the pulmonary circulation or the longitudinal distribution of resistances. Very high flows are associated with high capillary pressures, up to a 20–25 mmHg threshold associated with interstitial lung edema and altered ventilation/perfusion relationships. Pulmonary artery pressures of 40–50 mmHg, which can be achieved at maximal exercise, may correspond to the extreme of tolerable right ventricular afterload. Distension of capillaries that decrease resistance may be of adaptative value during exercise, but this is limited by hypoxemia from altered diffusion/perfusion relationships. Exercise in hypoxia is associated with higher pulmonary vascular pressures and lower maximal cardiac output, with increased likelihood of right ventricular function limitation and altered gas exchange by interstitial lung edema. Pharmacological interventions aimed at the reduction of pulmonary vascular tone have little effect on pulmonary vascular pressure-flow relationships in normoxia, but may decrease resistance in hypoxia, unloading the right ventricle and thereby improving exercise capacity. Exercise in patients with pulmonary hypertension is associated with sharp increases in pulmonary artery pressure and a right ventricular limitation of aerobic capacity. Exercise stress testing to determine multipoint pulmonary vascular pressures-flow relationships may uncover early stage pulmonary vascular disease. PMID:23105961

  8. Recent developments in video-assisted thoracoscopic surgery for pulmonary nodule management.

    PubMed

    Chow, Simon C Y; Ng, Calvin S H

    2016-07-01

    In the modern era when screening and early surveillance of pulmonary nodules is increasing in importance, the management of the pulmonary nodule represents a different challenge to thoracic surgeons. The difficulty lies in the merging of sound surgical and oncological principles with more minimally invasive and appropriate lung sparing surgery. Furthermore, the intra-operative identification and surgical management of small and sometimes multi-focal pulmonary lesions remain challenging. There have been many developments and innovations in the field of video-assisted thoracoscopic surgery (VATS) to cater for the demands from increasing incidence of pulmonary nodules with associated paradigm shift in their surgical management. Recently, uniportal VATS and non-intubated VATS represent an even less invasive alternative to the conventional multiport VATS. The emergence of image guided VATS, hybrid operating theatre and fluorescence thoracoscopy have all contributed to improved precision of VATS lung resection, and are becoming important adjuncts to lung sparing surgery. In this chapter, some of these recent developments in VATS with emphasize on their importance in surgical management of the pulmonary nodule will be discussed. PMID:27606081

  9. Recent developments in video-assisted thoracoscopic surgery for pulmonary nodule management

    PubMed Central

    Chow, Simon C. Y.

    2016-01-01

    In the modern era when screening and early surveillance of pulmonary nodules is increasing in importance, the management of the pulmonary nodule represents a different challenge to thoracic surgeons. The difficulty lies in the merging of sound surgical and oncological principles with more minimally invasive and appropriate lung sparing surgery. Furthermore, the intra-operative identification and surgical management of small and sometimes multi-focal pulmonary lesions remain challenging. There have been many developments and innovations in the field of video-assisted thoracoscopic surgery (VATS) to cater for the demands from increasing incidence of pulmonary nodules with associated paradigm shift in their surgical management. Recently, uniportal VATS and non-intubated VATS represent an even less invasive alternative to the conventional multiport VATS. The emergence of image guided VATS, hybrid operating theatre and fluorescence thoracoscopy have all contributed to improved precision of VATS lung resection, and are becoming important adjuncts to lung sparing surgery. In this chapter, some of these recent developments in VATS with emphasize on their importance in surgical management of the pulmonary nodule will be discussed.

  10. Recent developments in video-assisted thoracoscopic surgery for pulmonary nodule management

    PubMed Central

    Chow, Simon C. Y.

    2016-01-01

    In the modern era when screening and early surveillance of pulmonary nodules is increasing in importance, the management of the pulmonary nodule represents a different challenge to thoracic surgeons. The difficulty lies in the merging of sound surgical and oncological principles with more minimally invasive and appropriate lung sparing surgery. Furthermore, the intra-operative identification and surgical management of small and sometimes multi-focal pulmonary lesions remain challenging. There have been many developments and innovations in the field of video-assisted thoracoscopic surgery (VATS) to cater for the demands from increasing incidence of pulmonary nodules with associated paradigm shift in their surgical management. Recently, uniportal VATS and non-intubated VATS represent an even less invasive alternative to the conventional multiport VATS. The emergence of image guided VATS, hybrid operating theatre and fluorescence thoracoscopy have all contributed to improved precision of VATS lung resection, and are becoming important adjuncts to lung sparing surgery. In this chapter, some of these recent developments in VATS with emphasize on their importance in surgical management of the pulmonary nodule will be discussed. PMID:27606081

  11. The developing pulmonary veins and left atrium: implications for ablation strategy for atrial fibrillation.

    PubMed

    Sherif, Hisham M F

    2013-11-01

    The majority of cases of atrial fibrillation (AF) are the result of triggers originating in the area of the pulmonary veins. The reason for the predilection for that area remains unclear. We sought to examine the different mechanisms responsible for this observation through an extensive search of the medical literature, examining the development of the pulmonary veins, genetics of AF and left to -right cardiac chamber differentiation. Results confirm that the LAA is anatomically and embryologically different from other areas of the atrial walls and develops under distinct genetic and transcriptional pathways. Findings support an ablation strategy whose primary focus should be the creation of a 'box' lesion set, plus additional lines to prevent propagation to the left atrial appendage, the isthmus of the left atrium and the right atrium are likely to be more effective than simple pulmonary vein isolation.

  12. Endothelin-1 receptor antagonists in fetal development and pulmonary arterial hypertension.

    PubMed

    de Raaf, Michiel Alexander; Beekhuijzen, Manon; Guignabert, Christophe; Vonk Noordegraaf, Anton; Bogaard, Harm Jan

    2015-08-15

    The Pregnancy Prevention Program (PPP) is in place to prevent drug-induced developmental malformations. Remarkably, among the ten PPP-enlisted drugs are three endothelin-1 (ET-1) receptor antagonists (ERA's: ambrisentan, bosentan and macitentan), which are approved for the treatment of Pulmonary Arterial Hypertension (PAH). This review describes the effects of ERA's in PAH pathobiology and cardiopulmonary fetal development. While ERA's hamper pathological remodeling of the pulmonary vasculature and as such exert beneficial effects in PAH, they disturb fetal development of cardiopulmonary tissues. By blocking ET-1-mediated positive inotropic effects and myocardial fetal gene induction, ERA's may affect right ventricular adaptation to the increased pulmonary vascular resistance in both the fetus and the adult PAH patient.

  13. Pulmonary tissue volume, cardiac output, and diffusing capacity in sustained microgravity

    NASA Technical Reports Server (NTRS)

    Verbanck, S.; Larsson, H.; Linnarsson, D.; Prisk, G. K.; West, J. B.; Paiva, M.

    1997-01-01

    In microgravity (microG) humans have marked changes in body fluids, with a combination of an overall fluid loss and a redistribution of fluids in the cranial direction. We investigated whether interstitial pulmonary edema develops as a result of a headward fluid shift or whether pulmonary tissue fluid volume is reduced as a result of the overall loss of body fluid. We measured pulmonary tissue volume (Vti), capillary blood flow, and diffusing capacity in four subjects before, during, and after 10 days of exposure to microG during spaceflight. Measurements were made by rebreathing a gas mixture containing small amounts of acetylene, carbon monoxide, and argon. Measurements made early in flight in two subjects showed no change in Vti despite large increases in stroke volume (40%) and diffusing capacity (13%) consistent with increased pulmonary capillary blood volume. Late in-flight measurements in four subjects showed a 25% reduction in Vti compared with preflight controls (P < 0.001). There was a concomittant reduction in stroke volume, to the extent that it was no longer significantly different from preflight control. Diffusing capacity remained elevated (11%; P < 0.05) late in flight. These findings suggest that, despite increased pulmonary perfusion and pulmonary capillary blood volume, interstitial pulmonary edema does not result from exposure to microG.

  14. Dosimetric Predictors of Laryngeal Edema

    SciTech Connect

    Sanguineti, Giuseppe . E-mail: gisangui@utmb.edu; Adapala, Prashanth; Endres, Eugene J. C; Brack, Collin; Fiorino, Claudio; Sormani, Maria Pia; Parker, Brent

    2007-07-01

    Purpose: To investigate dosimetric predictors of laryngeal edema after radiotherapy (RT). Methods and Materials: A total of 66 patients were selected who had squamous cell carcinoma of the head and neck with grossly uninvolved larynx at the time of RT, no prior major surgical operation except for neck dissection and tonsillectomy, treatment planning data available for analysis, and at least one fiberoptic examination of the larynx within 2 years from RT performed by a single observer. Both the biologically equivalent mean dose at 2 Gy per fraction and the cumulative biologic dose-volume histogram of the larynx were extracted for each patient. Laryngeal edema was prospectively scored after treatment. Time to endpoint, moderate or worse laryngeal edema (Radiation Therapy Oncology Group Grade 2+), was calculated with log rank test from the date of treatment end. Results: At a median follow-up of 17.1 months (range, 0.4- 50.0 months), the risk of Grade 2+ edema was 58.9% {+-} 7%. Mean dose to the larynx, V30, V40, V50, V60, and V70 were significantly correlated with Grade 2+ edema at univariate analysis. At multivariate analysis, mean laryngeal dose (continuum, hazard ratio, 1.11; 95% confidence interval, 1.06-1.15; p < 0.001), and positive neck stage at RT (N0-x vs. N +, hazard ratio, 3.66; 95% confidence interval, 1.40-9.58; p = 0.008) were the only independent predictors. Further stratification showed that, to minimize the risk of Grade 2+ edema, the mean dose to the larynx has to be kept {<=}43.5 Gy at 2 Gy per fraction. Conclusion: Laryngeal edema is strictly correlated with various dosimetric parameters; mean dose to the larynx should be kept {<=}43.5 Gy.

  15. Excitotoxicity in the Lung: N-Methyl-D-Aspartate-Induced, Nitric Oxide-Dependent, Pulmonary Edema is Attenuated by Vasoactive Intestinal Peptide and by Inhibitors of Poly(ADP-Ribose) Polymerase

    NASA Astrophysics Data System (ADS)

    Said, Sami I.; Berisha, Hasan I.; Pakbaz, Hedayatollah

    1996-05-01

    Excitatory amino acid toxicity, resulting from overactivation of N-methyl-D-aspartate (NMDA) glutamate receptors, is a major mechanism of neuronal cell death in acute and chronic neurological diseases. We have investigated whether excitotoxicity may occur in peripheral organs, causing tissue injury, and report that NMDA receptor activation in perfused, ventilated rat lungs triggered acute injury, marked by increased pressures needed to ventilate and perfuse the lung, and by high-permeability edema. The injury was prevented by competitive NMDA receptor antagonists or by channel-blocker MK-801, and was reduced in the presence of Mg2+. As with NMDA toxicity to central neurons, the lung injury was nitric oxide (NO) dependent: it required L-arginine, was associated with increased production of NO, and was attenuated by either of two NO synthase inhibitors. The neuropeptide vasoactive intestinal peptide and inhibitors of poly(ADP-ribose) polymerase also prevented this injury, but without inhibiting NO synthesis, both acting by inhibiting a toxic action of NO that is critical to tissue injury. The findings indicate that: (i) NMDA receptors exist in the lung (and probably elsewhere outside the central nervous system), (ii) excessive activation of these receptors may provoke acute edematous lung injury as seen in the ``adult respiratory distress syndrome,'' and (iii) this injury can be modulated by blockade of one of three critical steps: NMDA receptor binding, inhibition of NO synthesis, or activation of poly(ADP-ribose) polymerase.

  16. [Perioperative management of a patient complicated with Quincke's edema].

    PubMed

    Nakaigawa, Naoko; Kamata, Kotoe; Komatsu, Ryu; Ozaki, Makoto

    2010-04-01

    We experienced perioperative management of a patient with Quincke's edema who underwent clipping of ruptured intracranial aneurysm. At the time of presentation, he complained of lip and tongue swelling. We administered dl-chlorpheniramine malate and tranexamic acid perioperatively to prevent further edema. Intraoperatively, we avoided contact of objects to the face and the oral cavity which might have caused mechanical stimuli, and infused albumin to maintain plasma osmotic pressure. The patient was kept intubated postoperatively because of significant tongue edema at the end of the procedure. On postoperative day 1, we extubated the trachea after prophylactic administration of methylpredonisolone. Significant upper airway edema was denied by flexible laryngoscopy. Pathophysiological cause of Quincke's edema is increased permeability of capillary vessels due to vasoactive substances. Aside from anti-histaminergic agents and steroids, tranexamic acid, which reduces production of kinin, is specifically effective for this condition. Although there is a reported case of Quincke's edema, eventually diagnosed after development of postoperative upper airway obstruction, there have been no reports of planned perioperative management of this condition. We demonstrated that Quincke's edema could be managed without life-threatening airway compromise by employing adequate pharmacologic interventions and sensible determination of the timing of extubation.

  17. The Employment of an Iterative Design Process to Develop a Pulmonary Graphical Display

    PubMed Central

    Wachter, S. Blake; Agutter, Jim; Syroid, Noah; Drews, Frank; Weinger, Matthew B.; Westenskow, Dwayne

    2003-01-01

    Objective: Data representations on today's medical monitors need to be improved to advance clinical awareness and prevent data vigilance errors. Simply building graphical displays does not ensure an improvement in clinical performance because displays have to be consistent with the user's clinical processes and mental models. In this report, the development of an original pulmonary graphical display for anesthesia is used as an example to show an iterative design process with built-in usability testing. Design: The process reported here is rapid, inexpensive, and requires a minimal number of subjects per development cycle. Three paper-based tests evaluated the anatomic, variable mapping, and graphical diagnostic meaning of the pulmonary display. Measurements: A confusion matrix compared the designer's intended answer with the subject's chosen answer. Considering deviations off the diagonal of the confusion matrix as design weaknesses, the pulmonary display was modified and retested. The iterative cycle continued until the anatomic and variable mapping cumulative test scores for a chosen design scored above 90% and the graphical diagnostic meaning test scored above 75%. Results: The iterative development test resulted in five design iterations. The final graphical pulmonary display improved the overall intuitiveness by 18%. The display was tested in three categories: anatomic features, variable mapping, and diagnostic accuracy. The anatomic intuitiveness increased by 25%, variable mapping intuitiveness increased by 34%, and diagnostic accuracy decreased slightly by 4%. Conclusion: With this rapid iterative development process, an intuitive graphical display can be developed inexpensively prior to formal testing in an experimental setting. PMID:12668693

  18. Development of pulmonary alveolar proteinosis following exposure to dust after the Great East Japan Earthquake.

    PubMed

    Hisata, Shu; Moriyama, Hiroshi; Tazawa, Ryushi; Ohkouchi, Shinya; Ichinose, Masakazu; Ebina, Masahito

    2013-12-01

    We report a unique case of pulmonary alveolar proteinosis that developed 3 weeks after the Great East Japan Earthquake and the subsequent tsunami. The patient had inhaled dust repeatedly while visiting her devastated neighborhood without wearing a protective mask. Five weeks after the earthquake, lung samples taken from the patient showed foreign particle deposition; however, her serum was negative for GM-CSF autoantibody. The patient's clinical symptoms resolved following whole lung lavage. We conclude that inhalation of fine dust particles after natural disasters may cause the onset of pulmonary alveolar proteinosis.

  19. Development of pulmonary alveolar proteinosis following exposure to dust after the Great East Japan Earthquake.

    PubMed

    Hisata, Shu; Moriyama, Hiroshi; Tazawa, Ryushi; Ohkouchi, Shinya; Ichinose, Masakazu; Ebina, Masahito

    2013-12-01

    We report a unique case of pulmonary alveolar proteinosis that developed 3 weeks after the Great East Japan Earthquake and the subsequent tsunami. The patient had inhaled dust repeatedly while visiting her devastated neighborhood without wearing a protective mask. Five weeks after the earthquake, lung samples taken from the patient showed foreign particle deposition; however, her serum was negative for GM-CSF autoantibody. The patient's clinical symptoms resolved following whole lung lavage. We conclude that inhalation of fine dust particles after natural disasters may cause the onset of pulmonary alveolar proteinosis. PMID:24238228

  20. Management of pseudophakic cystoid macular edema.

    PubMed

    Guo, Suqin; Patel, Shriji; Baumrind, Ben; Johnson, Keegan; Levinsohn, Daniel; Marcus, Edward; Tannen, Brad; Roy, Monique; Bhagat, Neelakshi; Zarbin, Marco

    2015-01-01

    Pseudophakic cystoid macular edema (PCME) is a common complication following cataract surgery. Acute PCME may resolve spontaneously, but some patients will develop chronic macular edema that affects vision and is difficult to treat. This disease was described more than 50 years ago, and there are multiple options for clinical management. We discuss mechanisms, clinical efficacy, and adverse effects of these treatment modalities. Topical non-steroidal anti-inflammatory agents and corticosteroids are widely used and, when combined, may have a synergistic effect. Intravitreal corticosteroids and anti-vascular endothelial growth factor (anti-VEGF) agents have shown promise when topical medications either fail or have had limited effects. Randomized clinical studies evaluating anti-VEGF agents are needed to fully evaluate benefits and risks. When PCME is either refractory to medical therapy or is associated with significant vitreous involvement, pars plana vitrectomy has been shown to improve outcomes, though it is associated with additional risks.

  1. Development and characterization of acellular porcine pulmonary valve scaffolds for tissue engineering.

    PubMed

    Luo, Ji; Korossis, Sotirios A; Wilshaw, Stacy-Paul; Jennings, Louise M; Fisher, John; Ingham, Eileen

    2014-11-01

    Currently available replacement heart valves all have limitations. This study aimed to produce and characterize an acellular, biocompatible porcine pulmonary root conduit for reconstruction of the right ventricular outflow tract e.g., during Ross procedure. A process for the decellularization of porcine pulmonary roots was developed incorporating trypsin treatment of the adventitial surface of the scraped pulmonary artery and sequential treatment with hypotonic Tris buffer (HTB; 10 mM Tris pH 8.0, 0.1% (w/v) EDTA, and 10 KIU aprotinin), 0.1% (w/v) sodium dodecyl sulfate in HTB, two cycles of DNase and RNase, and sterilization with 0.1% (v/v) peracetic acid. Histology confirmed an absence of cells and retention of the gross histoarchitecture. Immunohistochemistry further confirmed cell removal and partial retention of the extracellular matrix, but a loss of collagen type IV. DNA levels were reduced by more than 96% throughout all regions of the acellular tissue and no functional genes were detected using polymerase chain reaction. Total collagen levels were retained but there was a significant loss of glycosaminoglycans following decellularization. The biomechanical, hydrodynamic, and leaflet kinematics properties were minimally affected by the process. Both immunohistochemical labeling and antibody absorption assay confirmed a lack of α-gal epitopes in the acellular porcine pulmonary roots and in vitro biocompatibility studies indicated that acellular leaflets and pulmonary arteries were not cytotoxic. Overall the acellular porcine pulmonary roots have excellent potential for development of a tissue substitute for right ventricular outflow tract reconstruction e.g., during the Ross procedure. PMID:24786313

  2. Development of macitentan for the treatment of pulmonary arterial hypertension.

    PubMed

    Selej, Mona; Romero, Alain J; Channick, Richard N; Clozel, Martine

    2015-11-01

    Pulmonary arterial hypertension (PAH) is a serious, chronic condition that, without early recognition and treatment, leads to progressive right heart failure and death. The dual endothelin receptor antagonist macitentan was designed through a deliberate discovery process to maximize endothelin-axis blockade while improving adverse-effect profiles compared with previous compounds. Macitentan's efficacy was demonstrated in an event-driven morbidity and mortality study of treatment-naive and background PAH therapy-treated symptomatic patients. Compared to placebo, 10 mg of macitentan significantly reduced the relative risk of morbidity and mortality by 45%, primarily by delaying PAH worsening, most prominently in World Health Organization (WHO) functional class II and III PAH patients. Macitentan reduced the incidence of the composite end point of PAH-related hospitalizations and mortality and improved WHO FC and exercise capacity (6-min walk distance). Furthermore, it significantly improved cardiopulmonary hemodynamics and quality of life, and had a favorable safety and tolerability profile. To date, this was the largest and longest prospective trial for PAH. Macitentan, currently the only approved oral PAH treatment shown to be safe and effective in delaying long-term progression and reducing PAH-related hospitalizations, has changed treatment paradigms from goal-directed to long-term outcome-oriented therapy.

  3. Developments in the management and treatment of pulmonary embolism.

    PubMed

    Limbrey, Rachel; Howard, Luke

    2015-09-01

    Pulmonary embolism (PE) is a serious and costly disease for patients and healthcare systems. Guidelines emphasise the importance of differentiating between patients who are at high risk of mortality (those with shock and/or hypotension), who may be candidates for thrombolytic therapy or surgery, and those with less severe presentations. Recent clinical studies and guidelines have focused particularly on risk stratification of intermediate-risk patients. Although the use of thrombolysis has been investigated in these patients, anticoagulation remains the standard treatment approach. Individual risk stratification directs initial treatment. Rates of recurrence differ between subgroups of patients with PE; therefore, a review of provoking factors, along with the risks of morbidity and bleeding, guides the duration of ongoing anticoagulation. The direct oral anticoagulants have shown similar efficacy and, in some cases, reduced major bleeding compared with standard approaches for acute treatment. They also offer the potential to reduce the burden on patients and outpatient services in the post-hospital phase. Rivaroxaban, dabigatran and apixaban have been shown to reduce the risk of recurrent venous thromboembolism versus placebo, when given for >12 months. Patients receiving direct oral anticoagulants do not require regular coagulation monitoring, but follow-up, ideally in a specialist PE clinic in consultation with primary care providers, is recommended. PMID:26324810

  4. Acute Hemorrhagic Edema of Infancy.

    PubMed

    Serra E Moura Garcia, C; Sokolova, A; Torre, M L; Amaro, C

    2016-01-01

    Acute Hemorrhagic Edema of Infancy is a small vessel leucocytoclastic vasculitis affecting young infants. It is characterized by large, target-like, macular to purpuric plaques predominantly affecting the face, ear lobes and extremities. Non-pitting edema of the distal extremities and low-grade fever may also be present. Extra-cutaneous involvement is very rare. Although the lesions have a dramatic onset in a twenty-four to forty-eight hour period, usually the child has a non-toxic appearance. In most cases there are no changes in laboratory parameters. The cutaneous biopsy reveals an inflammatory perivascular infiltrate. It is a benign and auto-limited disease, with complete resolution within two to three weeks leaving no sequelae in the majority of cases. No recurrences are described. We report a case of a 42-day old girl admitted at our hospital with Acute Hemorrhagic Edema of Infancy.

  5. An Observational Study of the Development of Diabetic Macular Edema Following Panretinal (Scatter) Photocoagulation (PRP) Given in 1 or 4 Sittings

    PubMed Central

    2009-01-01

    Purpose To compare the effects of single-sitting vs. four-sitting panretinal photocoagulation (PRP) on macular edema in subjects with severe non-proliferative or early proliferative diabetic retinopathy with relatively good visual acuity and no or mild center involved macular edema. Method Subjects were treated with one sitting or 4 sittings of PRP in a non-randomized, prospective, multi-centered clinical trial. Main Outcome Measures Central subfield thickness on optical coherence tomography (OCT). Results Central subfield thickness was slightly greater in the 1 sitting group (n=84) than in the 4 sitting group (n=71) at the 3-day (P=0.01) and 4-week visits (P=0.003). At the 34-week primary outcome visit, the slight differences had reversed, with the thickness being slightly greater in the 4-sitting group than in the 1-sitting group (P=0.06). Visual acuity differences paralleled OCT differences. Conclusions Our results suggest that clinically meaningful differences are unlikely in OCT thickness or visual acuity following application of PRP in 1 sitting compared with 4 sittings in subjects in this cohort. More definitive results would require a large randomized trial. Application to Clinical Practice These results suggest PRP costs to some patients, in terms of travel and lost productivity, as well as to eye care providers, could be reduced. PMID:19204228

  6. Effects of buthionine sulfoximine on the development of ozone-induced pulmonary fibrosis

    SciTech Connect

    Sun, J.D.; Pickrell, J.A.; Harkema, J.R.; McLaughlin, S.I.; Hahn, F.F.; Henderson, R.F.

    1988-10-01

    The capacity of reduced glutathione (GSH) to protect lung tissue against ozone-induced pulmonary fibrosis was investigated. Male B6C3F1 mice were exposed to 0, 0.2, 0.5, and 1.0 ppm ozone for 23 hr/day for 14 days. During exposures and/or for a period of 90 days after exposures, subgroups of mice at each exposure level were given drinking water containing 30 mM L-buthionine-S,R-sulfoximine (BSO) to lower in vivo levels of GSH. These BSO treatments reduced blood glutamylcysteine synthetase (GCS) activity (regulatory enzyme for GSH biosynthesis) and lung nonprotein sulfhydryl (NPSH) levels in nonexposed animals by approximately half. In contrast, ozone exposures increased blood GCS activity and lung NPSH levels in a concentration-dependent manner, with smaller increases in the BSO-treated mice. Immediately after exposures, an ozone-related inflammatory response was seen in lungs, but no histopathological signs of developing fibrosis were evident. Ninety days later, mice exposed to 1 ppm ozone and not treated with BSO had modest evidence of pulmonary fibrosis. Mice exposed to 1 ppm ozone and treated with BSO during this post-exposure period (regardless of BSO treatment during exposures) showed histopathological evidence of exacerbated pulmonary fibrosis, compared to similarly exposed mice not treated with BSO postexposure. These results indicated that interference with the body's normal defense mechanisms against oxidant damage, including suppression of GSH biosynthesis, exacerbates the subsequent development of pulmonary fibrosis.

  7. Pulmonary arterial hypertension

    PubMed Central

    2013-01-01

    , essentially in the screening proposing criteria for estimating the presence of PH mainly based on tricuspid regurgitation peak velocity and systolic artery pressure (sPAP). The therapy of PAH consists of non-specific drugs including oral anticoagulation and diuretics as well as PAH specific therapy. Diuretics are one of the most important treatment in the setting of PH because right heart failure leads to fluid retention, hepatic congestion, ascites and peripheral edema. Current recommendations propose oral anticoagulation aiming for targeting an International Normalized Ratio (INR) between 1.5-2.5. Target INR for patients displaying chronic thromboembolic PH is between 2–3. Better understanding in pathophysiological mechanisms of PH over the past quarter of a century has led to the development of medical therapeutics, even though no cure for PAH exists. Several specific therapeutic agents were developed for the medical management of PAH including prostanoids (epoprostenol, trepoprostenil, iloprost), endothelin receptor antagonists (bosentan, ambrisentan) and phosphodiesterase type 5 inhibitors (sildenafil, tadalafil). This review discusses the current state of art regarding to epidemiologic aspects of PH, diagnostic approaches and the current classification of PH. In addition, currently available specific PAH therapy is discussed as well as future treatments. PMID:23829793

  8. Pulmonary arterial hypertension.

    PubMed

    Montani, David; Günther, Sven; Dorfmüller, Peter; Perros, Frédéric; Girerd, Barbara; Garcia, Gilles; Jaïs, Xavier; Savale, Laurent; Artaud-Macari, Elise; Price, Laura C; Humbert, Marc; Simonneau, Gérald; Sitbon, Olivier

    2013-01-01

    , essentially in the screening proposing criteria for estimating the presence of PH mainly based on tricuspid regurgitation peak velocity and systolic artery pressure (sPAP). The therapy of PAH consists of non-specific drugs including oral anticoagulation and diuretics as well as PAH specific therapy. Diuretics are one of the most important treatment in the setting of PH because right heart failure leads to fluid retention, hepatic congestion, ascites and peripheral edema. Current recommendations propose oral anticoagulation aiming for targeting an International Normalized Ratio (INR) between 1.5-2.5. Target INR for patients displaying chronic thromboembolic PH is between 2-3. Better understanding in pathophysiological mechanisms of PH over the past quarter of a century has led to the development of medical therapeutics, even though no cure for PAH exists. Several specific therapeutic agents were developed for the medical management of PAH including prostanoids (epoprostenol, trepoprostenil, iloprost), endothelin receptor antagonists (bosentan, ambrisentan) and phosphodiesterase type 5 inhibitors (sildenafil, tadalafil). This review discusses the current state of art regarding to epidemiologic aspects of PH, diagnostic approaches and the current classification of PH. In addition, currently available specific PAH therapy is discussed as well as future treatments. PMID:23829793

  9. Developing Pulmonary Vasculopathy in Systemic Sclerosis, Detected with Non-Invasive Cardiopulmonary Exercise Testing

    PubMed Central

    Dumitrescu, Daniel; Oudiz, Ronald J.; Karpouzas, George; Hovanesyan, Arsen; Jayasinghe, Amali; Hansen, James E.; Rosenkranz, Stephan; Wasserman, Karlman

    2010-01-01

    Background Patients with systemic sclerosis (SSc) may develop exercise intolerance due to musculoskeletal involvement, restrictive lung disease, left ventricular dysfunction, or pulmonary vasculopathy (PV). The latter is particularly important since it may lead to lethal pulmonary arterial hypertension (PAH). We hypothesized that abnormalities during cardiopulmonary exercise testing (CPET) in patients with SSc can identify PV leading to overt PAH. Methods Thirty SSc patients from the Harbor-UCLA Rheumatology clinic, not clinically suspected of having significant pulmonary vascular disease, were referred for this prospective study. Resting pulmonary function and exercise gas exchange were assessed, including peakVO2, anaerobic threshold (AT), heart rate- VO2 relationship (O2-pulse), exercise breathing reserve and parameters of ventilation-perfusion mismatching, as evidenced by elevated ventilatory equivalent for CO2 (VE/VCO2) and reduced end-tidal pCO2 (PETCO2) at the AT. Results Gas exchange patterns were abnormal in 16 pts with specific cardiopulmonary disease physiology: Eleven patients had findings consistent with PV, while five had findings consistent with left-ventricular dysfunction (LVD). Although both groups had low peak VO2 and AT, a higher VE/VCO2 at AT and decreasing PETCO2 during early exercise distinguished PV from LVD. Conclusions Previously undiagnosed exercise impairments due to LVD or PV were common in our SSc patients. Cardiopulmonary exercise testing may help to differentiate and detect these disorders early in patients with SSc. PMID:21179195

  10. Pulmonary Hypertension

    MedlinePlus

    Pulmonary hypertension (PH) is high blood pressure in the arteries to your lungs. It is a serious condition. If you have ... and you can develop heart failure. Symptoms of PH include Shortness of breath during routine activity, such ...

  11. Inflammasome genetics contributes to the development and control of active pulmonary tuberculosis.

    PubMed

    Souza de Lima, D; Ogusku, M M; Sadahiro, A; Pontillo, A

    2016-07-01

    Tuberculosis (TB) continues to be a major public health problem. An estimated one-third of the world's population is infected with Mycobacterium tuberculosis (Mtb) but remains asymptomatic (latent TB) and only 5% to 10% of these latent individuals will develop active pulmonary TB. Factors affecting the balance between latent and active TB are mostly unknown, even if host genome has been shown to contribute to the outcome of Mtb response. Acute inflammation and Th1 response are important in the early clearance of the bacteria as it was emphasized by the association between immune genes (i.e.: HLA, IFNG, TNF, NRPAM1, IL10) variants and the development of active pulmonary TB. Recently, the role of the inflammasome in experimental TB has been demonstrated, however, to our knowledge, no data still exist about the contribution of inflammasome genetics to Mtb susceptibility and/or to the development of active TB. For this reason, selected polymorphisms in inflammasome genes were analysed in a case/control cohort of individuals with active pulmonary TB from an endemic area of Brazil Amazon. Our data evidence the novel association between polymorphisms in NLRP3-inflammasome encoding genes and active pulmonary TB, and replicated the association between P2X7 and TB observed in other populations. These results emphasize the role of NLRP3-inflammasome also in human TB, and contribute to our knowledge about pathways involved in the development of active TB, even if deeper investigation are needed to fully elucidate the role of the complex in Mtb infection.

  12. Pulmonary vascular and alveolar development in preterm lambs chronically colonized with Ureaplasma parvum

    PubMed Central

    Polglase, Graeme R.; Dalton, Richard G. B.; Nitsos, Ilias; Knox, Christine L.; Pillow, J. Jane; Jobe, Alan H.; Moss, Timothy J. M.; Newnham, John P.

    2010-01-01

    Ureaplasma species, the most commonly isolated microorganisms in women with chorioamnionitis, are associated with preterm delivery. Chorioamnionitis increases the risk and severity of bronchopulmonary dysplasia and persistent pulmonary hypertension in newborns. It is not known whether the timing of exposure to inflammation in utero is an important contributor to the pathogenesis of bronchopulmonary dysplasia. We hypothesized that chronic inflammation would alter the pulmonary air space and vascular development after 70 days of exposure to infection. Pregnant ewes were given intra-amniotic injection of Ureaplasma parvum serovars 3 or 6 at low (2 × 104 cfu) or high doses (2 × 107 cfu) or media (controls) at 55 days gestational age. Fetuses were delivered at 125 days (term = 150 days). U. parvum was grown from the lungs of all exposed fetuses, and neutrophils and monocytes were increased in the air spaces. Lung mRNA expression of IL-1β and IL-8, but not IL-6, was modestly increased in U. parvum-exposed fetuses. U. parvum exposure increased surfactant and improved lung gas volumes. The changes in lung inflammation and maturation were independent of serovar or dose. Exposure to U. parvum did not change multiple indices of air space or vascular development. Parenchymal elastin and collagen content were similar between groups. Expression of several endothelial proteins and pulmonary resistance arteriolar media thickness were also not different between groups. We conclude that chronic exposure to U. parvum does not cause sustained effects on air space or vascular development in premature lambs. PMID:20495079

  13. Dose-Dependent Effects of Glucocorticoids on Pulmonary Vascular Development in a Murine Model of Hyperoxic Lung Injury

    PubMed Central

    Perez, Marta; Wisniewska, Kamila; Lee, Keng Jin; Cardona, Herminio J.; Taylor, Joann M.; Farrow, Kathryn N.

    2015-01-01

    BACKGROUND Exposure of neonatal mice to hyperoxia results in pulmonary vascular remodeling and aberrant phosphodiesterase-5 (PDE5) signaling. Although glucocorticoids are frequently utilized in the NICU, little is known about their effects on the developing pulmonary vasculature and on PDE5. We sought to determine the effects of hydrocortisone (HC) on pulmonary vascular development and on PDE5 in a neonatal mouse model of hyperoxic lung injury. METHODS C57BL/6 mice were placed in 21% O2 or 75% O2 within 24h of birth and received HC (1, 5, or 10 mg/kg subcutaneously every other day) or vehicle. At 14d, right ventricular hypertrophy (RVH), medial wall thickness (MWT), lung morphometry, and pulmonary artery (PA) PDE5 activity were assessed. PDE5 activity was measured in isolated pulmonary artery smooth muscle cells (PASMC) exposed to 21% or 95% O2 ± 100nM HC for 24h. RESULTS Hyperoxia resulted in alveolar simplification, RVH, increased MWT, and increased PA PDE5 activity. HC decreased hyperoxia-induced RVH and attenuated MWT. HC had dose-dependent effects on alveolar simplification. HC decreased hyperoxia-induced PDE5 activity in vivo and in vitro. CONCLUSIONS HC decreases hyperoxia-induced pulmonary vascular remodeling and attenuates PDE5 activity. These findings suggest that HC may protect against hyperoxic injury in the developing pulmonary vasculature. PMID:26756781

  14. Development and preclinical efficacy of novel transforming growth factor-β1 short interfering RNAs for pulmonary fibrosis.

    PubMed

    D'Alessandro-Gabazza, Corina N; Kobayashi, Tetsu; Boveda-Ruiz, Daniel; Takagi, Takehiro; Toda, Masaaki; Gil-Bernabe, Paloma; Miyake, Yasushi; Yasukawa, Atsushi; Matsuda, Yoshikazu; Suzuki, Noboru; Saito, Hiromitsu; Yano, Yutaka; Fukuda, Ayako; Hasegawa, Tetsuya; Toyobuku, Hidekazu; Rennard, Stephen I; Wagner, Peter D; Morser, John; Takei, Yoshiyuki; Taguchi, Osamu; Gabazza, Esteban C

    2012-03-01

    Idiopathic pulmonary fibrosis is a chronic devastating disease of unknown etiology. No therapy is currently available. A growing body of evidence supports the role of transforming growth factor (TGF)-β1 as the major player in the pathogenesis of the disease. However, attempts to control its expression and to improve the outcome of pulmonary fibrosis have been disappointing. We tested the hypothesis that TGF-β1 is the dominant factor in the acute and chronic phases of pulmonary fibrosis and developed short interfering (si)RNAs directed toward molecules implicated in the disease. This study developed novel sequences of siRNAs targeting the TGF-β1 gene and evaluated their therapeutic efficacy in two models of pulmonary fibrosis: a model induced by bleomycin and a novel model of the disease developed spontaneously in mice overexpressing the full length of human TGF-β1 in the lungs. Intrapulmonary delivery of aerosolized siRNAs of TGF-β1 with sequences common to humans and rodents significantly inhibited bleomycin-induced pulmonary fibrosis in the acute and chronic phases of the disease and in a dose-dependent manner. Aerosolized human-specific siRNA also efficiently inhibited pulmonary fibrosis, improved lung function, and prolonged survival in human TGF-β1 transgenic mice. Mice showed no off-target effects after intratracheal administration of siRNA. These results suggest the applicability of these novel siRNAs as tools for treating pulmonary fibrosis in humans. PMID:22033267

  15. Combination of ozone and silica on the development of pulmonary fibrosis

    SciTech Connect

    Shiotsuka, R.N.; Yermakoff, J.K.; Osheroff, M.R.; Drew, R.T.

    1986-01-01

    The biologic interactions of potentially fibrogenic agents commonly occurring as environmental pollutants remain to be rigorously characterized. Two agents that produce pulmonary fibrosis were selected for this study. Separate groups of male Sprague-Dawley rats were intratracheally instilled with 0, 2, 12, and 50 mg silica and then either sham-exposed or exposed to 0.8 ppm ozone 6 h/d, 5 d/w, for 37 exposure days. Interaction was not detected between silica and ozone in the development of pulmonary fibrosis as determined by quantitative biochemical indices (hydroxyproline and lysyl oxidase) or by histopathologic examination of the lungs. Thus, environmentally relevant levels of ozone appear unlikely to affect the progression of a concurrent silicotic lesion.

  16. [Perioperative Multiple Pulmonary Embolism in a Patient with Giant Right Atrial Myxoma: Report of a Case].

    PubMed

    Nakashima, Koki; Hanayama, Naoji; Kitamura, Tadashi; Sakaki, Kenjiro; Nie, Masaki; Miyaji, Kagami

    2016-02-01

    It is reported that 20% of cardiac myxomas are located in the right atrium. An 81-year-old man presented with dyspnea, general fatigue and leg edema lasting for a year. Echocardiography revealed an 80 mm tumor occupying the right atrium and the right ventricle. At surgery, the tumor attached to the atrial septum was removed with the surrounding septal wall. As the tricuspid annulus was dilated, tricuspid annuloplasty with an artificial ring was also carried out. After coming off cardiopulmonary bypass, the patient developed pulmonary hypertension with the pulmonary arterial pressure being 80% of the systemic pressure, which subsided gradually day by day. Histopathological diagnosis was cardiac myxoma. Postoperative lung perfusion scintigraphy revealed postoperative multiple defects. It was considered that multiple tumor embolisms in the distal pulmonary artery caused postoperative pulmonary hypertension. Careful follow-up for remote recurrence would be essential. PMID:27075159

  17. Plant lignan secoisolariciresinol suppresses pericardial edema caused by dioxin-like compounds in developing zebrafish: Implications for suppression of morphological abnormalities.

    PubMed

    Tokunaga, Saimi; Woodin, Bruce R; Stegeman, John J

    2016-10-01

    Dioxins and dioxin-like compounds (DLCs) enter the body mainly through diet and cause various toxicological effects through activation of the aryl hydrocarbon receptor (AhR), a ligand activated transcription factor. Some plant extracts and phytochemicals are reported to suppress this transformation. However, most of these reports have been from in vitro experiments and few reports have been from in vivo experiments. In addition, there has been no report of foodstuffs that effectively prevent AhR-associated morphological abnormalities such as deformities caused by dioxins and DLCs in vivo. In this study, we show that secoisolariciresinol (SECO), a natural lignan-type polyphenolic phytochemical found mainly in flaxseed, has a rescuing effect, actually suppressing morphological abnormalities (pericardial edema) in zebrafish embryos exposed to 3,3',4,4',5-pentachlorobiphenyl (PCB126), a dioxin-like PCB congener. Importantly, the rescuing effect of SECO was still evident when it was applied 16 h after the beginning of exposure to PCB126. This study suggests that SECO may be useful as a natural suppressive agent for morphological abnormalities caused by dioxins and DLCs. PMID:27427306

  18. Cerebral Edema in Traumatic Brain Injury: Pathophysiology and Prospective Therapeutic Targets.

    PubMed

    Winkler, Ethan A; Minter, Daniel; Yue, John K; Manley, Geoffrey T

    2016-10-01

    Traumatic brain injury is a heterogeneous disorder resulting from an external force applied to the head. The development of cerebral edema plays a central role in the evolution of injury following brain trauma and is closely associated with neurologic outcomes. Recent advances in the understanding of the molecular and cellular pathways contributing to the posttraumatic development of cerebral edema have led to the identification of multiple prospective therapeutic targets. The authors summarize the pathogenic mechanisms underlying cerebral edema and highlight the molecular pathways that may be therapeutically targeted to mitigate cerebral edema and associated sequelae following traumatic brain injury. PMID:27637397

  19. What predicts early volumetric edema increase following stereotactic radiosurgery for brain metastases?

    PubMed

    Hanna, Andrew; Boggs, D Hunter; Kwok, Young; Simard, Marc; Regine, William F; Mehta, Minesh

    2016-04-01

    A volumetric analysis of pre- and post-radiosurgery (PreSRS and PostSRS) edema in patients with cerebral metastases was performed to determine factors of a predictive model assessing the risk of developing increased edema relatively early after SRS. One-hundred-fourteen metastases in 55 patients were analyzed. Selection for this analysis required an MRI ≤ 30 days before SRS and an MRI ≤ 100 days after SRS. Tumor volumes were calculated on PreSRS, SRS, and PostSRS T1-weighted postgadolinium images while edema volumes were calculating using PreSRS and PostSRS fluid-attenuated inversion recovery MR images. An increase in edema was defined as an increase in measurable edema of at least 5%. We developed and evaluated a model predicting the relative risk (RR) of increased edema after SRS. Peritumoral edema increased in 18% (21/114) of the analyzed lesions. Melanoma/renal histology, recursive partitioning analysis class III, and prior WBRT carried RRs of developing postSRS edema increase of 2.45, 2.48, and 3.16, respectively (all P values <0.05). The PreSRS edema/tumor ratio predicted for a RR of 1.007/ratio unit, and steroid dose at time of SRS predicted for a RR of 0.89/mg (all P values <0.05). A predictive model for assessing the RR of increased edema after SRS was developed based from these data and may be useful in identifying patients who might benefit from prophylactic anti-edema therapies before, during, or after SRS. This model could be used as the basis of inclusion criteria for prospective trials investigating novel anti-edema therapies. PMID:26721241

  20. [Lung edema in scuba diving].

    PubMed

    Hempe, S; Lierz, P

    2003-10-01

    The management of a diving-related emergency is frequently a great challenge for an emergency physician without a special diving medicine training or experiences. Almost every physician knows something about the medical therapy of diving-related accidents which are combined with a barotrauma or a decompression sickness. But there are still some rare symptoms and organ affections of diving-related emergencies which are unknown in common. In consideration of the present case of an acute diving-related lung edema we discuss the different reasons and differential diagnosis of diving emergencies.

  1. [Pulmonary rehabilitation].

    PubMed

    Senjyu, Hideaki

    2016-05-01

    Pulmonary rehabilitation commenced in Japan in 1957. However, the development of pulmonary rehabilitation took a long time due to the lack of the necessary health and medical services. Pulmonary rehabilitation is a comprehensive intervention based on a thorough patient assessment followed by patient-tailored therapies that include, but are not limited to, exercise training, education, and behavior change, designed to improve the physical and psychological condition of people with chronic respiratory disease and to promote the long-term adherence to health-enhancing behaviors. The benefits of pulmonary rehabilitation include a decrease in breathlessness and an improvement in exercise tolerance. It is important that the gains in exercise tolerance lead to an increase in daily physical activity. PMID:27254948

  2. [Distal post-traumatic edema--symptom of a sympathetic reflex dystrophy (Sudeck's disease)?].

    PubMed

    Blumberg, H; Griesser, H J; Hornyak, M

    1992-01-01

    The present paper describes various mechanisms, possibly being involved in the development of the posttraumatic, distally generalized edema. New ideas point to a special importance of the sympathetic vasoconstrictor system for this clinical phenomenon, since this system could induce an enhanced venoconstriction at the exit of the capillary bed, which would result in an edema producing diminished venous return. Since the distally generalized edema is an initially and very commonly occurring symptom of reflex sympathetic dystrophy (M. Sudeck), the observation of such an edema should lead one to look for further symptoms of this disorder, especially for the typical triad of autonomic (sympathetic), motor, and sensory disturbances. PMID:1372460

  3. Photoacoustic diagnosis of edema in rat burned skin

    NASA Astrophysics Data System (ADS)

    Yoshida, Ken; Sato, Shunichi; Hatanaka, Kosuke; Saitoh, Daizoh; Ashida, Hiroshi; Sakamoto, Toshihisa; Obara, Minoru

    2010-02-01

    Diagnosis of edema, abnormal accumulation of water in tissue, is important for managing various traumatic injuries and diseases. However, there is no established method for real-time, noninvasive monitoring of edema. In severe extensive burn injuries, edema develops both topically and systemically due to the increased permeability of blood vessels. In this study, we examined photoacoustic (PA) monitoring of edema formed in rat burn models. Deep dermal burn with a 20% total body surface area was made in the dorsal skin of rats. Burn and its adjacent nonburn tissues were irradiated with 6-ns light pulses at 1430 nm, which is one of the absorption peak wavelengths of water in the near infrared. The PA signal amplitude increased until 12 - 24 hr postburn, and thereafter it gradually decreased to its initial level; the latter phase (after 24 hr postburn) coincided with a diuretic phase in the rats. There was a significant correlation between the PA signal amplitudes and water contents in the tissue measured by wet/dry weight method. These findings demonstrate the validity of PA measurement for real-time, noninvasive monitoring of edema.

  4. HIF2α–arginase axis is essential for the development of pulmonary hypertension

    PubMed Central

    Cowburn, Andrew S.; Crosby, Alexi; Macias, David; Branco, Cristina; Colaço, Renato D. D. R.; Southwood, Mark; Toshner, Mark; Crotty Alexander, Laura E.; Morrell, Nicholas W.; Chilvers, Edwin R.; Johnson, Randall S.

    2016-01-01

    Hypoxic pulmonary vasoconstriction is correlated with pulmonary vascular remodeling. The hypoxia-inducible transcription factors (HIFs) HIF-1α and HIF-2α are known to contribute to the process of hypoxic pulmonary vascular remodeling; however, the specific role of pulmonary endothelial HIF expression in this process, and in the physiological process of vasoconstriction in response to hypoxia, remains unclear. Here we show that pulmonary endothelial HIF-2α is a critical regulator of hypoxia-induced pulmonary arterial hypertension. The rise in right ventricular systolic pressure (RVSP) normally observed following chronic hypoxic exposure was absent in mice with pulmonary endothelial HIF-2α deletion. The RVSP of mice lacking HIF-2α in pulmonary endothelium after exposure to hypoxia was not significantly different from normoxic WT mice and much lower than the RVSP values seen in WT littermate controls and mice with pulmonary endothelial deletion of HIF-1α exposed to hypoxia. Endothelial HIF-2α deletion also protected mice from hypoxia remodeling. Pulmonary endothelial deletion of arginase-1, a downstream target of HIF-2α, likewise attenuated many of the pathophysiological symptoms associated with hypoxic pulmonary hypertension. We propose a mechanism whereby chronic hypoxia enhances HIF-2α stability, which causes increased arginase expression and dysregulates normal vascular NO homeostasis. These data offer new insight into the role of pulmonary endothelial HIF-2α in regulating the pulmonary vascular response to hypoxia. PMID:27432976

  5. [Therapeutic approach in persistent diabetic macular edema].

    PubMed

    Brănişteanu, Daniel; Moraru, Andreea

    2014-01-01

    Terminology of persistent diabetic macular edema has been initially reserved to cases unresponsive to conventional laser photocoagulation according to ETDRS criteria. While knowledge about pathophysiology of macular edema evolved and new drugs became available, the terminology of persistent diabetic macular edema expanded to include resistance to most current therapies. The purpose of this paper is to review medical and surgical options in the treatment of such difficult cases according to literature data and personal experience.

  6. Kawasaki Disease with Retropharyngeal Edema following a Blackfly Bite

    PubMed Central

    Watanabe, Toru

    2014-01-01

    We describe a patient with Kawasaki disease (KD) and retropharyngeal edema following a blackfly bite. An 8-year-old boy was referred to our hospital because of a 3-day-history of fever and left neck swelling and redness after a blackfly bite. Computed tomography of the neck revealed left cervical lymph nodes swelling with edema, increased density of the adjacent subcutaneous tissue layer, and low density of the retropharyngeum. The patient was initially presumed to have cervical cellulitis, lymphadenitis, and retropharyngeal abscess. He was administered antibiotics intravenously, which did not improve his condition. The patient subsequently exhibited other signs of KD and was diagnosed with KD and retropharyngeal edema. Intravenous immunoglobulin therapy and oral flurbiprofen completely resolved the symptoms and signs. A blackfly bite sometimes incites a systemic reaction in humans due to a hypersensitive reaction to salivary secretions, which may have contributed to the development of KD in our patient. PMID:25349761

  7. Metabolic Changes Precede the Development of Pulmonary Hypertension in the Monocrotaline Exposed Rat Lung

    PubMed Central

    Rafikova, Olga; Meadows, Mary L.; Kinchen, Jason M.; Mohney, Robert P.; Maltepe, Emin; Desai, Ankit A.; Yuan, Jason X.-J.; Garcia, Joe G. N.; Fineman, Jeffrey R.; Rafikov, Ruslan; Black, Stephen M.

    2016-01-01

    There is increasing interest in the potential for metabolic profiling to evaluate the progression of pulmonary hypertension (PH). However, a detailed analysis of the metabolic changes in lungs at the early stage of PH, characterized by increased pulmonary artery pressure but prior to the development of right ventricle hypertrophy and failure, is lacking in a preclinical animal model of PH. Thus, we undertook a study using rats 14 days after exposure to monocrotaline (MCT), to determine whether we could identify early stage metabolic changes prior to the manifestation of developed PH. We observed changes in multiple pathways associated with the development of PH, including activated glycolysis, increased markers of proliferation, disruptions in carnitine homeostasis, increased inflammatory and fibrosis biomarkers, and a reduction in glutathione biosynthesis. Further, our global metabolic profile data compare favorably with prior work carried out in humans with PH. We conclude that despite the MCT-model not recapitulating all the structural changes associated with humans with advanced PH, including endothelial cell proliferation and the formation of plexiform lesions, it is very similar at a metabolic level. Thus, we suggest that despite its limitations it can still serve as a useful preclinical model for the study of PH. PMID:26937637

  8. [Cigarette smoking is the most important causal factor for developing chronic obstructive pulmonary disease (COPD)].

    PubMed

    Muro, Shigeo

    2011-10-01

    Cigarette smoking is the most important causal factor for developing chronic obstructive pulmonary disease(COPD). On the other hand, a substantial proportion of COPD cases suffer from obstructive disorder by other causes than smoking, especially among younger persons, females, and residents of developing countries. There are evidences that several rare genetic syndromes(such as alpha 1-antitrypsin deficiency) and occupational exposures as causes of COPD. Environmental tobacco smoke, biomass smoke, and dietary factors are likely causes of COPD, although their contribution is much less compared to active smoking. Smoking during pregnancy may also pose a risk for the fetus, by affecting lung growth and development in uterus. The quicker the smoking cessation is achieved, the more improvements in the lung functions the COPD patients can obtain. Smoking should be avoided as soon as possible in all the COPD subjects and those who are at risk for developing COPD.

  9. Development of confocal immunofluorescence FRET microscopy to Investigate eNOS and GSNOR localization and interaction in pulmonary endothelial cells

    NASA Astrophysics Data System (ADS)

    Rehman, Shagufta; Brown-Steinke, Kathleen; Palmer, Lisa; Periasamy, Ammasi

    2015-03-01

    Confocal FRET microscopy is a widely used technique for studying protein-protein interactions in live or fixed cells. Endothelial nitric oxide synthase (eNOS) and S-nitrosoglutathione reductase (GSNOR) are enzymes involved in regulating the bioavailability of S-nitrosothiols (SNOs) in the pulmonary endothelium and have roles in the development of pulmonary arterial hypertension. Labeling of endogenous proteins to better understand a disease process can be challenging. We have used immunofluorescence to detect endogenous eNOS and GSNOR in primary pulmonary endothelial cells to co-localize these proteins as well as to study their interaction by FRET. The challenge has been in selecting the right immunofluorescence labeling condition, right antibody, the right blocking reagent, the right FRET pair and eliminating cross-reactivity of secondary antibodies. We have used Alexa488 and Alexa568 as a FRET pair. After a series of optimizations, the data from Confocal Laser Scanning Microscopy (CLSM) demonstrate co-localization of eNOS and GSNOR in the perinuclear region of the pulmonary endothelial cell primarily within the cis-Golgi with lower levels of co-localization seen within the trans-Golgi. FRET studies demonstrate, for the first time, interaction between eNOS and GSNOR in both murine and bovine pulmonary endothelial cells. Further characterization of eNOSGSNOR interaction and the subcellular location of this interaction will provide mechanistic insight into the importance of S-nitrosothiol signaling in pulmonary biology, physiology and pathology.

  10. Demographic, etiological, and histological pulmonary analysis of patients with acute respiratory failure: a study of 19 years of autopsies

    PubMed Central

    de Matos Soeiro, Alexandre; Ruppert, Aline D; Canzian, Mauro; Parra, Edwin R; Farhat, Cecília; Capelozzi, Vera L

    2011-01-01

    INTRODUCTION: Acute respiratory failure has been one of the most important causes of death in intensive care units, and certain aspects of its pulmonary pathology are currently unknown. OBJECTIVES: The objective was to describe the demographic data, etiology, and pulmonary histopathological findings of different diseases in the autopsies of patients with acute respiratory failure. METHOD: Autopsies of 4,710 patients with acute respiratory failure from 1990 to 2008 were reviewed, and the following data were obtained: age, sex, and major associated diseases. The pulmonary histopathology was categorized as diffuse alveolar damage, pulmonary edema, alveolar hemorrhage, and lymphoplasmacytic interstitial pneumonia. The odds ratio of the concordance between the major associated diseases and specific autopsy findings was calculated using logistic regression. RESULTS: Bacterial bronchopneumonia was present in 33.9% of the cases and cancer in 28.1%. The pulmonary histopathology showed diffuse alveolar damage in 40.7% (1,917) of the cases. A multivariate analysis showed a significant and powerful association between diffuse alveolar damage and bronchopneumonia, HIV/AIDS, sepsis, and septic shock, between liver cirrhosis and pulmonary embolism, between pulmonary edema and acute myocardial infarction, between dilated cardiomyopathy and cancer, between alveolar hemorrhage and bronchopneumonia and pulmonary embolism, and between lymphoplasmacytic interstitial pneumonia and HIV/AIDS and liver cirrhosis. CONCLUSIONS: Bronchopneumonia was the most common diagnosis in these cases. The most prevalent pulmonary histopathological pattern was diffuse alveolar damage, which was associated with different inflammatory conditions. Further studies are necessary to elucidate the complete pathophysiological mechanisms involved with each disease and the development of acute respiratory failure. PMID:21876973

  11. Development of an itraconazole-loaded nanostructured lipid carrier (NLC) formulation for pulmonary application.

    PubMed

    Pardeike, J; Weber, S; Haber, T; Wagner, J; Zarfl, H P; Plank, H; Zimmer, A

    2011-10-31

    Itraconazole-loaded NLC for pulmonary application were developed. In Precirol ATO 5 and oleic acid Itraconazole had the highest solubility. The solid lipid and the oil were mixable in a ratio 9:1 possessing a melting point above body temperature. 0.4% Itraconazole was dissolved in this lipid blend. Eumulgin SLM 20 was the stabilizer with the highest affinity to the lipid blend used as particle matrix. 2.5% Eumulgin SLM 20 was sufficient to obtain NLC with a narrow particle size distribution and sufficient stability. The tonicity of the formulation was adjusted with glycerol. Sterility was obtained by autoclaving. Neither the addition of glycerol nor autoclaving had an influence on the particle size and the zeta potential of Itraconazole-loaded NLC. SEM images showed spherical particles confirming the particle size measured by light scattering techniques. An entrapment efficiency of 98.78% was achieved. Burst release of Itraconazole from the developed carrier system was found. Itraconazole-loaded NLC possessed good storage stability. Nebulizing Itraconazole-loaded NLC with a jet stream and an ultrasonic nebulizer had no influence on the particle size and the entrapment efficiency of Itraconazole in the particle matrix, being a precondition for pulmonary application. PMID:21839157

  12. Development of pulmonary arterial hypertension during oral dasatinib therapy for chronic myelogenous leukemia.

    PubMed

    Morishita, Sakura; Hagihara, Maki; Itabashi, Megumi; Ishii, Yoshimi; Yamamoto, Wataru; Numata, Ayumi; Motohashi, Kenji; Matsumoto, Kenji; Fujisawa, Shin; Nakajima, Hideaki

    2016-08-01

    We present a 36-year-old woman who had been taking oral dasatinib for 3 years for the treatment of chronic myelogenous leukemia (CML). Although adverse events such as thrombocytopenia and pleural effusion developed, she showed a major molecular response (MMR) 22 months after the initiation of oral dasatinib administration, and the therapy was thus continued. Approximately 34 months after oral dasatinib initiation, she developed severe exertional dyspnea and had to be urgently hospitalized. There was no apparent pleural effusion increase, and neither imaging nor blood test results suggested pneumonia or other infections. Pulmonary arterial hypertension (PAH) was suspected on the basis of transthoracic echocardiography. PAH was then confirmed by right heart catheterization. Though dasatinib was discontinued on the day of hospitalization, pulmonary hypertension and heart failure progressed, and she did not respond to catecholamines or PDE5 (phosphodiesterase type 5) inhibitors. On the 4(th) hospital day, she experienced cardiopulmonary arrest and died 1 week later. Cases with PAH due to oral administration of dasatinib have been reported previously. However, cases showing the rapid progression documented in our patient are rare and we advocate that PAH be considered a potential adverse event associated with dasatinib therapy. PMID:27599415

  13. Pathogenesis of optic disc edema in raised intracranial pressure.

    PubMed

    Hayreh, Sohan Singh

    2016-01-01

    Optic disc edema in raised intracranial pressure was first described in 1853. Ever since, there has been a plethora of controversial hypotheses to explain its pathogenesis. I have explored the subject comprehensively by doing basic, experimental and clinical studies. My objective was to investigate the fundamentals of the subject, to test the validity of the previous theories, and finally, based on all these studies, to find a logical explanation for the pathogenesis. My studies included the following issues pertinent to the pathogenesis of optic disc edema in raised intracranial pressure: the anatomy and blood supply of the optic nerve, the roles of the sheath of the optic nerve, of the centripetal flow of fluids along the optic nerve, of compression of the central retinal vein, and of acute intracranial hypertension and its associated effects. I found that, contrary to some previous claims, an acute rise of intracranial pressure was not quickly followed by production of optic disc edema. Then, in rhesus monkeys, I produced experimentally chronic intracranial hypertension by slowly increasing in size space-occupying lesions, in different parts of the brain. Those produced raised cerebrospinal fluid pressure (CSFP) and optic disc edema, identical to those seen in patients with elevated CSFP. Having achieved that, I investigated various aspects of optic disc edema by ophthalmoscopy, stereoscopic color fundus photography and fluorescein fundus angiography, and light microscopic, electron microscopic, horseradish peroxidase and axoplasmic transport studies, and evaluated the effect of opening the sheath of the optic nerve on the optic disc edema. This latter study showed that opening the sheath resulted in resolution of optic disc edema on the side of the sheath fenestration, in spite of high intracranial CSFP, proving that a rise of CSFP in the sheath was the essential pre-requisite for the development of optic disc edema. I also investigated optic disc edema with

  14. Reinke Edema: Watch For Vocal Fold Cysts.

    PubMed

    Tüzüner, Arzu; Demirci, Sule; Yavanoglu, Ahmet; Kurkcuoglu, Melih; Arslan, Necmi

    2015-06-01

    Reinke edema is one of the common cause of dysphonia middle-aged population, and severe thickening of vocal folds require surgical treatment. Smoking plays a major role on etiology. Vocal fold cysts are also benign lesions and vocal trauma blamed for acquired cysts. We would like to present 3 cases with vocal fold cyst related with Reinke edema. First case had a subepidermal epidermoid cyst with Reinke edema, which could be easily observed before surgery during laryngostroboscopy. Second case had a mucous retention cyst into the edematous Reinke tissue, which was detected during surgical intervention, and third case had a epidermoid cyst that occurred 2 months after before microlaryngeal operation regarding Reinke edema reduction. These 3 cases revealed that surgical management of Reinke edema needs a careful dissection and close follow-up after surgery for presence of vocal fold cysts.

  15. Development of a diagnostic decision tree for obstructive pulmonary diseases based on real-life data

    PubMed Central

    in ’t Veen, Johannes C.C.M.; Dekhuijzen, P.N. Richard; van Heijst, Ellen; Kocks, Janwillem W.H.; Muilwijk-Kroes, Jacqueline B.; Chavannes, Niels H.; van der Molen, Thys

    2016-01-01

    The aim of this study was to develop and explore the diagnostic accuracy of a decision tree derived from a large real-life primary care population. Data from 9297 primary care patients (45% male, mean age 53±17 years) with suspicion of an obstructive pulmonary disease was derived from an asthma/chronic obstructive pulmonary disease (COPD) service where patients were assessed using spirometry, the Asthma Control Questionnaire, the Clinical COPD Questionnaire, history data and medication use. All patients were diagnosed through the Internet by a pulmonologist. The Chi-squared Automatic Interaction Detection method was used to build the decision tree. The tree was externally validated in another real-life primary care population (n=3215). Our tree correctly diagnosed 79% of the asthma patients, 85% of the COPD patients and 32% of the asthma–COPD overlap syndrome (ACOS) patients. External validation showed a comparable pattern (correct: asthma 78%, COPD 83%, ACOS 24%). Our decision tree is considered to be promising because it was based on real-life primary care patients with a specialist's diagnosis. In most patients the diagnosis could be correctly predicted. Predicting ACOS, however, remained a challenge. The total decision tree can be implemented in computer-assisted diagnostic systems for individual patients. A simplified version of this tree can be used in daily clinical practice as a desk tool. PMID:27730177

  16. Development of a pulmonary peptide delivery system using porous nanoparticle-aggregate particles for systemic application.

    PubMed

    Yang, Likai; Luo, Jing; Shi, Sanjun; Zhang, Qiang; Sun, Xun; Zhang, Zhirong; Gong, Tao

    2013-07-15

    As a non-invasive administration route, pulmonary peptide delivery for systemic application has shown great promise. However, many barriers exist that prevent effective peptide delivery. The use of porous nanoparticle-aggregate particles (PNAPs) is an excellent option because of their proper aerodynamic size and maximal deposition. However, in most cases, the spray drying heating process for PNAPs has been challenging in regard to maintaining peptide stability and activity. To overcome these issues, we developed a spray freeze-drying method for PNAP preparation. To solve the low entrapment efficiency problem of nanostructured lipid carriers, we used hydrophobic ion pair complexes to increase the lipophilicity of the peptide, thus increasing entrapment efficiency and drug loading. Here, we used a model peptide, octreotide acetate, for PNAP preparation, which has a high entrapment efficiency (>95%) and proper aerodynamic size (~3 μm). In addition, after intrapulmonary administration, we evaluated the pharmacokinetics and pharmacodynamics in a rat preventive hepatic ischemia-reperfusion injury model. Our in vivo data showed significantly increased area under the curve and improved plasma aspartate aminotransferase levels for our PNAP intrapulmonary delivery system vs. the clinically used octreotide acetate delivery via subcutaneous injection. Together, PNAPs may have great potential for carrying peptide drugs for pulmonary delivery.

  17. Response of pulmonary veins to increased intracranial pressure and pulmonary air embolization

    SciTech Connect

    Peterson, B.T.; Grauer, S.E.; Hyde, R.W.; Ortiz, C.; Moosavi, H.; Utell, M.J.

    1980-01-01

    To see whether air emboli to the lungs rather than brain compression caused these findings, anesthetized dogs received intravenous air infusions, subdural air infusions, or brain compression from balloons inflated in the subdural space. Subdural air and intravenous air resulted in similar vascular responses. Pulmonary artery pressure (Ppa) increased 160% (P < 0.01) and pulmonary venous pressure transiently rose 13 +- 5 Torr (P < 0.05) without an increase in left atrial pressure or cardiac output (Q). The end-tidal PCP/sub 2/ fell 55% (P < 0.01) and the postmortem weight of the lungs increased 55% (P < 0.05). Brain compression with a subdural balloon instead of air only caused a 20% rise in Ppa and Q without pulmonary edema. Thus, pulmonary air emboli rather than brain compression accounts for the edema and pulmonary hypertension caused by subdural air. Catheters in pulmonary veins and the left atrium showed that air emboli cause transient pulmonary venous hypertension as well as a reproducible form of noncardiogenic pulmonary edema.

  18. The Pulmonary Surfactant: Impact of Tobacco Smoke and Related Compounds on Surfactant and Lung Development

    PubMed Central

    Scott, J Elliott

    2004-01-01

    Cigarette smoking, one of the most pervasive habits in society, presents many well established health risks. While lung cancer is probably the most common and well documented disease associated with tobacco exposure, it is becoming clear from recent research that many other diseases are causally related to smoking. Whether from direct smoking or inhaling environmental tobacco smoke (ETS), termed secondhand smoke, the cells of the respiratory tissues and the lining pulmonary surfactant are the first body tissues to be directly exposed to the many thousands of toxic chemicals in tobacco. Considering the vast surface area of the lung and the extreme attenuation of the blood-air barrier, it is not surprising that this organ is the primary route for exposure, not just to smoke but to most environmental contaminants. Recent research has shown that the pulmonary surfactant, a complex mixture of phospholipids and proteins, is the first site of defense against particulates or gas components of smoke. However, it is not clear what effect smoke has on the surfactant. Most studies have demonstrated that smoking reduces bronchoalveolar lavage phospholipid levels. Some components of smoke also appear to have a direct detergent-like effect on the surfactant while others appear to alter cycling or secretion. Ultimately these effects are reflected in changes in the dynamics of the surfactant system and, clinically in changes in lung mechanics. Similarly, exposure of the developing fetal lung through maternal smoking results in postnatal alterations in lung mechanics and higher incidents of wheezing and coughing. Direct exposure of developing lung to nicotine induces changes suggestive of fetal stress. Furthermore, identification of nicotinic receptors in fetal lung airways and corresponding increases in airway connective tissue support a possible involvement of nicotine in postnatal asthma development. Finally, at the level of the alveoli of the lung, colocalization of nicotinic

  19. The Pulmonary Surfactant: Impact of Tobacco Smoke and Related Compounds on Surfactant and Lung Development

    PubMed Central

    Scott, J Elliott

    2004-01-01

    Cigarette smoking, one of the most pervasive habits in society, presents many well established health risks. While lung cancer is probably the most common and well documented disease associated with tobacco exposure, it is becoming clear from recent research that many other diseases are causally related to smoking. Whether from direct smoking or inhaling environmental tobacco smoke (ETS), termed secondhand smoke, the cells of the respiratory tissues and the lining pulmonary surfactant are the first body tissues to be directly exposed to the many thousands of toxic chemicals in tobacco. Considering the vast surface area of the lung and the extreme attenuation of the blood-air barrier, it is not surprising that this organ is the primary route for exposure, not just to smoke but to most environmental contaminants. Recent research has shown that the pulmonary surfactant, a complex mixture of phospholipids and proteins, is the first site of defense against particulates or gas components of smoke. However, it is not clear what effect smoke has on the surfactant. Most studies have demonstrated that smoking reduces bronchoalveolar lavage phospholipid levels. Some components of smoke also appear to have a direct detergent-like effect on the surfactant while others appear to alter cycling or secretion. Ultimately these effects are reflected in changes in the dynamics of the surfactant system and, clinically in changes in lung mechanics. Similarly, exposure of the developing fetal lung through maternal smoking results in postnatal alterations in lung mechanics and higher incidents of wheezing and coughing. Direct exposure of developing lung to nicotine induces changes suggestive of fetal stress. Furthermore, identification of nicotinic receptors in fetal lung airways and corresponding increases in airway connective tissue support a possible involvement of nicotine in postnatal asthma development. Finally, at the level of the alveoli of the lung, colocalization of nicotinic

  20. Development of a patient-specific model for calculation of pulmonary function

    NASA Astrophysics Data System (ADS)

    Zhong, Hualiang; Ding, Mingyue; Movsas, Benjamin; Chetty, Indrin J.

    2011-06-01

    The purpose of this paper is to develop a patient-specific finite element model (FEM) to calculate the pulmonary function of lung cancer patients for evaluation of radiation treatment. The lung model was created with an in-house developed FEM software with region-specific parameters derived from a four-dimensional CT (4DCT) image. The model was used first to calculate changes in air volume and elastic stress in the lung, and then to calculate regional compliance defined as the change in air volume corrected by its associated stress. The results have shown that the resultant compliance images can reveal the regional elastic property of lung tissue, and could be useful for radiation treatment planning and assessment.

  1. Factors affecting regional pulmonary blood flow in chronic ischemic heart disease

    SciTech Connect

    Pistolesi, M.; Miniati, M.; Bonsignore, M.; Andreotti, F.; Di Ricco, G.; Marini, C.; Rindi, M.; Biagini, A.; Milne, E.N.; Giuntini, C.

    1988-07-01

    To assess the effect of left heart disease on pulmonary blood flow distribution, we measured mean pulmonary arterial and wedge pressures, cardiac output, pulmonary vascular resistance, pulmonary blood volume, and arterial oxygen tension before and after treatment in 13 patients with longstanding ischemic heart failure and pulmonary edema. Pulmonary edema was evaluated by a radiographic score, and regional lung perfusion was quantified on a lung scan by the upper to lower third ratio (U:L ratio) of pulmonary blood flow per unit of lung volume. In all cases, redistribution of lung perfusion toward the apical regions was observed; this pattern was not affected by treatment. After treatment, pulmonary vascular pressures, resistance, and edema were reduced, while pulmonary blood volume did not change. At this time, pulmonary vascular resistance showed a positive correlation with the U:L ratio (r = 0.78; P less than 0.01), whereas no correlation was observed between U:L ratio and wedge pressure, pulmonary edema, or arterial oxygen tension. Hence, redistribution of pulmonary blood flow, in these patients, reflects chronic structural vascular changes prevailing in the dependent lung regions.

  2. Macular edema. A complication of diabetic retinopathy.

    PubMed

    Ferris, F L; Patz, A

    1984-05-01

    Diabetic macular edema is the leading cause of decreased vision from diabetic retinopathy. This decreased vision is caused by an increase in extracellular fluid within the retina distorting the retinal architecture and frequently taking on a pattern of cystoid macular edema. This fluid accumulates within the retina because of the breakdown of the barriers within the retinal blood vessels and possibly the pigment epithelium. Diabetic macular edema tends to be a chronic disorder. Although spontaneous recovery is not an uncommon occurrence, over one-half of diabetics with macular edema will lose two or more lines of visual acuity within two years. The most promising treatment for diabetic macular edema has been photocoagulation. It is recommended that in all patients with diabetic macular edema attempts be made to normalize elevated blood glucose, decrease elevated blood pressure, and improve cardiac or renal status. Reduction of serum lipids by diet or pharmacologic means is an unproven treatment at this time. The Early Treatment Diabetic Retinopathy Study hopefully will provide more definitive information as to whether photocoagulation is effective in various subgroups of patients with diabetic macular edema.

  3. Decreased light attenuation in cerebral cortex during cerebral edema detected using optical coherence tomography

    PubMed Central

    Rodriguez, Carissa L. R.; Szu, Jenny I.; Eberle, Melissa M.; Wang, Yan; Hsu, Mike S.; Binder, Devin K.; Park, B. Hyle

    2014-01-01

    Abstract. Cerebral edema develops in response to a variety of conditions, including traumatic brain injury and stroke, and contributes to the poor prognosis associated with these injuries. This study examines the use of optical coherence tomography (OCT) for detecting cerebral edema in vivo. Three-dimensional imaging of an in vivo water intoxication model in mice was performed using a spectral-domain OCT system centered at 1300 nm. The change in attenuation coefficient was calculated and cerebral blood flow was analyzed using Doppler OCT techniques. We found that the average attenuation coefficient in the cerebral cortex decreased over time as edema progressed. The initial decrease began within minutes of inducing cerebral edema and a maximum decrease of 8% was observed by the end of the experiment. Additionally, cerebral blood flow slowed during late-stage edema. Analysis of local regions revealed the same trend at various locations in the brain, consistent with the global nature of the cerebral edema model used in this study. These results demonstrate that OCT is capable of detecting in vivo optical changes occurring due to cerebral edema and highlights the potential of OCT for precise spatiotemporal detection of cerebral edema. PMID:25674578

  4. Flt1/VEGFR1 heterozygosity causes transient embryonic edema

    PubMed Central

    Otowa, Yasunori; Moriwaki, Kazumasa; Sano, Keigo; Shirakabe, Masanori; Yonemura, Shigenobu; Shibuya, Masabumi; Rossant, Janet; Suda, Toshio; Kakeji, Yoshihiro; Hirashima, Masanori

    2016-01-01

    Vascular endothelial growth factor-A is a major player in vascular development and a potent vascular permeability factor under physiological and pathological conditions by binding to a decoy receptor Flt1 and its primary receptor Flk1. In this study, we show that Flt1 heterozygous (Flt1+/−) mouse embryos grow up to adult without life-threatening abnormalities but exhibit a transient embryonic edema around the nuchal and back regions, which is reminiscent of increased nuchal translucency in human fetuses. Vascular permeability is enhanced and an intricate infolding of the plasma membrane and huge vesicle-like structures are seen in Flt1+/− capillary endothelial cells. Flk1 tyrosine phosphorylation is elevated in Flt1+/− embryos, but Flk1 heterozygosity does not suppress embryonic edema caused by Flt1 heterozygosity. When Flt1 mutants are crossed with Aspp1−/− mice which exhibit a transient embryonic edema with delayed formation and dysfunction of lymphatic vessels, only 5.7% of Flt1+/−; Aspp1−/− mice survive, compared to expected ratio (25%). Our results demonstrate that Flt1 heterozygosity causes a transient embryonic edema and can be a risk factor for embryonic lethality in combination with other mutations causing non-lethal vascular phenotype. PMID:27251772

  5. Lipid-based carriers for pulmonary products: preclinical development and case studies in humans.

    PubMed

    Cipolla, David; Shekunov, Boris; Blanchard, Jim; Hickey, Anthony

    2014-08-01

    A number of lipid-based technologies have been applied to pharmaceuticals to modify their drug release characteristics, and additionally, to improve the drug loading for poorly soluble drugs. These technologies, including solid-state lipid microparticles, many of which are porous in nature, liposomes, solid lipid nanoparticles and nanostructured lipid carriers, are increasingly being developed for inhalation applications. This article provides a review of the rationale for the use of these technologies in the pulmonary delivery of drugs, and summarizes the manufacturing processes and their limitations, the in vitro and in vivo performance of these systems, the safety of these lipid-based systems in the lung, and their promise for commercialization. PMID:24819218

  6. Renal sympathetic denervation prevents the development of pulmonary arterial hypertension and cardiac dysfunction in dogs.

    PubMed

    Hu, Wei; Yu, Sheng-Bo; Chen, Liao; Guo, Rui-Qiang; Zhao, Qing-Yan

    2015-08-01

    The renin-angiotensin-aldosterone system is activated in pulmonary arterial hypertension (PAH) patients, and this activation may have long-term negative effects on the progression of PAH. The purpose of this study was to evaluate the effects of transcatheter renal sympathetic denervation (RSD) on the development of pulmonary arterial hypertension and cardiac dysfunction in dogs using two-dimensional speckle tracking imaging. Twenty-two dogs were randomly divided into three groups: control group (n = 7), PAH group (n = 8), and PAH + RSD group (n = 7). All dogs were assessed using two-dimensional speckle tracking imaging. The ventricular strain, ventricular synchrony, left ventricular (LV) twist, and torsion rate were analyzed to evaluate cardiac function. After 8 weeks, the right ventricular lateral longitudinal strain and the septum longitudinal strain were reduced in the PAH group compared with the control group (p < 0.001). However, these values were significantly restored in the PAH + RSD group compared with the PAH group (p < 0.01). The degree of LV and RV dyssynchrony was significantly higher in the PAH group compared with the control group (p < 0.001), but the degree of LV and RV dyssynchrony was significantly lower in the PAH + RSD group compared to the PAH group (p < 0.01). The LV twist was significantly restored in the PAH + RSD group compared to the PAH group (p < 0.01). Similarly, the rotation rate was markedly decreased in the PAH group, and strikingly improved in the PAH + RSD group (p < 0.01). These results indicate that RSD prevents the development of PAH and cardiac dysfunction in dogs.

  7. Pulmonary hyalinizing granulomas in a patient with malignant lymphoma, with development nine years later of multiple myeloma and systemic amyloidosis.

    PubMed

    Drasin, H; Blume, M R; Rosenbaum, E H; Klein, H Z

    1979-07-01

    In our patient, multiple bilateral nodular pulmonary densities appeared on a chest x-ray at the time of diagnosis of stage IV diffuse lymphocytic lymphoma. After localized radiation therapy, the patient received no further systemic therapy. The pulmonary nodules slowly became larger and more numerous. Nine years later the patient developed proven multiple myeloma. Pulmonary hyalinizing granulomas have not heretofore been associated with proven lymphoreticular neoplasia, although this has long been suspected. The occurrence of two B-cell tumors at different points in time associated with systemic amyloidosis is an extremely rare event. The authors discuss the possibility that these conditions represent an abnormality in a common cell of origin with differing expression over time. Coincidence, however, remains a likely explanation for the different immunopathies that occurred in our patient. PMID:582294

  8. Development of a finite element-based injury metric for pulmonary contusion part I: model development and validation.

    PubMed

    Stitzel, Joel D; Gayzik, F Scott; Hoth, J Jason; Mercier, Jennifer; Gage, H Donald; Morton, Kathryn A; Duma, Stefan M; Payne, R Mark

    2005-11-01

    Pulmonary contusion is the most commonly identified thoracic soft tissue injury in an automobile crash and after blunt chest trauma and affects 10-17% of all trauma admissions. The mortality associated with pulmonary contusions is significant and is estimated to be 10-25%. Thus, there is a need to develop a finite element model based injury metric for pulmonary contusion for the purpose of predicting outcome. This will enable current and future finite element models of the lung to incorporate an understanding of how stress and strain may be related to contusion injuries. This study utilizes 14 impacts onto male Sprague-Dawley rats. In 5 of these tests, a calibrated weight (46 g) is dropped from a height of 44 cm directly onto the lungs of intubated, anesthetized rats in situ. Contused volume is estimated from MicroPET scans of the lung and normalized on the basis of liver uptake of 18F-FDG. The lungs are scanned at 24 hours, 7 days, and 28 days (15 scans), and the contused volume is measured. In addition, 9 controlled mechanical tests on in situ rat lung are used for model development and validation. Identical impacts are performed on a finite element model of the rat lung. The finite element model is developed from CT scans of normal rat and scaled to represent average rat lung volume. First principal strain is chosen as a candidate injury metric for pulmonary contusion. The volume of contused tissue at the three time points measured using PET is compared to the strain level achieved by a corresponding volume in the finite element model. For PET scans (n=5 scans per time point), the average contusion volume was 4.2 cm3 at 24 hours, 2.8 cm3 at 7 days, and 0.39 cm3 at 28 days. These volumes were used to identify threshold peak first principal strain levels measured by the finite element model. Maximum first principal strain from the finite element model for the three volume levels (4.2, 2.8, and 0.39 cm3) was 3.5%, 8.8%, and 35% strain, respectively. Furthermore

  9. Development of a finite element-based injury metric for pulmonary contusion part I: model development and validation.

    PubMed

    Stitzel, Joel D; Gayzik, F Scott; Hoth, J Jason; Mercier, Jennifer; Gage, H Donald; Morton, Kathryn A; Duma, Stefan M; Payne, R Mark

    2005-11-01

    Pulmonary contusion is the most commonly identified thoracic soft tissue injury in an automobile crash and after blunt chest trauma and affects 10-17% of all trauma admissions. The mortality associated with pulmonary contusions is significant and is estimated to be 10-25%. Thus, there is a need to develop a finite element model based injury metric for pulmonary contusion for the purpose of predicting outcome. This will enable current and future finite element models of the lung to incorporate an understanding of how stress and strain may be related to contusion injuries. This study utilizes 14 impacts onto male Sprague-Dawley rats. In 5 of these tests, a calibrated weight (46 g) is dropped from a height of 44 cm directly onto the lungs of intubated, anesthetized rats in situ. Contused volume is estimated from MicroPET scans of the lung and normalized on the basis of liver uptake of 18F-FDG. The lungs are scanned at 24 hours, 7 days, and 28 days (15 scans), and the contused volume is measured. In addition, 9 controlled mechanical tests on in situ rat lung are used for model development and validation. Identical impacts are performed on a finite element model of the rat lung. The finite element model is developed from CT scans of normal rat and scaled to represent average rat lung volume. First principal strain is chosen as a candidate injury metric for pulmonary contusion. The volume of contused tissue at the three time points measured using PET is compared to the strain level achieved by a corresponding volume in the finite element model. For PET scans (n=5 scans per time point), the average contusion volume was 4.2 cm3 at 24 hours, 2.8 cm3 at 7 days, and 0.39 cm3 at 28 days. These volumes were used to identify threshold peak first principal strain levels measured by the finite element model. Maximum first principal strain from the finite element model for the three volume levels (4.2, 2.8, and 0.39 cm3) was 3.5%, 8.8%, and 35% strain, respectively. Furthermore

  10. Percutaneous Pulmonary Valve Placement

    PubMed Central

    Prieto, Lourdes R.

    2015-01-01

    Patients with congenital heart disease and pulmonary valve disease need multiple procedures over their lifetimes to replace their pulmonary valves. Chronic pulmonary stenosis, regurgitation, or both have untoward effects on ventricular function and on the clinical status of these patients. To date, all right ventricle–pulmonary artery conduits have had relatively short lifespans. Percutaneous pulmonary valve implantation, although relatively new, will probably reduce the number of operative procedures that these patients will have to undergo over a lifetime. Refinement and further development of this procedure holds promise for the extension of this technology to other patient populations. PMID:26175629

  11. Effect of Decompressive Craniectomy on Perihematomal Edema in Patients with Intracerebral Hemorrhage

    PubMed Central

    Klinger-Gratz, Pascal P.; Fiechter, Michael; Z’Graggen, Werner J.; Gautschi, Oliver P.; El-Koussy, Marwan; Gralla, Jan; Schaller, Karl; Zbinden, Martin; Arnold, Marcel; Fischer, Urs; Mattle, Heinrich P.; Raabe, Andreas; Beck, Jürgen

    2016-01-01

    Background Perihematomal edema contributes to secondary brain injury in the course of intracerebral hemorrhage. The effect of decompressive surgery on perihematomal edema after intracerebral hemorrhage is unknown. This study analyzed the course of PHE in patients who were or were not treated with decompressive craniectomy. Methods More than 100 computed tomography images from our published cohort of 25 patients were evaluated retrospectively at two university hospitals in Switzerland. Computed tomography scans covered the time from admission until day 100. Eleven patients were treated by decompressive craniectomy and 14 were treated conservatively. Absolute edema and hematoma volumes were assessed using 3-dimensional volumetric measurements. Relative edema volumes were calculated based on maximal hematoma volume. Results Absolute perihematomal edema increased from 42.9 ml to 125.6 ml (192.8%) after 21 days in the decompressive craniectomy group, versus 50.4 ml to 67.2 ml (33.3%) in the control group (Δ at day 21 = 58.4 ml, p = 0.031). Peak edema developed on days 25 and 35 in patients with decompressive craniectomy and controls respectively, and it took about 60 days for the edema to decline to baseline in both groups. Eight patients (73%) in the decompressive craniectomy group and 6 patients (43%) in the control group had a good outcome (modified Rankin Scale score 0 to 4) at 6 months (P = 0.23). Conclusions Decompressive craniectomy is associated with a significant increase in perihematomal edema compared to patients who have been treated conservatively. Perihematomal edema itself lasts about 60 days if it is not treated, but decompressive craniectomy ameliorates the mass effect exerted by the intracerebral hemorrhage plus the perihematomal edema, as reflected by the reduced midline shift. PMID:26872068

  12. Hantavirus pulmonary syndrome.

    PubMed

    Macneil, Adam; Nichol, Stuart T; Spiropoulou, Christina F

    2011-12-01

    Hantavirus pulmonary syndrome (HPS) is a severe disease characterized by a rapid onset of pulmonary edema followed by respiratory failure and cardiogenic shock. The HPS associated viruses are members of the genus Hantavirus, family Bunyaviridae. Hantaviruses have a worldwide distribution and are broadly split into the New World hantaviruses, which includes those causing HPS, and the Old World hantaviruses [including the prototype Hantaan virus (HTNV)], which are associated with a different disease, hemorrhagic fever with renal syndrome (HFRS). Sin Nombre virus (SNV) and Andes virus (ANDV) are the most common causes of HPS in North and South America, respectively. Case fatality of HPS is approximately 40%. Pathogenic New World hantaviruses infect the lung microvascular endothelium without causing any virus induced cytopathic effect. However, virus infection results in microvascular leakage, which is the hallmark of HPS. This article briefly reviews the knowledge on HPS-associated hantaviruses accumulated since their discovery, less than 20 years ago.

  13. Water permeability and TCDD-induced edema in zebrafish early-life stages.

    PubMed

    Hill, Adrian J; Bello, Susan M; Prasch, Amy L; Peterson, Richard E; Heideman, Warren

    2004-03-01

    A common response to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure in teleost embryos is blue-sac disease, characterized by pericardial and yolk-sac edema. The cellular and extracellular fluids of freshwater fish are hyperosmotic compared to the surrounding water. In order to be in osmotic balance, freshwater fish must maintain a barrier to minimize water entry and excrete excess water that passes the barrier. We hypothesized that edema observed in TCDD-exposed zebrafish was caused by a failure of a barrier to incoming water. As a test of this hypothesis, we removed the osmotic gradient that drives water entry by increasing the osmolarity of the surrounding water with mannitol. Abolishing the osmotic gradient between the interior body fluids and the water environment of the developing zebrafish significantly reduced both pericardial and yolk-sac edema. When added after edema formation had already started, mannitol only partially reversed pre-existing edema. An alternate hypothesis is that TCDD impairs water excretion, allowing water to accumulate as edema fluid. However, we were unable to demonstrate an alteration in kidney function: expression of early markers for kidney development appeared normal, and we did not observe TCDD-induced changes in kidney filtration. An alteration in the overall shape of the kidney was observed, but this may be a consequence of compression by edema. In conclusion, TCDD exposure may inhibit the function of a permeability barrier to water, which is critical for maintaining osmotic balance in early development.

  14. A microsimulation model for the development and progression of chronic obstructive pulmonary disease.

    PubMed

    Tan, Emma; Boessen, Ruud; Fishwick, David; Klein Entink, Rinke; Meijster, Tim; Pronk, Anjoeka; van Duuren-Stuurman, Birgit; Warren, Nick

    2015-12-01

    Chronic obstructive pulmonary disease (COPD) is a chronic lung disease that is thought to affect over one million people in Great Britain. The main factor contributing to the development of COPD is tobacco smoke. This paper presents a microsimulation model for the development of COPD, incorporating population dynamics and trends in smoking. The model simulates a population longitudinally throughout their lifetimes, providing projections of future COPD prevalence and evaluation of the effects of changes in risk factor prevalence such as smoking. Sensitivity analysis provides information on the most influential model parameters. The model-predicted prevalence of COPD in 2040 was 17% in males over the age of 35 years (13% amongst non-smokers and 22% amongst smokers), and a modest decline over the next 25 years due to recent trends in smoking rates. The simulation model provides us with valuable information on current and future trends in COPD in Great Britain. It was developed primarily to enable easy extension to evaluate the effects of occupational and environmental exposures on lung function and the prevalence of COPD and to allow evaluation of interventions, such as introducing health surveillance or policy changes. As longitudinal studies for investigating COPD are difficult due to the lengthy follow-up time required and the potentially large number of drop-outs, we anticipate that the model will provide a valuable tool for health impact assessment. An extended model for occupational exposures is under development and will be presented in a subsequent paper.

  15. Developing a service for patients with very severe chronic obstructive pulmonary disease (COPD) within resources.

    PubMed

    Boland, Jason; Owen, Janet; Ainscough, Rachel; Mahdi, Hazim

    2013-03-01

    Chronic obstructive pulmonary disease (COPD) is a common life-limiting illness with significant burden for patient and carer. Despite this, access to supportive and specialist palliative care is inconsistent and implementation of published good practice recommendations may be challenging within current resources. The aim of this service development was to improve local service provision in Barnsley, within the currently available resources, for patients with very severe COPD, to improve patient identification and symptom management, increase advance care planning and the numbers of patients dying in their preferred place, and increase patient and carer support and satisfaction. To do this a working group was formed, the service problems identified and baseline data collected to identify the needs of people with very severe COPD. A multidisciplinary team meeting was piloted and assessed by community matron feedback, patient case studies and an after death analysis. These indicated a high level of satisfaction, with improvements in advance care planning, co-ordination of management and support for patients' preferred place of care at the end of life. In conclusion this is the first reported very severe COPD service development established in this way and within current resources. Preliminary data indicates the development of the multidisciplinary team meeting has been positive. The appointment of a coordinator will aid this development. Further evaluations particularly seeking patient views and estimations of cost savings will be performed. PMID:24644174

  16. Radioimmunotherapy Using Vascular Targeted 213Bi: The Role of TNF-Alpha in the Development of Pulmonary Fibrosis

    SciTech Connect

    Davis, I.A.; Kennel, S.J.

    1998-10-14

    A monoclonal antibody (201B) specific to murine thrombomodulin, covalently linked to CHX-b-DTPA, successfully delivers chelated 213Bi, an {alpha}-particle emitter, (213Bi-201B) rapidly to lungvascular endothelium. When injected at doses of l MBq/mouse, 213Bi-201B destroyed most of the 100 colonies of EMT-6 mammary carcinomas growing as lung tumors of up to 2000 cells/colony. Some mice were cured of lung tumors and others had extended life-spans compared to untreated control animals but eventually succumbed to tumor recurrence. At injected doses of 4-6 MBq/mouse, 100% of lung tumor colonies were eliminated; however, 3-4 months later these mice developed pulmonary fibrosis and died. The mechanisms leading to the fibrotic response in other pulmonary irradiation models strongly implicate tumor necrosis factor-alpha (TNF-{alpha}), released from damaged tissues, as the pivotal inflammatory cytokine in a cascade of events which culminate in fibrosis. Attempts to prevent the development of pulmonary fibrosis, by using antibodies or soluble receptor (Enbrel{trademark}) as inhibitors of TNF-{alpha}, were unsuccessful. Additionally, mice genetically deficient for TNF-{alpha} production developed pulmonary fibrosis following 213Bi-201B treatment. Interestingly, non-tumor bearing BALB/c mice receiving Enbrel{trademark} or mice genetically deficient in TNF-{alpha} production and treated with 213Bi-201B, had significantly reduced life spans compared to mice receiving no treatment or 213Bi-201B alone. We speculate that, in normal mice, while TNF-{alpha} may induce an inflammatory response following {alpha}-particle radiation mediated tumor clearance and pulmonary damage, its effects in the post-tumor clearance time period may actually retard the development of fibrosis.

  17. Diabetic Macular Edema Pathophysiology: Vasogenic versus Inflammatory

    PubMed Central

    Baget-Bernaldiz, Marc; Pareja-Rios, Alicia; Lopez-Galvez, Maribel; Navarro-Gil, Raul; Verges, Raquel

    2016-01-01

    Diabetic macular edema (DME) can cause blindness in diabetic patients suffering from diabetic retinopathy (DR). DM parameters controls (glycemia, arterial tension, and lipids) are the gold standard for preventing DR and DME. Although the vascular endothelial growth factor (VEGF) is known to play a role in the development of DME, the pathological processes leading to the onset of this disease are highly complex and the exact sequence in which they occur is still not completely understood. Angiogenesis and inflammation have been shown to be involved in the pathogenesis of this disease. However, it still remains to be clarified whether angiogenesis following VEGF overexpression is a cause or a consequence of inflammation. This paper provides a review of the data currently available, focusing on VEGF, angiogenesis, and inflammation. Our analysis suggests that angiogenesis and inflammation act interdependently during the development of DME. Knowledge of DME etiology seems to be important in treatments with anti-VEGF or anti-inflammatory drugs. Current diagnostic techniques do not permit us to differentiate between both etiologies. In the future, diagnosing the physiopathology of each patient with DME will help us to select the most effective drug. PMID:27761468

  18. Pulmonary Rehabilitation

    MedlinePlus

    ... Topics Bronchitis COPD Cystic Fibrosis Idiopathic Pulmonary Fibrosis Sarcoidosis Send a link to NHLBI to someone by ... people who have COPD (chronic obstructive pulmonary disease), sarcoidosis (sar-koy-DOE-sis), idiopathic pulmonary fibrosis , or ...

  19. Development and application of pulmonary structure-function registration methods: towards pulmonary image-guidance tools for improved airway targeted therapies and outcomes

    NASA Astrophysics Data System (ADS)

    Guo, Fumin; Pike, Damien; Svenningsen, Sarah; Coxson, Harvey O.; Drozd, John J.; Yuan, Jing; Fenster, Aaron; Parraga, Grace

    2014-03-01

    Objectives: We aimed to develop a way to rapidly generate multi-modality (MRI-CT) pulmonary imaging structurefunction maps using novel non-rigid image registration methods. This objective is part of our overarching goal to provide an image processing pipeline to generate pulmonary structure-function maps and guide airway-targeted therapies. Methods: Anatomical 1H and functional 3He MRI were acquired in 5 healthy asymptomatic ex-smokers and 7 ex-smokers with chronic obstructive pulmonary disease (COPD) at inspiration breath-hold. Thoracic CT was performed within ten minutes of MRI using the same breath-hold volume. Landmark-based affine registration methods previously validated for imaging of COPD, was based on corresponding fiducial markers located in both CT and 1H MRI coronal slices and compared with shape-based CT-MRI non-rigid registration. Shape-based CT-MRI registration was developed by first identifying the shapes of the lung cavities manually, and then registering the two shapes using affine and thin-plate spline algorithms. We compared registration accuracy using the fiducial localization error (FLE) and target registration error (TRE). Results: For landmark-based registration, the TRE was 8.4±5.3 mm for whole lung and 7.8±4.6 mm for the R and L lungs registered independently (p=0.4). For shape-based registration, the TRE was 8.0±4.6 mm for whole lung as compared to 6.9±4.4 mm for the R and L lung registered independently and this difference was significant (p=0.01). The difference for shape-based (6.9±4.4 mm) and landmark-based R and L lung registration (7.8±4.6 mm) was also significant (p=.04) Conclusion: Shape-based registration TRE was significantly improved compared to landmark-based registration when considering L and R lungs independently.

  20. Prostatic edema in {sup 125}I permanent prostate implants: Dynamical dosimetry taking volume changes into account

    SciTech Connect

    Leclerc, Ghyslain; Lavallee, Marie-Claude; Roy, Rene; Vigneault, Eric; Beaulieu, Luc

    2006-03-15

    The purpose of this study is to determine the impact of edema on the dose delivered to the target volume. An evaluation of the edema characteristics was first made, and then a dynamical dosimetry algorithm was developed and used to compare its results to a standard clinical (static) dosimetry. Source positions and prostate contours extracted from 66 clinical cases on images taken at different points in time (planning, implant day, post-implant evaluation) were used, via the mean interseed distance, to characterize edema [initial increase ({delta}r{sub 0}), half-life ({tau})]. An algorithm was developed to take into account the edema by summing a time series of dose-volume histograms (DVHs) with a weight based on the fraction of the dose delivered during the time interval considered. The algorithm was then used to evaluate the impact of edema on the dosimetry of permanent implants by comparing its results to those of a standard clinical dosimetry. The volumetric study yielded results as follows: the initial prostate volume increase was found to be 1.58 (ranging from 1.15 to 2.48) and the edema half-life, approximately 30 days (range: 3 to 170 days). The dosimetric differences in D{sub 90} observed between the dynamic dosimetry and the clinical one for a single case were up to 15 Gy and depended on the edema half-life and the initial volume increase. The average edema half-life, 30 days, is about 3 times longer than the previously reported 9 days. Dosimetric differences up to 10% of the prescription dose are observed, which can lead to differences in the quality assertion of an implant. The study of individual patient edema resorption with time might be necessary to extract meaningful clinical correlation or biological parameters in permanent implants.

  1. Aplastic anemia induced disc edema and visual loss in pregnancy: a case report

    PubMed Central

    Gupta, Shailesh K; Brar, Vikram S; Keshavamurthy, Ravi; Chalam, Kakarla V

    2008-01-01

    Introduction A case of aplastic anemia diagnosed during pregnancy, which developed bilateral disc edema and acute pre-retinal hemorrhage leading to vision loss. Case Presentation A 20 year old primagravid female developed acute vision loss in her right eye, during hospitalization for treatment of aplastic anemia diagnosed during her pregnancy. Her best-corrected visual acuity (BCVA) was hand motions and fundus evaluation revealed a large pre-macular hemorrhage in the right eye (OD) and bilateral disc edema. Neuro-imaging studies did not reveal any signs of intracranial mass lesion or edema. Conclusion There was resolution of the disc edema with improvement in the pre-macular hemorrhage resulting in 20/50 vision in the right eye, following supportive transfusions. Ophthalmic manifestations developing in a pregnant patient with aplastic anemia can be successfully managed with supportive care including red blood cell and platelet transfusions. PMID:19017378

  2. Development and maintenance of a biospecimen repository for clinical samples derived from pulmonary patients.

    PubMed

    Schwiebert, Lisa M; Estell, Kim; Meadows, Tonja; Thannickal, Victor J; Rowe, Steven; Sorscher, Eric J; Harris, W Thomas; Gaggar, Amit; Dransfield, Mark; de Andrade, Joao A

    2014-08-01

    The Pulmonary Biospecimen Repository (PBR) at the University of Alabama at Birmingham (UAB) was launched in 2009. The purpose of the UAB PBR is to provide investigators within the pulmonary community at UAB and elsewhere with clinical samples derived from multiple lung diseases, including transplant recipients, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, cystic fibrosis, and asthma. Cell and fluid samples isolated from bronchoalveolar lavage (BAL), plasma, and serum are collected and stored; samples are assessed routinely for viability. Each sample is linked directly with the respective patient information via the Pulmonary Translational Research and Clinical Database, a Health Insurance Portability and Accountability Act compliant database that includes detailed information allowing for the study of specific patient cohorts. To access samples, investigators must complete a request form, which is reviewed by the UAB PBR Steering Committee. To date, more than 800 patients have provided approximately 7,000 BAL, serum and plasma fluid, and cell samples. Over the past 4 years, nearly 800 of these samples have been distributed to investigators at UAB and elsewhere. Future plans for the UAB PBR include expanding sample collection to additional pulmonary diseases, such as mycobacterial infections, increasing the number of sample users and obtaining external funding to ensure its continued sustainability.

  3. Development and maintenance of a biospecimen repository for clinical samples derived from pulmonary patients.

    PubMed

    Schwiebert, Lisa M; Estell, Kim; Meadows, Tonja; Thannickal, Victor J; Rowe, Steven; Sorscher, Eric J; Harris, W Thomas; Gaggar, Amit; Dransfield, Mark; de Andrade, Joao A

    2014-08-01

    The Pulmonary Biospecimen Repository (PBR) at the University of Alabama at Birmingham (UAB) was launched in 2009. The purpose of the UAB PBR is to provide investigators within the pulmonary community at UAB and elsewhere with clinical samples derived from multiple lung diseases, including transplant recipients, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, cystic fibrosis, and asthma. Cell and fluid samples isolated from bronchoalveolar lavage (BAL), plasma, and serum are collected and stored; samples are assessed routinely for viability. Each sample is linked directly with the respective patient information via the Pulmonary Translational Research and Clinical Database, a Health Insurance Portability and Accountability Act compliant database that includes detailed information allowing for the study of specific patient cohorts. To access samples, investigators must complete a request form, which is reviewed by the UAB PBR Steering Committee. To date, more than 800 patients have provided approximately 7,000 BAL, serum and plasma fluid, and cell samples. Over the past 4 years, nearly 800 of these samples have been distributed to investigators at UAB and elsewhere. Future plans for the UAB PBR include expanding sample collection to additional pulmonary diseases, such as mycobacterial infections, increasing the number of sample users and obtaining external funding to ensure its continued sustainability. PMID:24889057

  4. Mechanisms of Astrocyte-Mediated Cerebral Edema

    PubMed Central

    Stokum, Jesse A.; Kurland, David B.; Gerzanich, Volodymyr; Simard, J. Marc

    2014-01-01

    Cerebral edema formation stems from disruption of blood brain barrier (BBB) integrity and occurs after injury to the CNS. Due to the restrictive skull, relatively small increases in brain volume can translate into impaired tissue perfusion and brain herniation. In excess, cerebral edema can be gravely harmful. Astrocytes are key participants in cerebral edema by virtue of their relationship with the cerebral vasculature, their unique compliment of solute and water transport proteins, and their general role in brain volume homeostasis. Following the discovery of aquaporins, passive conduits of water flow, aquaporin 4 (AQP4) was identified as the predominant astrocyte water channel. Normally, AQP4 is highly enriched at perivascular endfeet, the outermost layer of the BBB, whereas after injury, AQP4 expression disseminates to the entire astrocytic plasmalemma, a phenomenon termed dysregulation. Arguably, the most important role of AQP4 is to rapidly neutralize osmotic gradients generated by ionic transporters. In pathological conditions, AQP4 is believed to be intimately involved in the formation and clearance of cerebral edema. In this review, we discuss aquaporin function and localization in the BBB during health and injury, and we examine post-injury ionic events that modulate AQP4- dependent edema formation. PMID:24996934

  5. Hantavirus fever without pulmonary syndrome in Panama.

    PubMed

    Armien, Blas; Pascale, Juan M; Muñoz, Carlos; Mariñas, Jamileth; Núñez, Heydy; Herrera, Milagro; Trujillo, José; Sánchez, Deyanira; Mendoza, Yaxelis; Hjelle, Brian; Koster, Frederick

    2013-09-01

    In Panama, hantavirus pulmonary syndrome (HPS) is caused by Choclo virus, a species phylogenetically related to Andes and Maporal viruses. Up to 60% of the population has been positive for specific serum antibody in community-based surveys, but mortality is very uncommon. In four western Panama clinics, we tested individuals presenting with a severe febrile prodrome for acute hantavirus (HV) infection by immunoglobulin M enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction as well as clinically similar infections, such as dengue and leptospirosis. From 2006 to 2009, at least 21% of 117 patients diagnosed with HV infection had HV Fever (HF) with no evidence of pulmonary edema (no respiratory distress or radiographic lung infiltrates), and 44% of patients had very mild HPS (radiographic pulmonary edema but no respiratory insufficiency). HV infection caused by Choclo virus in Panama presents often as HF, which contrasts with HV in the Americas but is consistent with the high seroprevalence in endemic regions.

  6. Enterovirus 71 Infection Causes Severe Pulmonary Lesions in Gerbils, Meriones unguiculatus, Which Can Be Prevented by Passive Immunization with Specific Antisera

    PubMed Central

    Xia, Yong; Qian, Lei; Yang, Zhang-Nv; Xie, Rong-Hui; Sun, Yi-Sheng; Lu, Hang-Jing; Miao, Zi-Ping; Li, Chan; Li, Xiao; Liang, Wei-Feng; Huang, Xiao-Xiao; Xia, Shi-Chang; Chen, Zhi-Ping; Jiang, Jian-Min; Zhang, Yan-Jun; Mei, Ling-Ling; Liu, She-Lan; Gu, Hua; Xu, Zhi-Yao; Fu, Xiao-Fei; Zhu, Zhi-Yong; Zhu, Han-Ping

    2015-01-01

    Neurogenic pulmonary edema caused by severe brainstem encephalitis is the leading cause of death in young children infected by Enterovirus 71 (EV71). However, no pulmonary lesions have been found in EV71-infected transgenic or non-transgenic mouse models. Development of a suitable animal model is important for studying EV71 pathogenesis and assessing effect of therapeutic approaches. We had found neurological disorders in EV71-induced young gerbils previously. Here, we report severe pulmonary lesions characterized with pulmonary congestion and hemorrhage in a gerbil model for EV71 infection. In the EV71-infected gerbils, six 21-day-old or younger gerbils presented with a sudden onset of symptoms and rapid illness progression after inoculation with 1×105.5 TCID50 of EV71 via intraperitoneal (IP) or intramuscular (IM) route. Respiratory symptoms were observed along with interstitial pneumonia, pulmonary congestion and extensive lung hemorrhage could be detected in the lung tissues by histopathological examination. EV71 viral titer was found to be peak at late stages of infection. EV71-induced pulmonary lesions, together with severe neurological disorders were also observed in gerbils, accurately mimicking the disease process in EV71-infected patients. Passive transfer with immune sera from EV71 infected adult gerbils with a neutralizing antibody (GMT=89) prevented severe pulmonary lesion formation after lethal EV71 challenge. These results establish this gerbil model as a useful platform for studying the pathogenesis of EV71-induced pulmonary lesions, immunotherapy and antiviral drugs. PMID:25767882

  7. Aberrant pulmonary lymphatic development in the nitrofen mouse model of congenital diaphragmatic hernia

    PubMed Central

    Shue, Eveline; Wu, Jianfeng; Schecter, Samuel; Miniati, Doug

    2013-01-01

    Purpose Many infants develop a postsurgical chylothorax after diaphragmatic hernia repair. The pathogenesis remains elusive but may be due to dysfunctional lymphatic development. This study characterizes pulmonary lymphatic development in the nitrofen mouse model of CDH. Methods CD1 pregnant mice were fed nitrofen/bisdiamine (N/B) or olive oil at E8.5. At E14.5 and E15.5, lung buds were categorized by phenotype: normal, N/B without CDH (N/B−CDH), or N/B with CDH (N/B+CDH). Anti-CD31 was used to localize all endothelial cells, while anti-LYVE-1 was used to identify lymphatic endothelial cells in lung buds using immunofluorescence. Differential protein expression of lymphatic-specific markers was analyzed. Results Lymphatic endothelial cells localized to the mesenchyme surrounding the airway epithelium at E15.5. CD31 and LYVE-1 colocalization identified lymphatic endothelial cells. LYVE-1 expression was upregulated in N/B+CDH lung buds in comparison to N/B−CDH and normal lung buds by immunofluorescence. Western blotting shows that VEGF-D, LYVE-1, Prox-1, and VEGFR-3 expression was upregulated in N/B+CDH lung buds in comparison to N/B−CDH or control lung buds at E14.5. Conclusions Lung lymphatics are hyperplastic in N/B+CDH. Upregulation of lymphatic-specific genes suggest that lymphatic hyperplasia plays an important role in dysfunctional lung lymphatic development in the nitrofen mouse model of CDH. PMID:23845607

  8. Hantavirus Pulmonary Syndrome

    PubMed Central

    Zaki, Sherif R.; Greer, Patricia w.; Coffield, Lisa M.; Goldsmith, Cynthia S.; Nolte, Kurt B.; Foucar, Kathy; Feddersen, Richard M.; Zumwalt, Ross E.; Miller, Gayle L.; Khan, Ali S.; Rollin, Pierre E.; Ksiazek, Thomas G.; Nichol, Stuart T.; Mahy, Brian W.J.; Peters, Clarence J.

    1995-01-01

    A recent outbreak of a severe pulmonary disease in the southwestern United States was etiologically linked to a previously unrecognized bantavirus. The virus has been isolated from its majorreservoir, the deer mouse, Peromyscus maniculatus,and recently named Sin Nombre virus. Clinically, the disease has become known as the bantavirus pulmonary syndrome (HPS). Since May 1993, 44 fatal cases of HPS have been identified through clinicopathological review and immunobistochemical(IHC) testing of tissues from 273 patients who died of an unexplained noncardiogenic pulmonary edema. In 158 cases for which suitable specimens were available, serologicaltesting and/or reverse transcription-polymerase chain reaction (RT-PCR) amplification of extracted RNA was also performed. IHC, serological, and PCR results were concordant for virtually all HPS and non-HPS patients when more than one assay was performed. The prodromal ilness of HPS is similar to that of many other viral diseases. Consistent bematological features include thrombocytopenia, bemoconcentration, neutropbilic leukocytosis with a left shift, and reactivel lymphocytes. Pulmonary bistopatbological features were similar in most of the fatal HPS cases (40/44) and consisted of an interstitial pneumonitis with a variable mononuclear cell infiltrate, edema, and focal byaline membranes. In four cases, bowever, pulmonary features were significantly different and included diffuse alveolar damage and variable degrees of severe air space disorganization. IHC analysis showed widespread presence of bantaviral antigens in endothelial cells of the microvasculature, particularly in the lung. Hantaviral antigens were also observed within follicular dendritic cells, macrophages, and lymphocytes. Hantaviral inclusions were observed in endothelial cells of lungs by thinsection electron microscopy, and their identity was verified by immunogold labeling. Virus-like particles were seen in pulmonary endothelial cells and macropbages. HPS is

  9. Impact of pre-transplant pulmonary infection developed in horizontal laminar flow unit on the outcome of subsequent allogeneic hematopoietic stem cell transplantation

    PubMed Central

    He, Gan-Lin; Chang, Ying-Jun; Xu, Lan-Ping; Zhang, Xiao-Hui; Wang, Yu; Liu, Kai-Yan

    2016-01-01

    Background So far, there is very little literature on how pre-transplant pulmonary infection developed in horizontal laminar flow unit (HLFU) affects outcomes of allogeneic hematopoietic stem cell transplantation (allo-HSCT). Methods A retrospective analysis was performed on allo-HSCT recipients who were diagnosed with pre-transplant pulmonary infection developed in HLFU between January 2012 and December 2012. Various tests were analyzed to evaluate the overall survival (OS) and pulmonary infection rate after allo-HSCT. Results Among 317 patients who received allo-HSCT from related donors, 7 cases of human leukocyte antigen (HLA)-haploidentical transplantation reported a fever, cough, and other symptoms before transplantation. Chest radiography findings showed pulmonary infection, and the C-reactive protein (CRP) level was higher than normal, which confirmed pulmonary infection (incidence rate 2.21%). The Breslow test suggested that the early survival rate was lower in the group with pre-transplant pulmonary infection than in the group without pre-transplant pulmonary infection (OS: 28.4 vs. 42.4 months; P=0.023); the early survival rate was lower in patients with a pulmonary infection accompanied by bilateral pleural effusion than in patients without pleural effusion (OS: 1.5 vs. 36.3 months; P=0.010). In the first month after transplantation, the difference in the CD4CD45RO+CD45RA- and CD4CD45RO-CD45RA+ between the groups with and without pre-transplant pulmonary infection was statistically significant (P<0.05). Patients with pre-transplant pulmonary infection who survived >3 years had a higher rate of pulmonary infection in the first 2 months after allo-HSCT than those without pre-transplant pulmonary infection [100% (5/5 patients) vs. 38.1% (118/310); χ2=5.542, P=0.019]. Conclusions Development of pre-transplant pulmonary infection in the HLFU in patients with hematological malignancies who receive HLA-haploidentical HSCT is associated with an increased risk

  10. Impact of pre-transplant pulmonary infection developed in horizontal laminar flow unit on the outcome of subsequent allogeneic hematopoietic stem cell transplantation

    PubMed Central

    He, Gan-Lin; Chang, Ying-Jun; Xu, Lan-Ping; Zhang, Xiao-Hui; Wang, Yu; Liu, Kai-Yan

    2016-01-01

    Background So far, there is very little literature on how pre-transplant pulmonary infection developed in horizontal laminar flow unit (HLFU) affects outcomes of allogeneic hematopoietic stem cell transplantation (allo-HSCT). Methods A retrospective analysis was performed on allo-HSCT recipients who were diagnosed with pre-transplant pulmonary infection developed in HLFU between January 2012 and December 2012. Various tests were analyzed to evaluate the overall survival (OS) and pulmonary infection rate after allo-HSCT. Results Among 317 patients who received allo-HSCT from related donors, 7 cases of human leukocyte antigen (HLA)-haploidentical transplantation reported a fever, cough, and other symptoms before transplantation. Chest radiography findings showed pulmonary infection, and the C-reactive protein (CRP) level was higher than normal, which confirmed pulmonary infection (incidence rate 2.21%). The Breslow test suggested that the early survival rate was lower in the group with pre-transplant pulmonary infection than in the group without pre-transplant pulmonary infection (OS: 28.4 vs. 42.4 months; P=0.023); the early survival rate was lower in patients with a pulmonary infection accompanied by bilateral pleural effusion than in patients without pleural effusion (OS: 1.5 vs. 36.3 months; P=0.010). In the first month after transplantation, the difference in the CD4CD45RO+CD45RA- and CD4CD45RO-CD45RA+ between the groups with and without pre-transplant pulmonary infection was statistically significant (P<0.05). Patients with pre-transplant pulmonary infection who survived >3 years had a higher rate of pulmonary infection in the first 2 months after allo-HSCT than those without pre-transplant pulmonary infection [100% (5/5 patients) vs. 38.1% (118/310); χ2=5.542, P=0.019]. Conclusions Development of pre-transplant pulmonary infection in the HLFU in patients with hematological malignancies who receive HLA-haploidentical HSCT is associated with an increased risk

  11. Movement, Function, Pain, and Postoperative Edema in Axillary Web Syndrome

    PubMed Central

    Blaes, Anne H.; Haddad, Tuffia C.; Hunter, David W.; Hirsch, Alan T.; Ludewig, Paula M.

    2015-01-01

    Background Axillary web syndrome (AWS) is a condition that may develop following breast cancer surgery and that presents as a palpable axillary cord of tissue. Objective The purposes of this study were: (1) to determine the clinical characteristics of AWS related to movement, function, pain, and postoperative edema and (2) to define the incidence of and risk factors for AWS within the first 3 months following breast cancer surgery. Design This was a prospective cohort study with a repeated-measures design. Methods Women who underwent breast cancer surgery with sentinel node biopsy or axillary lymph node dissection (N=36) were assessed for AWS, shoulder range of motion, function, pain, and postoperative edema (using girth measurements, bioimpedance, and tissue dielectric constant) at 2, 4, and 12 weeks. Demographic characteristics were used for risk analysis. Results Seventeen women (47.2%) developed AWS, and AWS persisted in 10 participants (27.8%) at 12 weeks. Abduction range of motion was significantly lower in the AWS group compared with the non-AWS group at 2 and 4 weeks. There were no differences between groups in measurements of function, pain, or edema at any time point. Trunk edema measured by dielectric constant was present in both groups, with an incidence of 55%. Multivariate analysis determined lower body mass index as being significantly associated with AWS (odds ratio=0.86; 95% confidence interval=0.74, 1.00). Limitations Limitations included a short follow-up time and a small sample size. Conclusion Axillary web syndrome is prevalent following breast/axilla surgery for early-stage breast cancer and may persist beyond 12 weeks. The early consequences include movement restriction, but the long-term effects of persistent AWS cords are yet unknown. Low body mass index is considered a risk factor for AWS. PMID:25977305

  12. Drug-induced pulmonary disease

    MedlinePlus

    ... improve. Some drug-induced lung diseases, such as pulmonary fibrosis, may never go away. ... Complications that may develop include: Diffuse interstitial pulmonary fibrosis Hypoxemia (low blood oxygen) Respiratory failure

  13. International brain edema symposia 1967-2011.

    PubMed

    Kuroiwa, Toshihiko

    2013-01-01

    This is a brief review of previous international brain edema symposia. The symposia that took place from 1965 to 1999 were summarized by Igor Klatzo and A. Marmarou in the proceedings Brain Edema XI [1]. In this article the author summarized the symposia, including latest five. Images from previous symposia such as the cover pages of the proceedings and snapshots of organizers were included. The outline and key words of the symposia were summarized in tables. The name of the prize winner and the title of the memorial lectures in recent symposia were also summarized in a table. PMID:23564096

  14. Oxidative and nitrosative signalling in pulmonary arterial hypertension - Implications for development of novel therapies.

    PubMed

    Hansen, Thomas; Galougahi, Keyvan-Karimi; Celermajer, David; Rasko, Nathalie; Tang, Owen; Bubb, Kristen J; Figtree, Gemma

    2016-09-01

    Pulmonary arterial hypertension (PAH) is a syndrome characterised by an increase in pulmonary vascular resistance. This results in elevated resting pulmonary artery pressure and leads to progressive right ventricular (RV) failure, secondary to increased afterload. Although initially thought to be a disease driven primarily by endothelial dysfunction with a resultant vasoconstrictor versus vasodilator imbalance, it has become increasingly apparent that the rise in pulmonary vascular resistance that causes RV failure is also attributable to pulmonary vascular remodelling. This inflammatory, hyper-proliferative and anti-apoptotic phenotype is accompanied by a metabolic switch from physiological mitochondrial oxidative phosphorylation to aerobic glycolysis. The molecular pathways triggering this cellular metabolic shift have been the subject of extensive investigation, as their discovery will inevitably lead to new therapeutic targets. Reactive oxygen/nitrogen species (ROS/RNS) including hydrogen peroxide, superoxide and peroxynitrite are second messenger molecules that are involved in functional oxidative and nitrosative modification of proteins. Dysregulation of oxidative signalling caused by an excess of ROS and RNS relative to antioxidants has been heavily implicated in the underlying pathophysiology of PAH and likely participates in this metabolic reprogramming. This review will focus on the role of oxidative signalling and redox reactions to the molecular pathology of PAH. In addition, promising novel therapeutic agents targeting these pathways will be discussed.

  15. Significance of bone marrow edema in pathogenesis of rheumatoid arthritis

    PubMed Central

    Sudoł-Szopińska, Iwona; Kontny, Ewa; Maśliński, Włodzimierz; Prochorec-Sobieszek, Monika; Warczyńska, Agnieszka; Kwiatkowska, Brygida

    2013-01-01

    Summary Assessing the pathology of the synovium, its thickening and increased vascularity through ultrasound and magnetic resonance examinations (more often an ultrasound study alone) is still considered a sensitive parameter in the diagnosis of rheumatoid arthritis and in monitoring of treatment efficacy. Magnetic resonance studies showed that, aside from the joint pannus, the subchondral bone tissue constitutes an essential element in the development of rheumatoid arthritis. Bone marrow edema correlates with inflammation severity, joint destruction, clinical signs and symptoms of rheumatoid arthritis, and thus is considered a predictor of rapid radiological progression of the disease. The newest studies reveal that bone marrow edema may be a more sensitive indicator of the response to therapy than appearance of the synovium. Bone marrow edema presents with increased signal in T2-weighted images, being most visible in fat saturation or IR sequences (STIR, TIRM). On the other hand, it is hypointense and less evident in T1-weighted images. It becomes enhanced (hyperintense) after contrast administration. Histopathological studies confirmed that it is a result of bone inflammation (osteitis/osteomyelitis), i.e. replacememt of bone marrow fat by inflammatory infiltrates containing macrophages, T lymphocytes, B lymphocytes, plasma cells and osteoclasts. Bone marrow edema appears after a few weeks from occurrence of symptoms and therefore is considered an early marker of inflammation. It correlates with clinical assessment of disease activity and elevated markers of acute inflammatory phase, i.e. ESR and CRP. It is a reversible phenomenon and may become attenuated due to biological treatment. It is considered a “herald” of erosions, as the risk of their formation is 6-fold higher in sites where BME was previously noted PMID:23493495

  16. An Independent Risk of Gout on the Development of Deep Vein Thrombosis and Pulmonary Embolism

    PubMed Central

    Huang, Chien-Chung; Huang, Po-Hao; Chen, Jiunn-Horng; Lan, Joung-Liang; Tsay, Gregory J.; Lin, Hsiao-Yi; Tseng, Chun-Hung; Lin, Cheng-Li; Hsu, Chung-Yi

    2015-01-01

    Abstract Previous studies indicated that gout is a risk factor of cardiovascular diseases. This study aimed to determine if patients with gout have an increased risk of deep vein thrombosis (DVT) or pulmonary embolism (PE). We used the Longitudinal Health Insurance Database, a subset of the national insurance claim dataset, which enrolled 1 million Taiwanese to identify 57,981 patients with gout and 115,961 reference subjects matched by sex, age, and entry date of diagnosis. The risk of DVT and PE was analyzed using the Cox proportional hazards model. In this Taiwanese dataset observed from 2000 to 2010, we found the incidence of DVT was 5.26 per 104 person-years in the gout cohort, which was twofold higher than the incidence of 2.63 per 104 person-years in the reference cohort. After adjusting for age, sex, and 9 comorbidities, the hazard ratio (HR) of developing DVT was 1.66 (95% confidence interval [CI] = 1.37–2.01). Among patients with gout, the youngest age group had the highest increase in the risk of developing DVT (HR [95% CI] = 2.04 [1.24–3.37] for ages 20 to 49 years, 1.80 [1.28–2.51] for ages 50 to 64 years, and 1.45 [1.11–1.91] for ages ≥65 years). The incidence of PE was about one-fifth that of DVT in gout patients, but the effect of gout on the risk was similar (HR [95% CI] = 1.53 [1.01–2.29]). Our analysis confirmed that gout increased the risk of DVT and PE. Further exploration is needed in the future. PMID:26705202

  17. Meandering right pulmonary vein associated with severe and progressive "idiopathic-like" pulmonary hypertensive vascular disease.

    PubMed

    Cuenca, Sofia; Bret, Montserrat; del Cerro, Maria Jesus

    2016-03-01

    Congenital anomalies of the pulmonary veins are rare. Meandering right pulmonary vein, considered a part of the Scimitar syndrome spectrum, is often an incidental finding during chest imaging. We present the case of a 4-year-old girl diagnosed with meandering pulmonary vein, who developed pulmonary hypertensive disease with an aggressive course, in spite of absence of hypoxia or elevated pulmonary wedge pressure.

  18. Brain Edema after Repeat Gamma Knife Radiosurgery for a Large Arteriovenous Malformation: A Case Report

    PubMed Central

    Kim, Joo Whan; Chung, Hyun-Tai; Han, Moon Hee; Kim, Dong Gyu

    2016-01-01

    Brain edema due to venous thrombosis following stereotactic radiosurgery for a cerebral arteriovenous malformation (AVM) has rarely been reported. We report a patient with a large AVM in the eloquent area, and brain edema developed in this area after repeat Gamma knife stereotactic radiosurgery (GKRS). An 18-year-old female presented with a 4-year-history of persistent headache. Magnetic resonance imaging and transfemoral carotid angiogram revealed a high-flow large AVM in the left parieto-occipital area. Brain edema developed and aggravated patient's symptoms after time-staged GKRS. The cause of edema was thought to be the failure of the surrounding venous channels to drain the venous flow from the normal brain and the drainage was hampered by the persistent shunt flow from the AVM, which was due to the thrombosis of one huge draining vein of the AVM. The microsurgical resection of the AVM nidus eliminated shunt flow and completely normalized the brain edema. Microsurgical resection of the AVM nidus completely normalized the brain edema due to thrombosis of a draining vein of an AVM develops after SRS. PMID:27574486

  19. Brain Edema after Repeat Gamma Knife Radiosurgery for a Large Arteriovenous Malformation: A Case Report.

    PubMed

    Kim, Joo Whan; Chung, Hyun-Tai; Han, Moon Hee; Kim, Dong Gyu; Paek, Sun Ha

    2016-08-01

    Brain edema due to venous thrombosis following stereotactic radiosurgery for a cerebral arteriovenous malformation (AVM) has rarely been reported. We report a patient with a large AVM in the eloquent area, and brain edema developed in this area after repeat Gamma knife stereotactic radiosurgery (GKRS). An 18-year-old female presented with a 4-year-history of persistent headache. Magnetic resonance imaging and transfemoral carotid angiogram revealed a high-flow large AVM in the left parieto-occipital area. Brain edema developed and aggravated patient's symptoms after time-staged GKRS. The cause of edema was thought to be the failure of the surrounding venous channels to drain the venous flow from the normal brain and the drainage was hampered by the persistent shunt flow from the AVM, which was due to the thrombosis of one huge draining vein of the AVM. The microsurgical resection of the AVM nidus eliminated shunt flow and completely normalized the brain edema. Microsurgical resection of the AVM nidus completely normalized the brain edema due to thrombosis of a draining vein of an AVM develops after SRS. PMID:27574486

  20. Elevated Intracranial Pressure and Cerebral Edema following Permanent MCA Occlusion in an Ovine Model

    PubMed Central

    Wells, Adam J.; Vink, Robert; Helps, Stephen C.; Knox, Steven J.; Blumbergs, Peter C.; Turner, Renée J.

    2015-01-01

    Introduction Malignant middle cerebral artery (MCA) stroke has a disproportionately high mortality due to the rapid development of refractory space-occupying cerebral edema. Animal models are essential in developing successful anti-edema therapies; however to date poor clinical translation has been associated with the predominately used rodent models. As such, large animal gyrencephalic models of stroke are urgently needed. The aim of the study was to characterize the intracranial pressure (ICP) response to MCA occlusion in our recently developed ovine stroke model. Materials and Methods 30 adult female Merino sheep (n = 8–12/gp) were randomized to sham surgery, temporary or permanent proximal MCA occlusion. ICP and brain tissue oxygen were monitored for 24 hours under general anesthesia. MRI, infarct volume with triphenyltetrazolium chloride (TTC) staining and histology were performed. Results No increase in ICP, radiological evidence of ischemia within the MCA territory but without space-occupying edema, and TTC infarct volumes of 7.9+/-5.1% were seen with temporary MCAO. Permanent MCAO resulted in significantly elevated ICP, accompanied by 30% mortality, radiological evidence of space-occupying cerebral edema and TTC infarct volumes of 27.4+/-6.4%. Conclusions Permanent proximal MCAO in the sheep results in space-occupying cerebral edema, raised ICP and mortality similar to human malignant MCA stroke. This animal model may prove useful for pre-clinical testing of anti-edema therapies that have shown promise in rodent studies. PMID:26121036

  1. Plasma Fibrinogen Qualification as a Drug Development Tool in Chronic Obstructive Pulmonary Disease. Perspective of the Chronic Obstructive Pulmonary Disease Biomarker Qualification Consortium.

    PubMed

    Miller, Bruce E; Tal-Singer, Ruth; Rennard, Stephen I; Furtwaengler, Armin; Leidy, Nancy; Lowings, Michael; Martin, Ubaldo J; Martin, Thomas R; Merrill, Debora D; Snyder, Jeffrey; Walsh, John; Mannino, David M

    2016-03-15

    The COPD Foundation Biomarker Qualification Consortium (CBQC) is a unique public-private partnership established in 2010 between the COPD Foundation, the pharmaceutical industry, and academic chronic obstructive pulmonary disease (COPD) experts with advisors from the U.S. NHLBI and the Food and Drug Administration (FDA). This was a direct response to the 2009 publication of a guidance on qualification of drug development tools by the FDA. Although data were believed to be available from publicly funded and industry-funded studies that could support qualification of several tools, the necessary data resided in disparate databases. The initial intent of the CBQC was to integrate these data and submit a dossier for the qualification. This led to the FDA qualification of plasma fibrinogen as a prognostic or enrichment biomarker for all-cause mortality and COPD exacerbations in July 2015. It is the first biomarker drug development tool qualified for use in COPD under the FDA's drug development tool qualification program. This perspective summarizes the FDA's qualification process, the formation of the CBQC, and the effort that led to a successful outcome for plasma fibrinogen and discusses implications for future biomarker qualification efforts.

  2. Plasma Fibrinogen Qualification as a Drug Development Tool in Chronic Obstructive Pulmonary Disease. Perspective of the Chronic Obstructive Pulmonary Disease Biomarker Qualification Consortium.

    PubMed

    Miller, Bruce E; Tal-Singer, Ruth; Rennard, Stephen I; Furtwaengler, Armin; Leidy, Nancy; Lowings, Michael; Martin, Ubaldo J; Martin, Thomas R; Merrill, Debora D; Snyder, Jeffrey; Walsh, John; Mannino, David M

    2016-03-15

    The COPD Foundation Biomarker Qualification Consortium (CBQC) is a unique public-private partnership established in 2010 between the COPD Foundation, the pharmaceutical industry, and academic chronic obstructive pulmonary disease (COPD) experts with advisors from the U.S. NHLBI and the Food and Drug Administration (FDA). This was a direct response to the 2009 publication of a guidance on qualification of drug development tools by the FDA. Although data were believed to be available from publicly funded and industry-funded studies that could support qualification of several tools, the necessary data resided in disparate databases. The initial intent of the CBQC was to integrate these data and submit a dossier for the qualification. This led to the FDA qualification of plasma fibrinogen as a prognostic or enrichment biomarker for all-cause mortality and COPD exacerbations in July 2015. It is the first biomarker drug development tool qualified for use in COPD under the FDA's drug development tool qualification program. This perspective summarizes the FDA's qualification process, the formation of the CBQC, and the effort that led to a successful outcome for plasma fibrinogen and discusses implications for future biomarker qualification efforts. PMID:26745765

  3. Neostigmine and pulmonary oedema

    PubMed Central

    Nagella, Amrutha Bindu; Bijapur, Mubina Begum; Shreyavathi, Shreyavathi; R S, Raghavendra Rao

    2014-01-01

    A 1-year-old child with no pre-existing cardiac or respiratory disease developed frank pulmonary oedema after administration of a neostigmine–glycopyrrolate mixture to reverse neuromuscular blockade during general anaesthesia. Possible cardiac and extra-cardiac factors that could cause pulmonary oedema in this child were ruled out by appropriate investigations. As the pulmonary oedema manifested shortly after administration of the neostigmine–glycopyrrolate mixture, we concluded that neostigmine was the most probable cause. This article briefly reports the occurrence of events and successful management of perioperative pulmonary oedema. PMID:25199191

  4. Dose calculation for permanent prostate implants incorporating spatially anisotropic linearly time-resolving edema

    SciTech Connect

    Monajemi, T. T.; Clements, Charles M.; Sloboda, Ron S.

    2011-04-15

    Purpose: The objectives of this study were (i) to develop a dose calculation method for permanent prostate implants that incorporates a clinically motivated model for edema and (ii) to illustrate the use of the method by calculating the preimplant dosimetry error for a reference configuration of {sup 125}I, {sup 103}Pd, and {sup 137}Cs seeds subject to edema-induced motions corresponding to a variety of model parameters. Methods: A model for spatially anisotropic edema that resolves linearly with time was developed based on serial magnetic resonance imaging measurements made previously at our center to characterize the edema for a group of n=40 prostate implant patients [R. S. Sloboda et al., ''Time course of prostatic edema post permanent seed implant determined by magnetic resonance imaging,'' Brachytherapy 9, 354-361 (2010)]. Model parameters consisted of edema magnitude, {Delta}, and period, T. The TG-43 dose calculation formalism for a point source was extended to incorporate the edema model, thus enabling calculation via numerical integration of the cumulative dose around an individual seed in the presence of edema. Using an even power piecewise-continuous polynomial representation for the radial dose function, the cumulative dose was also expressed in closed analytical form. Application of the method was illustrated by calculating the preimplant dosimetry error, RE{sub preplan}, in a 5x5x5 cm{sup 3} volume for {sup 125}I (Oncura 6711), {sup 103}Pd (Theragenics 200), and {sup 131}Cs (IsoRay CS-1) seeds arranged in the Radiological Physics Center test case 2 configuration for a range of edema relative magnitudes ({Delta}=[0.1,0.2,0.4,0.6,1.0]) and periods (T=[28,56,84] d). Results were compared to preimplant dosimetry errors calculated using a variation of the isotropic edema model developed by Chen et al. [''Dosimetric effects of edema in permanent prostate seed implants: A rigorous solution,'' Int. J. Radiat. Oncol., Biol., Phys. 47, 1405-1419 (2000

  5. Etiology and treatment of the inflammatory causes of cystoid macular edema.

    PubMed

    Cho, Hyung; Madu, Assumpta

    2009-01-01

    Cystoid macular edema in its various forms can be considered one of the leading causes of central vision loss in the developed world. It occurs in a wide variety of pathologic conditions and represents the final common pathway of several basic processes. Therapeutic approaches to cystoid macular edema depend on a clear understanding of its contributing pathophysiologic mechanisms. This review will discuss the mechanism of ocular inflammation in cystoid macular edema with a particular focus on the inflammatory causes: post-operative, uveitic, and after laser procedures. A variety of pharmacologic agents targeting inflammatory molecules have been shown to reduce macular edema and improve visual function. However, the long-term efficacy and safety of most new therapies have yet to be established in controlled clinical trials.

  6. Etiology and treatment of the inflammatory causes of cystoid macular edema

    PubMed Central

    Cho, Hyung; Madu, Assumpta

    2009-01-01

    Cystoid macular edema in its various forms can be considered one of the leading causes of central vision loss in the developed world. It occurs in a wide variety of pathologic conditions and represents the final common pathway of several basic processes. Therapeutic approaches to cystoid macular edema depend on a clear understanding of its contributing pathophysiologic mechanisms. This review will discuss the mechanism of ocular inflammation in cystoid macular edema with a particular focus on the inflammatory causes: post-operative, uveitic, and after laser procedures. A variety of pharmacologic agents targeting inflammatory molecules have been shown to reduce macular edema and improve visual function. However, the long-term efficacy and safety of most new therapies have yet to be established in controlled clinical trials. PMID:22096351

  7. The pulmonary veins of the pig as an anatomical model for the development of a new treatment for atrial fibrillation.

    PubMed

    Vandecasteele, T; Vandevelde, K; Doom, M; Van Mulken, E; Simoens, P; Cornillie, P

    2015-02-01

    The layout of the porcine atriopulmonary junction and immediately adjacent structures was investigated by gross anatomical and vascular corrosion casting studies to meet the need for more in-depth anatomical insights when using the pig as an animal model in the development of innovative approaches for surgical cardiac ablation in man. The veins from the right cranial and middle lung lobes drain through a common ostium in the left atrium, whereas a second ostium receives the blood returning from all other lung lobes, although limited variation to this pattern was observed. Surrounding anatomical structures that are most vulnerable to ablation damage as reported in man are located at a safer distance from the pulmonary veins in pigs, yet a certain locations, comparable risks are to be considered. Additionally, it was histologically confirmed that myocardial sleeves extend to over a centimetre in the wall of the pulmonary veins.

  8. Dysphagia Caused by Chronic Laryngeal Edema.

    PubMed

    Delides, Alexander; Sakagiannis, George; Maragoudakis, Pavlos; Gouloumi, Αlina-Roxani; Katsimbri, Pelagia; Giotakis, Ioannis; Panayiotides, John G

    2015-10-01

    A rare case of a young female with chronic diffuse laryngeal edema causing severe swallowing difficulty is presented. The patient was previously treated with antibiotics and steroids with no improvement. Diagnosis was made with biopsy of the epiglottis under local anesthesia in the office.

  9. The Role of Circulating Serotonin in the Development of Chronic Obstructive Pulmonary Disease

    PubMed Central

    Lau, Way K. W.; Chan-Yeung, Moira M. W.; Yip, Benjamin H. K.; Cheung, Amy H. K.; Ip, Mary S. M.; Mak, Judith C. W.

    2012-01-01

    Background Cigarette smoking is a major risk factor in the development of age-related chronic obstructive pulmonary disease (COPD). The serotonin transporter (SERT) gene polymorphism has been reported to be associated with COPD, and the degree of cigarette smoking has been shown to be a significant mediator in this relationship. The interrelation between circulating serotonin (5-hydroxytyptamine, 5-HT), cigarette smoking and COPD is however largely unknown. The current study aimed at investigating the mediation effects of plasma 5-HT on cigarette smoking-induced COPD and the relation between plasma 5-HT levels and age. Methods The association between plasma 5-HT, age and COPD was analyzed in a total of 62 COPD patients (ever-smokers) and 117 control subjects (healthy non-smokers and ever-smokers). Plasma 5-HT levels were measured by enzyme-linked immuno assay (EIA). Results The elevated plasma 5-HT levels were significantly associated with increased odds for COPD (OR = 1.221, 95% CI = 1.123 to 1.319, p<0.0001). The effect remained significant after being adjusted for age and pack-years smoked (OR = 1.271, 95% CI = 1.134 to 1.408, p = 0.0003). Furthermore, plasma 5-HT was found to mediate the relation between pack-years smoked and COPD. A positive correlation (r = 0.303, p = 0.017) was found between plasma 5-HT levels and age in COPD, but not in the control subjects (r = −0.149, p = 0.108). Conclusion Our results suggest that cigarette smoke-induced COPD is partially mediated by the plasma levels of 5-HT, and that these become elevated with increased age in COPD. The elevated plasma 5-HT levels in COPD might contribute to the pathogenesis of this disease. PMID:22319639

  10. A Sex-Specific MicroRNA-96/5-Hydroxytryptamine 1B Axis Influences Development of Pulmonary Hypertension

    PubMed Central

    Wallace, Emma; Morrell, Nicholas W.; Yang, Xudong D.; Long, Lu; Stevens, Hannah; Nilsen, Margaret; Loughlin, Lynn; Mair, Kirsty M.; Baker, Andrew H.

    2015-01-01

    Rationale: Females are predisposed to pulmonary arterial hypertension (PAH); evidence suggests that serotonin, mutations in the bone morphogenetic protein receptor (BMPR) II gene, and estrogens influence development of PAH. The 5-hydroxytryptamine 1B receptor (5-HT1BR) mediates human pulmonary artery smooth muscle cell (hPASMC) proliferation. Objectives: We aimed to determine whether selected microRNAs (miRNAs) expressed in PASMCs are influenced by sex, BMPR-II mutations, and estrogens, and contribute to PASMC proliferation in PAH. Methods: Expression levels of miRNAs targeting genes related to PAH, estrogen, and serotonin were determined by quantitative RT-PCR in hPASMCs and mouse PASMCs harboring a heterozygous mutation in BMPR-II (BMPR-IIR899X+/− PASMCs). miRNA-96 targets 5-HT1BR and was selected for further investigation. miRNA target validation was confirmed by luciferase reporter assay. Precursor miRNA-96 was transfected into hPASMCs to examine effects on proliferation and 5-HT1BR expression. The effect of a miRNA-96 mimic on the development of hypoxic pulmonary hypertension in mice was also assessed. Measurements and Main Results: miRNA-96 expression was reduced in BMPR-IIR899X+/− PASMCs from female mice and hPASMCs from female patients with PAH; this was associated with increased 5-HT1BR expression and serotonin-mediated proliferation. 5-HT1BR was validated as a target for miRNA-96. Transfection of precursor miRNA-96 into hPASMCs reduced 5-HT1BR expression and inhibited serotonin-induced proliferation. Restoration of miRNA-96 expression in pulmonary arteries in vivo via administration of an miRNA-96 mimic reduced the development of hypoxia-induced pulmonary hypertension in the mouse. Conclusions: Increased 5-HT1BR expression may be a consequence of decreased miRNA-96 expression in female patient PASMCs, and this may contribute to the development of PAH. PMID:25871906

  11. Hereditary angioneurotic edema and HLA types in two Danish families.

    PubMed

    Eggert, J; Zachariae, H; Svejgaard, E; Svejgaard, A; Kissmeyer-Nielsen, F

    1982-01-01

    HLA types were determined in 19 patients and 9 healthy members of 2 Danish families with hereditary angioneurotic edema. The study revealed no connections between hereditary angioneurotic edema and the HLA system. PMID:7165360

  12. Arginine-Restricted Therapy Resistant Bilateral Macular Edema Associated with Gyrate Atrophy.

    PubMed

    Doguizi, Sibel; Sekeroglu, Mehmet Ali; Anayol, Mustafa Alpaslan; Yilmazbas, Pelin

    2015-01-01

    Introduction. Gyrate atrophy is a rare genetical metabolic disorder affecting vision. Here, we report a 9-year-old boy with gyrate atrophy associated with bilateral macular edema at the time of diagnosis and the effect of long term metabolic control on macular edema. Case Presentation. A 9-year-old boy presented with a complaint of low visual acuity (best corrected visual acuity: 20/80 in both eyes, refractive error: -12.00 D). Dilated fundus examination revealed multiple bilateral, sharply defined, and scalloped chorioretinal atrophy areas in the midperipheral and peripheral zone. Spectral-domain optical coherence tomography revealed bilateral cystoid macular edema in both eyes. Serum ornithine level was high (622 μmol/L). An arginine-restricted diet reduced serum ornithine level (55 μmol/L). However, visual findings including macular edema remained unchanged in 2 years of follow-up. Conclusion. Arginine-restricted diet did not improve macular edema in our patient with gyrate atrophy. A more comprehensive understanding of the underlying factors for macular edema will lead to the development of effective therapies.

  13. Pulmonary Embolism

    MedlinePlus

    ... pulmonary embolism is a sudden blockage in a lung artery. The cause is usually a blood clot ... loose and travels through the bloodstream to the lung. Pulmonary embolism is a serious condition that can ...

  14. Pulmonary Fibrosis

    MedlinePlus

    Pulmonary fibrosis is a condition in which the tissue deep in your lungs becomes scarred over time. This tissue ... may not get enough oxygen. Causes of pulmonary fibrosis include environmental pollutants, some medicines, some connective tissue ...

  15. Pulmonary Rehabilitation

    MedlinePlus

    Pulmonary Rehabilitation If you have shortness of breath because of lung problems, you may have asked yourself: • Can I ... medications do I really need to take? Pulmonary rehabilitation can help answer these and other questions. Enrolling ...

  16. Development of grafted xyloglucan micelles for pulmonary delivery of curcumin: In vitro and in vivo studies.

    PubMed

    Mahajan, Hitendra S; Mahajan, Prashant R

    2016-01-01

    A novel grafted copolymer consisting of l-lactide grafted xyloglucan was synthesized by polymerization reaction and characterized. The grafted copolymers were analyzed by Fourier-transform infrared spectrometry (FTIR) and (1)H nuclear magnetic resonance ((1)H NMR) was performed to confirm the grafting of l-poly lactic acid on xyloglucan. The grafted polymer forms micelles at the critical micelle concentration of 0.0150 wt% with the average particle size of 102 nm, as determined by particle size analyzer. The zeta potential of the curcumin loaded micelles was -18.2 mV, an acceptable drug loading efficiency of 68.9 ± 0.02% and the entrapment efficiency of 96.38 ± 0.2%. The release study for 5h showed a sustained release property. In vitro assessment demonstrates suitability of micelles as dry powder for inhalation. In vivo studies showed significant improvement in bioavailability on pulmonary administration of curcumin micelles as DPI formulation. The potential for pulmonary delivery curcumin loaded in micelles was evaluated. In conclusion, polymeric micelle based on a newly synthesized grafted xyloglucan could be suitable carrier for pulmonary delivery of curcumin.

  17. Cystoid Macular Edema in Bietti's Crystalline Retinopathy

    PubMed Central

    2014-01-01

    A 27-year-old man with progressive bilateral visual decline was diagnosed to have Bietti's crystalline dystrophy (BCD). Fluorescein angiography revealed bilateral petaloid type late hyperfluorescence implicating concurrent cystoid macular edema (CME). Optical coherence tomography exhibited cystoid foveal lacunas OU. During the follow-up of six years, intraretinal crystals reduced in amount but CME persisted angiographically and tomographically. CME is among the rare macular features of BCD including subfoveal sensorial detachment, subretinal neovascular membrane, and macular hole. PMID:24949209

  18. Cortical edema in moderate fluid percussion brain injury is attenuated by vagus nerve stimulation.

    PubMed

    Clough, R W; Neese, S L; Sherill, L K; Tan, A A; Duke, A; Roosevelt, R W; Browning, R A; Smith, D C

    2007-06-29

    Development of cerebral edema (intracellular and/or extracellular water accumulation) following traumatic brain injury contributes to mortality and morbidity that accompanies brain injury. Chronic intermittent vagus nerve stimulation (VNS) initiated at either 2 h or 24 h (VNS: 30 s train of 0.5 mA, 20 Hz, biphasic pulses every 30 min) following traumatic brain injury enhances recovery of motor and cognitive function in rats in the weeks following brain injury; however, the mechanisms of facilitated recovery are unknown. The present study examines the effects of VNS on development of acute cerebral edema following unilateral fluid percussion brain injury (FPI) in rats, concomitant with assessment of their behavioral recovery. Two hours following FPI, VNS was initiated. Behavioral testing, using both beam walk and locomotor placing tasks, was conducted at 1 and 2 days following FPI. Edema was measured 48 h post-FPI by the customary method of region-specific brain weights before and after complete dehydration. Results of this study replicated that VNS initiated at 2 h after FPI: 1) effectively facilitated the recovery of vestibulomotor function at 2 days after FPI assessed by beam walk performance (P<0.01); and 2) tended to improve locomotor placing performance at the same time point (P=0.18). Most interestingly, results of this study showed that development of edema within the cerebral cortex ipsilateral to FPI was significantly attenuated at 48 h in FPI rats receiving VNS compared with non-VNS FPI rats (P<0.04). Finally, a correlation analysis between beam walk performance and cerebral edema following FPI revealed a significant inverse correlation between behavior performance and cerebral edema. Together, these results suggest that VNS facilitation of motor recovery following experimental brain injury in rats is associated with VNS-mediated attenuation of cerebral edema. PMID:17543463

  19. Lethal brain edema, shock, and coagulopathy after scorpion envenomation.

    PubMed

    Cavari, Yuval; Lazar, Isaac; Shelef, Ilan; Sofer, Shaul

    2013-03-01

    We report the case of a 2-year-old Bedouin boy in whom developed severe and unusual complications after being stung, most probably, by the yellow scorpion Leiurus quinquestriatus hebraeus. Five hours after arrival to the emergency department, the boy had multisystem organ failure involving the central nervous system (seizure activity followed by coma with dilated, nonreactive pupils, and severe brain edema), shock (noncardiogenic), disseminated intravascular coagulation, renal failure, hepatic failure, and watery diarrhea, causing his death. In view of the relevant literature, we discuss the pathophysiologic events ultimately leading to his death. PMID:23280335

  20. Pulmonary delivery of an ultra-fine oxytocin dry powder formulation: potential for treatment of postpartum haemorrhage in developing countries.

    PubMed

    Prankerd, Richard J; Nguyen, Tri-Hung; Ibrahim, Jibriil P; Bischof, Robert J; Nassta, Gemma C; Olerile, Livesey D; Russell, Adrian S; Meiser, Felix; Parkington, Helena C; Coleman, Harold A; Morton, David A V; McIntosh, Michelle P

    2013-01-01

    Oxytocin is recommended by the World Health Organisation as the most effective uterotonic for the prevention and treatment of postpartum haemorrhage. The requirement for parenteral administration by trained healthcare providers and the need for the drug solution to be maintained under cold-chain storage limit the use of oxytocin in the developing world. In this study, a spray-dried ultrafine formulation of oxytocin was developed with an optimal particle size diameter (1-5 µm) to facilitate aerosolised delivery via the lungs. A powder formulation of oxytocin, using mannitol, glycine and leucine as carriers, was prepared with a volume-based median particle diameter of 1.9 µm. Oxytocin content in the formulation was assayed using high-performance liquid chromatography-mass spectroscopy and was found to be unchanged after spray-drying. Ex vivo contractility studies utilising human and ovine uterine tissue indicated no difference in the bioactivity of oxytocin before and after spray-drying. Uterine electromyographic (EMG) activity in postpartum ewes following pulmonary (in vivo) administration of oxytocin closely mimicked that observed immediately postpartum (0-12 h following normal vaginal delivery of the lamb). In comparison to the intramuscular injection, pulmonary administration of an oxytocin dry powder formulation to postpartum ewes resulted in generally similar EMG responses, however a more rapid onset of uterine EMG activity was observed following pulmonary administration (129 ± 18 s) than intramuscular injection (275 ± 22 s). This is the first study to demonstrate the potential for oxytocin to elicit uterine activity after systemic absorption as an aerosolised powder from the lungs. Aerosolised oxytocin has the potential to provide a stable and easy to administer delivery system for effective prevention and treatment of postpartum haemorrhage in resource-poor settings in the developing world.

  1. Aquaporin-1 Deficiency Protects Against Myocardial Infarction by Reducing Both Edema and Apoptosis in Mice

    PubMed Central

    Li, Lihua; Weng, Zhiyong; Yao, Chenjuan; Song, Yuanlin; Ma, Tonghui

    2015-01-01

    Many studies have determined that AQP1 plays an important role in edema formation and resolution in various tissues via water transport across the cell membrane. The aim of this research was to determine both if and how AQP1 is associated with cardiac ischemic injury, particularly the development of edema following myocardial infarction (MI). AQP1+/+ and AQP1−/− mice were used to create the MI model. Under physiological conditions, AQP1−/− mice develop normally; however, in the setting of MI, they exhibit cardioprotective properties, as shown by reduced cardiac infarct size determined via NBT staining, improved cardiac function determined via left ventricular catheter measurements, decreased AQP1-dependent myocardial edema determined via water content assays, and decreased apoptosis determined via TUNEL analysis. Cardiac ischemia caused by hypoxia secondary to AQP1 deficiency stabilized the expression of HIF-1α in endothelial cells and subsequently decreased microvascular permeability, resulting in the development of edema. The AQP1-dependent myocardial edema and apoptosis contributed to the development of MI. AQP1 deficiency protected cardiac function from ischemic injury following MI. Furthermore, AQP1 deficiency reduced microvascular permeability via the stabilization of HIF-1α levels in endothelial cells and decreased cellular apoptosis following MI. PMID:26348407

  2. Aquaporin-1 Deficiency Protects Against Myocardial Infarction by Reducing Both Edema and Apoptosis in Mice.

    PubMed

    Li, Lihua; Weng, Zhiyong; Yao, Chenjuan; Song, Yuanlin; Ma, Tonghui

    2015-01-01

    Many studies have determined that AQP1 plays an important role in edema formation and resolution in various tissues via water transport across the cell membrane. The aim of this research was to determine both if and how AQP1 is associated with cardiac ischemic injury, particularly the development of edema following myocardial infarction (MI). AQP1+/+ and AQP1-/- mice were used to create the MI model. Under physiological conditions, AQP1-/- mice develop normally; however, in the setting of MI, they exhibit cardioprotective properties, as shown by reduced cardiac infarct size determined via NBT staining, improved cardiac function determined via left ventricular catheter measurements, decreased AQP1-dependent myocardial edema determined via water content assays, and decreased apoptosis determined via TUNEL analysis. Cardiac ischemia caused by hypoxia secondary to AQP1 deficiency stabilized the expression of HIF-1α in endothelial cells and subsequently decreased microvascular permeability, resulting in the development of edema. The AQP1-dependent myocardial edema and apoptosis contributed to the development of MI. AQP1 deficiency protected cardiac function from ischemic injury following MI. Furthermore, AQP1 deficiency reduced microvascular permeability via the stabilization of HIF-1α levels in endothelial cells and decreased cellular apoptosis following MI. PMID:26348407

  3. Relationship between colloid osmotic pressure and pulmonary artery wedge pressure in patients with acute cardiorespiratory failure.

    PubMed

    Weil, M H; Henning, R J; Morissette, M; Michaels, S

    1978-04-01

    Close relationships between progressive respiratory failure, roentgenographic signs of pulmonary opacification and decreases in the difference between colloid osmotic pressure of plasma and the pulmonary artery wedge pressure (colloid-hydrosatic pressure gradient) were demonstrated in 49 critically ill patients with multisystem failure, in patients in shock. The potential importance of this relationship is underscored by the observation that fatal progression of pulmonary edema was related to a critical reduction in the colloid-hydrostatic pressure gradient to levels of less than 0 mm Hg. More often, reduction in colloid osmotic pressure rather than increases in left ventricular filling pressure (pulmonary artery wedge pressure) accounted for the decline in colloid-hydrostatic pressure gradient. Routine measurement of colloid osmotic pressure, preferably in conjunction with pulmonary artery wedge pressure, is likely to improve understanding of the mechanisms of acute pulmonary edema.

  4. Pulmonary Hypertension

    PubMed Central

    Newman, John H.

    2005-01-01

    The modern era in cardiopulmonary medicine began in the 1940s, when Cournand and Richards pioneered right-heart catheterization. Until that time, no direct measurement of central vascular pressure had been performed in humans. Right-heart catheterization ignited an explosion of insights into function and dysfunction of the pulmonary circulation, cardiac performance, ventilation–perfusion relationships, lung–heart interactions, valvular function, and congenital heart disease. It marked the beginnings of angiocardiography with its diagnostic implications for diseases of the left heart and peripheral circulation. Pulmonary hypertension was discovered to be the consequence of a large variety of diseases that either raised pressure downstream of the pulmonary capillaries, induced vasoconstriction, increased blood flow to the lung, or obstructed the pulmonary vessels, either by embolism or in situ fibrosis. Hypoxic vasoconstriction was found to be a major cause of acute and chronic pulmonary hypertension, and surprising vasoreactivity of the pulmonary vascular bed was discovered to be present in many cases of severe pulmonary hypertension, initially in mitral stenosis. Diseases as disparate as scleroderma, cystic fibrosis, kyphoscoliosis, sleep apnea, and sickle cell disease were found to have shared consequences in the pulmonary circulation. Some of the achievements of Cournand and Richards and their scientific descendents are discussed in this article, including success in the diagnosis and treatment of idiopathic pulmonary arterial hypertension, chronic thromboembolic pulmonary hypertension, and management of hypoxic pulmonary hypertension. PMID:15994464

  5. Potential and development of inhaled RNAi therapeutics for the treatment of pulmonary tuberculosis.

    PubMed

    Man, Dede K W; Chow, Michael Y T; Casettari, Luca; Gonzalez-Juarrero, Mercedes; Lam, Jenny K W

    2016-07-01

    Tuberculosis (TB), caused by the infection of Mycobacterium tuberculosis (Mtb), continues to pose a serious threat to public health, and the situation is worsening with the rapid emergence of multidrug resistant (MDR) TB. Current TB regimens require long duration of treatment, and their toxic side effects often lead to poor adherence and low success rates. There is an urgent need for shorter and more effective treatment for TB. In recent years, RNA interference (RNAi) has become a powerful tool for studying gene function by silencing the target genes. The survival of Mtb in host macrophages involves the attenuation of the antimicrobial responses mounted by the host cells. RNAi technology has helped to improve our understanding of how these bacilli interferes with the bactericidal effect and host immunity during TB infection. It has been suggested that the host-directed intervention by modulation of host pathways can be employed as a novel and effective therapy against TB. This therapeutic approach could be achieved by RNAi, which holds enormous potential beyond a laboratory to the clinic. RNAi therapy targeting TB is being investigated for enhancing host antibacterial capacity or improving drug efficacy on drug resistance strains while minimizing the associated adverse effects. One of the key challenges of RNAi therapeutics arises from the delivery of the RNAi molecules into the target cells, and inhalation could serve as a direct administration route for the treatment of pulmonary TB in a non-invasive manner. However, there are still major obstacles that need to be overcome. This review focuses on the RNAi candidates that are currently explored for the treatment of TB and discusses the major barriers of pulmonary RNAi delivery. From this, we hope to stimulate further studies of local RNAi therapeutics for pulmonary TB treatment.

  6. Development of a Fuzzy Decision Support System to Determine the Severity of Obstructive Pulmonary in Chemical Injured Victims

    PubMed Central

    Samad-Soltani, Taha; Ghanei, Mostafa; Langarizadeh, Mostafa

    2015-01-01

    Background: Chronic Obstructive Pulmonary Disease (COPD) is the most common known complication of exposure to mustard gas. Thus, all clinical guidelines have provided some recommendation for diagnosis, clinical management and treatment of this disease. Decision support systems are used to increase the acceptance of clinical guidelines. The purpose of this research is to develop a CDSS to determine the severity of COPD in chemical injured victims. Objectives: Development of a decision support system to determine the severity of COPD. Patients and Methods: First, the variables influencing to determining the severity of the disease was classified through studying the clinical guidelines. Then, the fuzzy model was implemented. To testing the system, the data from 50 patients were used. Results: the overall accuracy in determining the severity of the injury is equal to 92%, these indicators reflect the proper functioning of the system to assist the physician regarding the diagnosis of chronic obstructive pulmonary disease and determining its severity. Conclusions: The CDSS has efficient results and satisfactory performance. Although, the medical expert systems cannot be expected to provide 100 percent correct responses, however, they can be useful in the areas of patient management, diagnosis and treatment planning. PMID:26236078

  7. Influences of high-voltage electrical burns on the pulmonary microcirculation in rabbits.

    PubMed

    Zhou, H M; Xu, S J; Wang, L; Shao, H B; Xie, B; Feng, J K; Wang, C J; Bai, Y Q; Zhang, Q F

    2016-01-01

    This study was performed to investigate the effects of high-voltage electrical burns (HEB) on the pulmonary microcirculation in rabbits. Total of 120 rabbits were randomly divided into control and HEB group using a random number table. HEB model was developed with a voltage regulator and experimental transformer. Laser Doppler perfusion imager was utilized to monitor and quantify the blood perfusion in pulmonary microcirculation. The microvascular morphologic changes of the lung were observed using light microscopy and transmission electron microscope (TEM). The lung wet/dry weight ratio and the PaO2 were determined. The values of blood perfusion in rabbit pulmonary microcirculation in the HEB group were decreased at 5 min, but increased at 1 h after burn (P <  0.01) and then decreased gradually. Light microscopy reveals microthrombus formation in pulmonary venules and bleeding in venous capillaries in HEB group. We found the number of microvilli in the capillary endothelial cells decreased, the rough endoplasmic reticulum expanded and severe degranulation occurred, the mitochondrial cristae fused or disappeared, and severe edema surrounded the capillary endothelial cells by TEM. The values of lung wet/dry weight ratio were higher and the PaO2 were lower than that of before burn group (P <  0.01). These results demonstrated that microcirculatory disorders play a major role in the development of progressive lung damage after high-voltage electrical burns.

  8. Isosmotic media prevent edema in amphibian larvae without cardiac function.

    PubMed

    Smith, S C

    2000-03-01

    The absence of cardiac and circulatory function causes severe edema in amphibian embryos. Analyzing the roles of embryonic and larval circulation in respiration may thus be confounded by the increased diffusion distance and decreased surface area/volume ratio caused by edema. Similarly, detailed morphological analyses of embryos/larvae with defective circulatory or renal function is difficult or impossible due to the gross morphological anomalies engendered by edematous swelling. To circumvent these problems, two media have been developed which are isosmotic with the plasma of a common experimental amphibian species (Ambystoma mexicanun). These media are remarkably effective in preventing fluid accumulation in embryos and larvae lacking heart function and, when used in slightly lower concentrations, cause no apparent harm to embryos and larvae with normal circulation for periods up to 3 weeks. These media should prove useful for a variety of studies on the developmental physiology of the circulatory system and possibly also when examining the development of renal function and ionoregulation. PMID:10764226

  9. [Chronic thromboembolic pulmonary hypertension].

    PubMed

    Kim, Nick H; Delcroix, Marion; Jenkins, David P; Channick, Richard; Dartevelle, Philippe; Jansa, Pavel; Lang, Irene; Madani, Michael M; Ogino, Hitoshi; Pengo, Vittorio; Mayer, Eckhard

    2014-10-01

    Since the last World Symposium on Pulmonary Hypertension in 2008, we have witnessed numerous and exciting developments in chronic thromboembolic pulmonary hypertension (CTEPH). Emerging clinical data and advances in technology have led to reinforcing and updated guidance on diagnostic approaches to pulmonary hypertension, guidelines that we hope will lead to better recognition and more timely diagnosis of CTEPH. We have new data on treatment practices across international boundaries as well as long-term outcomes for CTEPH patients treated with or without pulmonary endarterectomy. Furthermore, we have expanded data on alternative treatment options for select CTEPH patients, including data from multiple clinical trials of medical therapy, including 1 recent pivotal trial, and compelling case series of percutaneous pulmonary angioplasty. Lastly, we have garnered more experience, and on a larger international scale, with pulmonary endarterectomy, which is the treatment of choice for operable CTEPH. This report overviews and highlights these important interval developments as deliberated among our task force of CTEPH experts and presented at the 2013 World Symposium on Pulmonary Hypertension in Nice, France. (J Am Coil Cardiol 2013;62:D92-9) ©2013 by the American College of Cardiology Foundation.

  10. Development and analysis of a finite element model to simulate pulmonary emphysema in CT imaging.

    PubMed

    Diciotti, Stefano; Nobis, Alessandro; Ciulli, Stefano; Landini, Nicholas; Mascalchi, Mario; Sverzellati, Nicola; Innocenti, Bernardo

    2015-01-01

    In CT imaging, pulmonary emphysema appears as lung regions with Low-Attenuation Areas (LAA). In this study we propose a finite element (FE) model of lung parenchyma, based on a 2-D grid of beam elements, which simulates pulmonary emphysema related to smoking in CT imaging. Simulated LAA images were generated through space sampling of the model output. We employed two measurements of emphysema extent: Relative Area (RA) and the exponent D of the cumulative distribution function of LAA clusters size. The model has been used to compare RA and D computed on the simulated LAA images with those computed on the models output. Different mesh element sizes and various model parameters, simulating different physiological/pathological conditions, have been considered and analyzed. A proper mesh element size has been determined as the best trade-off between reliable results and reasonable computational cost. Both RA and D computed on simulated LAA images were underestimated with respect to those calculated on the models output. Such underestimations were larger for RA (≈ -44 ÷ -26%) as compared to those for D (≈ -16 ÷ -2%). Our FE model could be useful to generate standard test images and to design realistic physical phantoms of LAA images for the assessment of the accuracy of descriptors for quantifying emphysema in CT imaging.

  11. Proton nuclear magnetic resonance studies on brain edema

    SciTech Connect

    Naruse, S.; Horikawa, Y.; Tanaka, C.; Hirakawa, K.; Nishikawa, H.; Yoshizaki, K.

    1982-06-01

    The water in normal and edematous brain tissues of rats was studied by the pulse nuclear magnetic resonance (NMR) technique, measuring the longitudinal relaxation time (T1) and the transverse relaxation time (T2). In the normal brain, T1 and T2 were single components, both shorter than in pure water. Prolongation and separation of T2 into two components, one fast and one slow, were the characteristic findings in brain edema induced by both cold injury and triethyl tin (TET), although some differences between the two types of edema existed in the content of the lesion and in the degree of changes in T1 and T2 values. Quantitative analysis of T1 and T2 values in their time course relating to water content demonstrated that prolongation of T1 referred to the volume of increased water in tissues examined, and that two phases of T2 reflected the distribution and the content of the edema fluid. From the analysis of the slow component of T2 versus water content during edema formation, it was demonstrated that the increase in edema fluid was steady, and its content was constant during formation of TET-induced edema. On the contrary, during the formation of cold-injury edema, water-rich edema fluid increased during the initial few hours, and protein-rich edema fluid increased thereafter. It was concluded that proton NMR relaxation time measurements may provide new understanding in the field of brain edema research.

  12. Effect of dl-3-n-butylphthalide on brain edema in rats subjected to focal cerebral ischemia.

    PubMed

    Deng, W; Feng, Y

    1997-06-01

    The present study evaluated the effect of dl-3-n-butylphthalide(NBP), a novel brain protective agent, on brain edema in rats following focal ischemia. Edema was induced by occluding the right middle cerebral artery (MCAO), producing permanent focal ischemia in the right cerebral hemisphere, which developed ipsilateral brain edema reproducibly. Edema was assessed 24 h after MCA occlusion by determining the brain water content from wet and dry weight measurements, and the sodium, potassium concentrations with ion-selective electrodes. In this model, NBP at the dose of 80, 160 and 240 mg/kg p.o. 15 min after MCAO prevented from brain edema in a dose-dependent manner. A significant reduction of sodium content and an increase in potassium level were observed in all drug-treated groups. It showed that NBP strongly attenuated brain water entry, sodium accumulation and potassium loss. Nimodipine treatment (5 mg/kg s.c.) also reduced brain edema (P < 0.05). The results suggest that a strong anti-edema activity of NBP may play an important role to contribute to the treatment of ischemic damage.

  13. Neurological deficits and brain edema after intracerebral hemorrhage in Mongolian gerbils.

    PubMed

    Kuroiwa, T; Okauchi, M; Hua, Y; Schallert, T; Keep, R F; Xi, G

    2008-01-01

    We examined the time course of neurological deficits in gerbils after an intracerebral hemorrhage (ICH) induced by autologous blood infusion and examined its correlation with the severity of perihematomal edema. Mongolian gerbils (n = 15) were subjected to stereotaxic autologous blood infusion (30 or 60 microL) into the left caudate nucleus. Corner-turn and forelimb-placing tests were performed before, and 1 and 3 days after ICH. Perihematomal water content was measured by tissue gravimetry. Gerbils developed neurological deficits and perihematomal edema at day 1 after ICH. Both neurological deficits and perihematomal edema were significantly greater in animals with 60 microL blood infusion compared to the 30 microL infusion group, and both neurological deficits and edema were also greater at 3 days compared to 1 day after ICH. The severity of neurological deficits paralleled the degree of perihematomal edema. We conclude that the Mongolian gerbil is a suitable model for studies on the behavioral effects of ICH. PMID:19066097

  14. The malar septum: the anatomic basis of malar mounds and malar edema.

    PubMed

    Pessa, J E; Garza, J R

    1997-01-01

    The anatomy of malar mounds and malar edema is evaluated in a series of 18 fresh cadaver dissections. Dye injection, histologic evaluation, and gross anatomic dissection are used to identify a previously unrecognized fascial structure of the lower eyelid and cheek. The malar septum originates from orbital rim periosteum superiorly and inserts into cheek skin 2.5 to 3 cm inferior to the lateral canthus. This fascial structure acts as a relatively impermeable barrier that allows tissue edema and hemoglobin pigment to accumulate above its cutaneous insertion. The malar septum, which acts as both a functional and a structural barrier, defines the lower boundary of several clinical entities: malar mounds, malar edema, malar festoons, and periorbital ecchymosis. The permeability characteristics of the malar septum suggest that, at least in some persons, malar mounds may be accentuated by chronic lower eyelid edema, and these characteristics may imply a time course in the progressive development from malar edema to malar mounds and, ultimately, to malar festoons. The anatomy of the malar septum is clinically relevant because it defines the four anatomic compartments of the malar mound that should be considered during surgery: the superior compartment of suborbicularis oculi fat, orbicularis oculi muscle, and superficial cheek fat and cheek skin superior to the cutaneous insertion of the malar septum.

  15. The Effect of Complete Decongestive Therapy on Edema Volume Reduction and Pain in Women With Post Breast Surgery Lymph Edema

    PubMed Central

    Angooti Oshnari, Leila; Hosseini, Seyed Ali; Haghighat, Shahpar; Hossein Zadeh, Samaneh

    2016-01-01

    Background Upper extremity lymph edema is the most common side effect of breast cancer treatment that may produce significant physical and psychological morbidity. Pain is the frequent symptom of lymph edema that causes impairment of activities in daily life. Objectives The aim of this study was assessment of the effect of complex decongestive therapy (CDT) on upper extremity lymph edema and pain in women with post breast surgery lymph edema. Patients and Methods In this quasi- experimental research with before- after design, 36 women with moderate lymph edema after breast surgery participated in the program. Edema volume was measured by water displacement method; pain values were evaluated by visual analog scale (VAS). Data were recorded before intervention and 2 and 4 weeks after it. CDT included the first phase (intensive phase) and the second phase (maintenance phase). Each phase lasted 2 weeks. After use of Shapiro Wilk test for normality, analysis of variances with GEE and repeated measurements were used to analyze the data. Results After one month doing CDT program, significant decrease of edema was noticed (P < 0.0001), also pain decreased during 2 and 4 weeks after intervention (P < 0.0001). Conclusions This study indicated that CDT program is effective in reducing lymph edema volume and pain in women with moderate post breast surgery lymph edema. It seems that raising patients’ awareness and training healthcare professionals regarding lymph edema preventive strategies have an important role in earlier and better combating this complication. PMID:27482330

  16. Diffusion tensor-based tumor infiltration index cannot discriminate vasogenic edema from tumor-infiltrated edema.

    PubMed

    Kinoshita, Manabu; Goto, Tetsu; Okita, Yoshiko; Kagawa, Naoki; Kishima, Haruhiko; Hashimoto, Naoya; Yoshimine, Toshiki

    2010-02-01

    Diffusion tensor imaging (DTI) by magnetic resonance imaging (MRI) is now used not only for delineating white matter fiber tracts, but also for assessing the histological characteristics of pathological tissues. Among these uses, predicting the extent or existence of tumor cell invasion into white matter by DTI is under extensive investigation. The previously reported tumor infiltration index (TII) holds great potential for the discrimination of pure vasogenic edema from tumor-infiltrated edema. However, conflicting data are being reported questioning the clinical value of TII. The present investigation reevaluated the utility of TII in patients with meningioma or glioma. We found that TII was unable to discriminate vasogenic from tumor-infiltrated edema. Conversely, detailed voxel-by-voxel comparison of TII and (11)C-methionie PET in the T2-hyperintense area of gliomas showed that TII and (11)C-methionie PET has a positive correlation, suggesting that, although TII is unable to discriminate the cause of edema, the extent of tumor cell invasion into white matter is depicted in gliomas by TII. These data suggest that TII involves both vasogenic and tumor-infiltrated factors, rather than only a single factor. A more intensive investigation is required to reach a complete understanding of TII.

  17. Macular edema in branch retinal vein occlusion: types and treatment.

    PubMed

    Jalkh, A E; Trempe, C L

    1989-01-01

    In this study of branch retinal vein occlusion, we distinguished between cystoid macular edema caused by increased capillary pressure and noncystoid edema due to hard exudates in the macula caused by chronic leakage from vascular abnormalities in the posterior pole or midperiphery. We performed laser photocoagulation in 51 eyes with cystoid macular edema to achieve focal narrowing of the retinal arterioles perfusing the macular area affected by the cystoid edema; good anatomic and functional results were achieved in 40 of these eyes (78%). In 25 of the five eyes, the treated segment of the retinal arteriole was outside the area of macular edema; results were successful in 19 of these eyes (76%). In 14 eyes with noncystoid exudative macular edema, we performed laser photocoagulation to the vascular abnormalities; good anatomic and functional results were obtained in 12 of these (86%). PMID:2927879

  18. Pneumocystis murina infection and cigarette smoke exposure interact to cause increased organism burden, development of airspace enlargement, and pulmonary inflammation in mice.

    PubMed

    Christensen, Paul J; Preston, Angela M; Ling, Tony; Du, Ming; Fields, W Bradley; Curtis, Jeffrey L; Beck, James M

    2008-08-01

    Chronic obstructive pulmonary disease (COPD) is characterized by the presence of airflow obstruction and lung destruction with airspace enlargement. In addition to cigarette smoking, respiratory pathogens play a role in pathogenesis, but specific organisms are not always identified. Recent reports demonstrate associations between the detection of Pneumocystis jirovecii DNA in lung specimens or respiratory secretions and the presence of emphysema in COPD patients. Additionally, human immunodeficiency virus-infected individuals who smoke cigarettes develop early emphysema, but a role for P. jirovecii in pathogenesis remains speculative. We developed a new experimental model using immunocompetent mice to test the interaction of cigarette smoke exposure and environmentally acquired Pneumocystis murina infection in vivo. We hypothesized that cigarette smoke and P. murina would interact to cause increases in total lung capacity, airspace enlargement, and pulmonary inflammation. We found that exposure to cigarette smoke significantly increases the lung organism burden of P. murina. Pulmonary infection with P. murina, combined with cigarette smoke exposure, results in changes in pulmonary function and airspace enlargement characteristic of pulmonary emphysema. P. murina and cigarette smoke exposure interact to cause increased lung inflammatory cell accumulation. These findings establish a novel animal model system to explore the role of Pneumocystis species in the pathogenesis of COPD. PMID:18490462

  19. Pulmonary rehabilitation.

    PubMed

    Troosters, Thierry; Demeyer, Heleen; Hornikx, Miek; Camillo, Carlos Augusto; Janssens, Wim

    2014-03-01

    Pulmonary rehabilitation is a therapy that offers benefits to patients with chronic obstructive pulmonary disease that are complementary to those obtained by pharmacotherapy. The main objective of pulmonary rehabilitation is to restore muscle function and exercise tolerance, reverse other nonrespiratory consequences of the disease, and help patients to self-manage chronic obstructive pulmonary disease and its exacerbations and symptoms. To do so, a multidisciplinary program tailored to the patient in terms of program content, exercise prescription, and setting must be offered. Several settings and programs have shown to spin off in significant immediate results. The challenge lies in maintaining the benefits outside the program. PMID:24507849

  20. Chronic thromboembolic pulmonary hypertension: time for research in pathophysiology to catch up with developments in treatment

    PubMed Central

    Toshner*, Mark

    2014-01-01

    The modern treatment era in chronic thromboembolic disease has seen significant advances in both surgical and medical treatment. One such treatment, the pulmonary endarterectomy (where established chronic organized thrombus is removed), has dramatically affected morbidity and mortality. These advances have outstripped basic research into the causes and pathophysiology of disease, which remain largely poorly understood. In this review, we will set out to explain some of the historical reasons for this, including the difficulties inherent in human studies and the lack of good animal models. We will review some of the recent advances in pathophysiology from registries and translational research, and we will summarize the treatment options, with some discussion of very recently published work, including medical and surgical treatments, both traditional and more experimental work in non-invasive techniques. PMID:24991415

  1. Early Macrophage Recruitment and Alternative Activation Are Critical for the Later Development of Hypoxia-induced Pulmonary Hypertension

    PubMed Central

    Vergadi, Eleni; Chang, Mun Seog; Lee, Changjin; Liang, Olin; Liu, Xianlan; Fernandez-Gonzalez, Angeles; Mitsialis, S. Alex; Kourembanas, Stella

    2011-01-01

    Background Lung inflammation precedes the development of hypoxia-induced pulmonary hypertension (HPH); however its role in the pathogenesis of HPH is poorly understood. We sought to characterize the hypoxic inflammatory response and elucidate its role in the development of HPH. We also aimed to investigate the mechanisms by which heme oxygenase-1 (HO-1), an anti-inflammatory enzyme, is protective in HPH. Methods and Results We generated bitransgenic mice that overexpress human HO-1 under doxycycline (dox) control in an inducible, lung-specific manner. Hypoxic exposure of mice in the absence of dox resulted in early transient accumulation of monocytes/macrophages in the bronchoalveolar lavage. Alveolar macrophages acquired an alternatively activated phenotype (M2) in response to hypoxia, characterized by the expression of Found in Inflammatory Zone-1, Arginase-1 and Chitinase-3-like-3. A brief, two-day pulse of dox delayed but did not prevent the peak of hypoxic inflammation, and could not protect from HPH. In contrast, a seven-day dox treatment sustained high HO-1 levels during the entire period of hypoxic inflammation, inhibited macrophage accumulation and activation, induced macrophage IL-10 expression, and prevented the development of HPH. Supernatants from hypoxic M2 macrophages promoted proliferation of pulmonary artery smooth muscle cells while treatment with carbon monoxide, a HO-1 enzymatic product, abrogated this effect. Conclusions Early recruitment and alternative activation of macrophages in hypoxic lungs is critical for the later development of HPH. HO-1 may confer protection from HPH by effectively modifing macrophage activation state in hypoxia. PMID:21518986

  2. Observational study of subclinical diabetic macular edema

    PubMed Central

    Bressler, N M; Miller, K M; Beck, R W; Bressler, S B; Glassman, A R; Kitchens, J W; Melia, M; Schlossman, D K

    2012-01-01

    Purpose To determine the rate of progression of eyes with subclinical diabetic macular edema (DME) to clinically apparent DME or DME necessitating treatment during a 2-year period. Methods In all, 43 eyes from 39 study participants with subclinical DME, defined as absence of foveal center edema as determined with slit lamp biomicroscopy but a center point thickness (CPT) between 225 and 299 μm on time domain (Stratus, Carl Zeiss Meditec) optical coherence tomography (OCT) scan, were enrolled from 891 eyes of 582 subjects screened. Eyes were evaluated annually for up to 2 years for the primary outcome, which was an increase in OCT CPT of at least 50 μm from baseline and a CPT of at least 300 μm, or treatment for DME (performed at the discretion of the investigator). Results The cumulative probability of meeting an increase in OCT CPT of at least 50 μm from baseline and a CPT of at least 300 μm, or treatment for DME was 27% (95% confidence interval (CI): 14%, 38%) by 1 year and 38% (95% CI: 23%, 50%) by 2 years. Conclusions Although subclinical DME may be uncommon, this study suggests that between approximately one-quarter and one-half of eyes with subclinical DME will progress to more definite thickening or be judged to need treatment for DME within 2 years after its identification. PMID:22441027

  3. CARDIOVASCULAR AND BLOOD COAGULATION EFFECTS OF PULMONARY ZINC EXPOSURE

    EPA Science Inventory

    Cardiovascular damage induced by pulmonary exposure to environmental chemicals can result from direct action or, secondarily, from pulmonary injury. We have developed a rat model of pulmonary exposure to zinc to demonstrate cardiac, coagulative, and fibrinolytic alterations. Mal...

  4. [Effect of prostaglandin synthesis inhibitors of diabetic cystoid macular edema].

    PubMed

    Kieselbach, G; Juen, S

    1990-01-01

    In most cases, diabetic macular edema is treated successfully with central laser photocoagulation. However, only few studies report such favorable results in cystoid macular edema, which has a poor visual prognosis. In the present prospective study on diabetics with cystoid macular edema, aged less than 40 years, a better visual outcome was obtained in patients treated with prostaglandin synthesis inhibitors than in an untreated group. PMID:2345629

  5. The Presence of Chronic Mucus Hypersecretion across Adult Life in Relation to Chronic Obstructive Pulmonary Disease Development

    PubMed Central

    Shaheen, Seif O.

    2016-01-01

    Rationale: Chronic mucus hypersecretion (CMH) is common among smokers and is associated with chronic obstructive pulmonary disease development and progression. Objectives: To understand how the relationships between smoking, CMH, and chronic obstructive pulmonary disease develop during adult life, and facilitate earlier disease detection and intervention. Methods: We analyzed data on CMH, smoking, and lung function prospectively collected by the Medical Research Council National Survey of Health and Development, a nationally representative British cohort followed since birth in 1946. We analyzed the longitudinal relationships between smoking and CMH, how symptoms during life related to airflow limitation at 60–64 years, and how CMH duration between ages 43 and 60–64 years related to concurrent FEV1 decline. Measurements and Main Results: From 5,362 individuals enrolled at birth, 4,427 contributed data between ages 20 and 64 years (52% male; 63% ever-smoker). Among smokers CMH prevalence escalated between ages 36 and 43 from 7.6 ± 2.0% to 13.0 ± 2.6%. At these ages, symptoms were associated with a higher risk of subsequent airflow limitation (odds ratio [95% confidence interval], 3.70 [1.62–8.45] and 4.11 [1.85–9.13], respectively). Across adult life, CMH followed a dynamic remitting–relapsing course. Symptom prevalence following smoking cessation returned to levels seen among never-smokers. The longer CMH was present across three occasions (ages 43, 53, and 60–64 yr), the greater the concurrent FEV1 decline, corresponding to an additional decrement of 3.6 ± 2.5 ml/yr per occasion that CMH was present (P = 0.005). Conclusions: CMH among middle-aged smokers represents an early developmental phase of chronic obstructive pulmonary disease. Smoking-related CMH usually resolves following smoking cessation but the longer its duration the greater the FEV1 lost, suggesting the course of CMH across adult life may reflect the underlying course

  6. Cerebral edema following iodine-131 therapy for thyroid carcinoma metastatic to the brain

    SciTech Connect

    Datz, F.L.

    1986-05-01

    Brain metastases are rare in well-differentiated thyroid carcinoma but when present they can lead to the patient's death. Iodine-131 therapy for intracerebral thyroid carcinoma metastases causes radiation-induced acute cerebral edema that can lead to CNS complications and even death. We present a case in which a patient with intracerebral /sup 131/I uptake developed seizures, slurred speech, and muscle weakness 12 hr following /sup 131/I therapy. The patient's CT scan, post-therapy, confirmed an intracranial metastasis with a significant amount of surrounding edema. Radiotherapists, when using external beam radiation to treat intracerebral metastases, commonly place these patients on steroids, glycerol, or mannitol prior to instituting therapy, to prevent complications from radiation-induced cerebral edema. This technique could be applied to /sup 131/I therapy of intracranial thyroid carcinoma metastases as well.

  7. A Descriptive Study of the Temporal Patterns of Volume and Contents Change in Human Acute Burn Edema: Application in Evidence-Based Intervention and Research Design.

    PubMed

    Edgar, Dale W; Fear, Mark; Wood, Fiona M

    2016-01-01

    Edema after burn contributes significantly to burn wound depth conversion. In humans after burn injury, there is a lack of detailed understanding of the contents and temporal changes in volume of acute tissue edema. The novel findings of these studies relate to the collection of edema fluid after partial-thickness burn injury. Edema volume peaks on day 1 after burn without formal fluid resuscitation. The studies indicated that the peak was on day 2 for a resuscitated burn. In contrast, animal studies suggest that the peak of edema occurs by or before day 1 after injury. The findings confirm the pitfalls of evidence derived from animal models and assuming direct transference to humans. Postburn edema was demonstrated to be a high-protein fluid (ie, ≥10 g/L) for the duration of the inflammatory period. The presence of high-protein edema presents greater challenges to clinicians developing novel treatment options. The rate of volume change over time tapered to insignificant levels after day 4 following burn. Greater than 98% of the edema contents was fluid. However, the size of particulate matter did not preclude it passing through patent lymphatic collectors. The results indicate a necessity for urgent postburn intervention, which should incorporate the active stimulation of the lymphatic system to improve efficacy of edema removal.

  8. A Descriptive Study of the Temporal Patterns of Volume and Contents Change in Human Acute Burn Edema: Application in Evidence-Based Intervention and Research Design.

    PubMed

    Edgar, Dale W; Fear, Mark; Wood, Fiona M

    2016-01-01

    Edema after burn contributes significantly to burn wound depth conversion. In humans after burn injury, there is a lack of detailed understanding of the contents and temporal changes in volume of acute tissue edema. The novel findings of these studies relate to the collection of edema fluid after partial-thickness burn injury. Edema volume peaks on day 1 after burn without formal fluid resuscitation. The studies indicated that the peak was on day 2 for a resuscitated burn. In contrast, animal studies suggest that the peak of edema occurs by or before day 1 after injury. The findings confirm the pitfalls of evidence derived from animal models and assuming direct transference to humans. Postburn edema was demonstrated to be a high-protein fluid (ie, ≥10 g/L) for the duration of the inflammatory period. The presence of high-protein edema presents greater challenges to clinicians developing novel treatment options. The rate of volume change over time tapered to insignificant levels after day 4 following burn. Greater than 98% of the edema contents was fluid. However, the size of particulate matter did not preclude it passing through patent lymphatic collectors. The results indicate a necessity for urgent postburn intervention, which should incorporate the active stimulation of the lymphatic system to improve efficacy of edema removal. PMID:27322367

  9. Life-threatening Cerebral Edema Caused by Acute Occlusion of a Superior Vena Cava Stent

    SciTech Connect

    Sofue, Keitaro Takeuchi, Yoshito Arai, Yasuaki; Sugimura, Kazuro

    2013-02-15

    A71-year-old man with advanced lung cancer developed a life-threatening cerebral edema caused by the acute occlusion of a superior vena cava (SVC) stent and was successfully treated by an additional stent placement. Although stent occlusion is a common early complication, no life-threatening situations have been reported until now. Our experience highlights the fact that acute stent occlusion can potentially lead to the complete venous shutdown of the SVC, resulting in life-threatening cerebral edema, after SVC stent placement. Immediate diagnosis and countermeasures are required.

  10. A Ruptured Basilar Tip Aneurysm Showing Repeated Perianeurysmal Edema after Endovascular Coil Embolization: Case Report

    PubMed Central

    TAKESHITA, Tomonori; HORIE, Nobutaka; FUKUDA, Yutaka; SO, Gohei; HAYASHI, Kentaro; MORIKAWA, Minoru; SUYAMA, Kazuhiko; NAGATA, Izumi

    The authors present an extremely rare case of a 48-year-old female who developed repeated perianeurysmal edema at 2, 9, and 16 weeks after endovascular coil embolization for the ruptured intracranial aneurysm. Interestingly, the mechanism for this edema could be different at each time point in this case; acute thrombosis formation, chemical inflammation, and aneurysm recanalization. We have to be aware of this potential complication in the long term after endovascular coil embolization for the intracranial aneurysm, especially with large size or buried into the brain parenchyma. The clinical implications of this case are discussed with a review of the literature. PMID:24390180

  11. Vascular Remodeling in Pulmonary Hypertension

    PubMed Central

    Shimoda, Larissa A; Laurie, Steven S.

    2013-01-01

    Pulmonary hypertension is a complex, progressive condition arising from a variety of genetic and pathogenic causes. Patients present with a spectrum of histologic and pathophysiological features, likely reflecting the diversity in underlying pathogenesis. It is widely recognized that structural alterations in the vascular wall contribute to all forms of pulmonary hypertension. Features characteristic of the remodeled vasculature in patients with pulmonary hypertension include increased stiffening of the elastic proximal pulmonary arteries, thickening of the intimal and/or medial layer of muscular arteries, development of vaso-occlusive lesions and the appearance of cells expressing smooth muscle specific markers in normally non-muscular small diameter vessels, resulting from proliferation and migration of pulmonary arterial smooth muscle cells and cellular trans-differentiation. The development of several animal models of pulmonary hypertension has provided the means to explore the mechanistic underpinnings of pulmonary vascular remodeling, although none of the experimental models currently used entirely replicates the pulmonary arterial hypertension observed in patients. Herein, we provide an overview of the histological abnormalities observed in humans with pulmonary hypertension and in preclinical models and discuss insights gained regarding several key signaling pathways contributing to the remodeling process. In particular, we will focus on the roles of ion homeostasis, endothelin-1, serotonin, bone morphogenetic proteins, Rho kinase and hypoxia-inducible factor 1 in pulmonary arterial smooth muscle and endothelial cells, highlighting areas of cross-talk between these pathways and potentials for therapeutic targeting. PMID:23334338

  12. Telmisartan reduced cerebral edema by inhibiting NLRP3 inflammasome in mice with cold brain injury.

    PubMed

    Wei, Xin; Hu, Chen-Chen; Zhang, Ya-Li; Yao, Shang-Long; Mao, Wei-Ke

    2016-08-01

    The aim of this study was to investigate the possible beneficial role of telmisartan in cerebral edema after traumatic brain injury (TBI) and the potential mechanisms related to the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) pyrin domain-containing 3 (NLRP3) inflammasome activation. TBI model was established by cold-induced brain injury. Male C57BL/6 mice were randomly assigned into 3, 6, 12, 24, 48 and 72 h survival groups to investigate cerebral edema development with time and received 0, 5, 10, 20 and 40 mg/kg telmisartan by oral gavage, 1 h prior to TBI to determine the efficient anti-edemic dose. The therapeutic window was identified by post-treating 30 min, 1 h, 2 h and 4 h after TBI. Blood-brain barrier (BBB) integrity, the neurological function and histological injury were assessed, at the same time, the mRNA and protein expression levels of NLRP3 inflammasome, IL-1β and IL-18 concentrations in peri-contused brain tissue were measured 24 h post TBI. The results showed that the traumatic cerebral edema occurred from 6 h, reached the peak at 24 h and recovered to the baseline 72 h after TBI. A single oral dose of 5, 10 and 20 mg/kg telmisartan could reduce cerebral edema. Post-treatment up to 2 h effectively limited the edema development. Furthermore, prophylactic administration of telmisartan markedly inhibited BBB impairment, NLRP3, apoptotic speck-containing protein (ASC) and Caspase-1 activation, as well as IL-1β and IL-18 maturation, subsequently improved the neurological outcomes. In conclusion, telmisartan can reduce traumatic cerebral edema by inhibiting the NLRP3 inflammasome-regulated IL-1β and IL-18 accumulation. PMID:27465336

  13. [A CASE OF PULMONARY MYCOBACTERIUM ABSCESSUS INFECTION THAT DEVELOPED DURING IMMUNOSUPPRESSIVE THERAPY FOR MYASTHENIA GRAVIS WITH RECURRENT THYMOMA].

    PubMed

    Matsuse, Hiroto; Oshio, Takeshi; Kishimoto, Kumiko; Nakayama, Haruo

    2016-02-01

    A 58-year-old man developed cough, sputum, and low-grade fever during immunosuppressive treatment with corticosteroids and cyclosporine for myasthenia gravis with recurrent thymoma. Since chest CT revealed diffuse nodular opacities in both lung fields, he was referred to our department. Mycobacterium abscessus was repeatedly cultured from his sputum, and he was diagnosed with pulmonary M. abscessus infection. Although both chest radiological findings and clinical symptoms were mild, he required treatment with immunosuppressive agents and systemic anesthesia for resection of the recurrent thymoma. Based on complications and according to the patient's preference, oral treatment with clarithromycin 600 mg/day, levofloxacin 500 mg/day, and faropenem 600 mg/day was initiated on an outpatient basis. Following these treatments, his chest CT findings and clinical symptoms subsided, and the thymoma was successfully resected. Our experience with the present case suggests a possible treatment strategy for M. abscessus infection in immunocompromised and complicated cases. PMID:27263226

  14. [A CASE OF PULMONARY MYCOBACTERIUM ABSCESSUS INFECTION THAT DEVELOPED DURING IMMUNOSUPPRESSIVE THERAPY FOR MYASTHENIA GRAVIS WITH RECURRENT THYMOMA].

    PubMed

    Matsuse, Hiroto; Oshio, Takeshi; Kishimoto, Kumiko; Nakayama, Haruo

    2016-02-01

    A 58-year-old man developed cough, sputum, and low-grade fever during immunosuppressive treatment with corticosteroids and cyclosporine for myasthenia gravis with recurrent thymoma. Since chest CT revealed diffuse nodular opacities in both lung fields, he was referred to our department. Mycobacterium abscessus was repeatedly cultured from his sputum, and he was diagnosed with pulmonary M. abscessus infection. Although both chest radiological findings and clinical symptoms were mild, he required treatment with immunosuppressive agents and systemic anesthesia for resection of the recurrent thymoma. Based on complications and according to the patient's preference, oral treatment with clarithromycin 600 mg/day, levofloxacin 500 mg/day, and faropenem 600 mg/day was initiated on an outpatient basis. Following these treatments, his chest CT findings and clinical symptoms subsided, and the thymoma was successfully resected. Our experience with the present case suggests a possible treatment strategy for M. abscessus infection in immunocompromised and complicated cases.

  15. Pulmonary extramedullary hematopoiesis involving the pulmonary artery.

    PubMed

    Monga, Varun; Silverman, Margarida

    2015-02-24

    Extramedullary hematopoiesis (EMH) occurs as a complication of hematologic disorders such as myelofibrosis, sickle cell anemia and thalassemia. The extramedullary tissue usually involves liver, spleen and lymph nodes, less frequently the chest. We present a recent case of a man with myeloproliferative neoplasm who developed pulmonary hemorrhage secondary to EMH in the lung and pulmonary artery. Radiation therapy was considered the best approach, but it didn't work and the patient died a week after radiation therapy was completed. We also review herein the present literature. PMID:25852851

  16. Update on corticosteroids for diabetic macular edema.

    PubMed

    Schwartz, Stephen G; Scott, Ingrid U; Stewart, Michael W; Flynn, Harry W

    2016-01-01

    Diabetic macular edema (DME) remains an important cause of visual loss. Although anti-vascular endothelial growth factor (VEGF) agents are generally used as first-line treatments for patients with center-involving DME, there is an important role for corticosteroids as well. Corticosteroids may be especially useful in pseudophakic patients poorly responsive to anti-VEGF therapies, in patients wishing to reduce the number of required injections, and in pregnant patients. Intravitreal triamcinolone acetonide has been used for many years but is not approved for this indication. An extended-release bioerodable dexamethasone delivery system and an extended-release nonbioerodable fluocinolone acetonide insert have both achieved regulatory approval for the treatment of DME. All intravitreal corticosteroids are associated with risks of cataract progression, elevation of intraocular pressure, and endophthalmitis. There is no current consensus regarding the use of corticosteroids, but they are valuable for selected patients with center-involving DME. PMID:27660409

  17. Update on corticosteroids for diabetic macular edema

    PubMed Central

    Schwartz, Stephen G; Scott, Ingrid U; Stewart, Michael W; Flynn, Harry W

    2016-01-01

    Diabetic macular edema (DME) remains an important cause of visual loss. Although anti-vascular endothelial growth factor (VEGF) agents are generally used as first-line treatments for patients with center-involving DME, there is an important role for corticosteroids as well. Corticosteroids may be especially useful in pseudophakic patients poorly responsive to anti-VEGF therapies, in patients wishing to reduce the number of required injections, and in pregnant patients. Intravitreal triamcinolone acetonide has been used for many years but is not approved for this indication. An extended-release bioerodable dexamethasone delivery system and an extended-release nonbioerodable fluocinolone acetonide insert have both achieved regulatory approval for the treatment of DME. All intravitreal corticosteroids are associated with risks of cataract progression, elevation of intraocular pressure, and endophthalmitis. There is no current consensus regarding the use of corticosteroids, but they are valuable for selected patients with center-involving DME. PMID:27660409

  18. Update on corticosteroids for diabetic macular edema

    PubMed Central

    Schwartz, Stephen G; Scott, Ingrid U; Stewart, Michael W; Flynn, Harry W

    2016-01-01

    Diabetic macular edema (DME) remains an important cause of visual loss. Although anti-vascular endothelial growth factor (VEGF) agents are generally used as first-line treatments for patients with center-involving DME, there is an important role for corticosteroids as well. Corticosteroids may be especially useful in pseudophakic patients poorly responsive to anti-VEGF therapies, in patients wishing to reduce the number of required injections, and in pregnant patients. Intravitreal triamcinolone acetonide has been used for many years but is not approved for this indication. An extended-release bioerodable dexamethasone delivery system and an extended-release nonbioerodable fluocinolone acetonide insert have both achieved regulatory approval for the treatment of DME. All intravitreal corticosteroids are associated with risks of cataract progression, elevation of intraocular pressure, and endophthalmitis. There is no current consensus regarding the use of corticosteroids, but they are valuable for selected patients with center-involving DME.

  19. Nonproliferative diabetic retinopathy and macular edema.

    PubMed

    Smith, S C

    1999-01-01

    As previously noted, although visual loss usually does not fall below 20/200 in the presence of ME, it may nevertheless be a significant disability. Additional interventions may include referral to low vision clinics, home health agencies, visual loss support groups, and local or regional blindness agencies to aid the patient's occupational rehabilitation, coping mechanisms, and adaptation responses in the presence of this potentially debilitating process. Control of blood sugar, blood pressure, and the intervention of focal/grid laser treatments to seal leaks and prevent further edema provide the best chance of maintaining useful vision throughout life. Patient education is paramount to improve comprehension of the condition, recommended treatment modalities, and compliance with prescribed regimens. Assessments and interventions related to knowledge and sensory deficits, anxiety, discomfort, ineffective coping mechanisms, and health maintenance behaviors add a quality link in the multidisciplinary approach surrounding the delivery of care to patients with NPDR and clinically significant ME. PMID:11907881

  20. Pseudophakic cystoid macular edema: update 2016

    PubMed Central

    Grzybowski, Andrzej; Sikorski, Bartosz L; Ascaso, Francisco J; Huerva, Valentín

    2016-01-01

    Pseudophakic cystoid macular edema (PCME) is the most common complication of cataract surgery, leading in some cases to a decrease in vision. Although the pathogenesis of PCME is not completely understood, the contribution of postsurgical inflammation is generally accepted. Consequently, anti-inflammatory medicines, including steroids and nonsteroidal anti-inflammatory drugs, have been postulated as having a role in both the prophylaxis and treatment of PCME. However, the lack of a uniformly accepted PCME definition, conflicting data on some risk factors, and the scarcity of studies comparing the role of nonsteroidal anti-inflammatory drugs to steroids in PCME prevention make the problem of PCME one of the puzzles of ophthalmology. This paper presents an updated review on the pathogenesis, risk factors, and use of anti-inflammatory drugs in PCME that reflect current research and practice.

  1. Pseudophakic cystoid macular edema: update 2016

    PubMed Central

    Grzybowski, Andrzej; Sikorski, Bartosz L; Ascaso, Francisco J; Huerva, Valentín

    2016-01-01

    Pseudophakic cystoid macular edema (PCME) is the most common complication of cataract surgery, leading in some cases to a decrease in vision. Although the pathogenesis of PCME is not completely understood, the contribution of postsurgical inflammation is generally accepted. Consequently, anti-inflammatory medicines, including steroids and nonsteroidal anti-inflammatory drugs, have been postulated as having a role in both the prophylaxis and treatment of PCME. However, the lack of a uniformly accepted PCME definition, conflicting data on some risk factors, and the scarcity of studies comparing the role of nonsteroidal anti-inflammatory drugs to steroids in PCME prevention make the problem of PCME one of the puzzles of ophthalmology. This paper presents an updated review on the pathogenesis, risk factors, and use of anti-inflammatory drugs in PCME that reflect current research and practice. PMID:27672316

  2. Heme oxygenase-1-mediated autophagy protects against pulmonary endothelial cell death and development of emphysema in cadmium-treated mice.

    PubMed

    Surolia, Ranu; Karki, Suman; Kim, Hyunki; Yu, Zhihong; Kulkarni, Tejaswini; Mirov, Sergey B; Carter, A Brent; Rowe, Steven M; Matalon, Sadis; Thannickal, Victor J; Agarwal, Anupam; Antony, Veena B

    2015-08-01

    Pulmonary exposure to cadmium, a major component of cigarette smoke, has a dramatic impact on lung function and the development of emphysema. Cigarette smoke exposure induces heme oxygenase-1 (HO-1), a cytoprotective enzyme. In this study, we employed a truncated mouse model of emphysema by intratracheal instillation of cadmium (CdCl2) solution (0.025% per 1 mg/kg body wt) in HO-1(+/+), HO-1(-/-), and overexpressing humanized HO-1 bacterial artificial chromosome (hHO-1BAC) mice. We evaluated the role of HO-1 in cadmium-induced emphysema in mice by analyzing histopathology, micro-computed tomography scans, and lung function tests. CdCl2-exposed HO-1(-/-) mice exhibited more severe emphysema compared with HO-1(+/+) or hHO-1BAC mice. Loss of pulmonary endothelial cells (PECs) from the alveolar capillary membrane is recognized to be a target in emphysema. PECs from HO-1(+/+), HO-1(-/-), and hHO-1BAC were employed to define the underlying molecular mechanism for the protection from emphysema by HO-1. Electron microscopy, expression of autophagic markers (microtubule-associated protein 1B-light chain 3 II, autophagy protein 5, and Beclin1) and apoptotic marker (cleaved caspase 3) suggested induction of autophagy and apoptosis in PECs after CdCl2 treatment. CdCl2-treated HO-1(-/-) PECs exhibited downregulation of autophagic markers and significantly increased cleaved caspase 3 expression and activity (∼4-fold higher). Moreover, hHO-1BAC PECs demonstrated upregulated autophagy and absence of cleaved caspase 3 expression or activity. Pretreatment of HO-1(+/+) PECs with rapamycin induced autophagy and resulted in reduced cell death upon cadmium treatment. Induction of autophagy following CdCl2 treatment was found to be protective from apoptotic cell death. HO-1 induced protective autophagy in PECs and mitigated cadmium-induced emphysema.

  3. Heme oxygenase-1-mediated autophagy protects against pulmonary endothelial cell death and development of emphysema in cadmium-treated mice

    PubMed Central

    Surolia, Ranu; Karki, Suman; Kim, Hyunki; Yu, Zhihong; Kulkarni, Tejaswini; Mirov, Sergey B.; Carter, A. Brent; Rowe, Steven M.; Matalon, Sadis; Thannickal, Victor J.; Agarwal, Anupam

    2015-01-01

    Pulmonary exposure to cadmium, a major component of cigarette smoke, has a dramatic impact on lung function and the development of emphysema. Cigarette smoke exposure induces heme oxygenase-1 (HO-1), a cytoprotective enzyme. In this study, we employed a truncated mouse model of emphysema by intratracheal instillation of cadmium (CdCl2) solution (0.025% per 1 mg/kg body wt) in HO-1+/+, HO-1−/−, and overexpressing humanized HO-1 bacterial artificial chromosome (hHO-1BAC) mice. We evaluated the role of HO-1 in cadmium-induced emphysema in mice by analyzing histopathology, micro-computed tomography scans, and lung function tests. CdCl2-exposed HO-1−/− mice exhibited more severe emphysema compared with HO-1+/+ or hHO-1BAC mice. Loss of pulmonary endothelial cells (PECs) from the alveolar capillary membrane is recognized to be a target in emphysema. PECs from HO-1+/+, HO-1−/−, and hHO-1BAC were employed to define the underlying molecular mechanism for the protection from emphysema by HO-1. Electron microscopy, expression of autophagic markers (microtubule-associated protein 1B-light chain 3 II, autophagy protein 5, and Beclin1) and apoptotic marker (cleaved caspase 3) suggested induction of autophagy and apoptosis in PECs after CdCl2 treatment. CdCl2-treated HO-1−/− PECs exhibited downregulation of autophagic markers and significantly increased cleaved caspase 3 expression and activity (∼4-fold higher). Moreover, hHO-1BAC PECs demonstrated upregulated autophagy and absence of cleaved caspase 3 expression or activity. Pretreatment of HO-1+/+ PECs with rapamycin induced autophagy and resulted in reduced cell death upon cadmium treatment. Induction of autophagy following CdCl2 treatment was found to be protective from apoptotic cell death. HO-1 induced protective autophagy in PECs and mitigated cadmium-induced emphysema. PMID:26071551

  4. Aflibercept for the treatment of diabetic macular edema.

    PubMed

    Harkins, Keegan A; Haschke, Mary; Do, Diana V

    2016-05-01

    Diabetic macular edema (DME) is an accumulation of fluid in the central retina, secondary to vascular-leakage from diabetic vascular damage. DME and other ophthalmic sequela of diabetes are the leading cause of blindness in 20 to 74-year-olds. The development of VEGF-inhibitors (anti-VEGF) has revolutionized DME treatment improving the clinician's ability to remove excess fluid from the macula, improving visual-acuity. Aflibercept is an anti-VEGF agent made of a recombinant fusion protein (consisting of VEGF receptors 1 and 2 extracellular domains) fused with the Fc-portion of human-IgG1, which binds both VEGF isoforms A and B, and placental growth factor. Phase III clinical trials and published scientific studies have demonstrated the efficacy of intravitreal aflibercept injection in the treatment of DME. PMID:26907516

  5. Drowning stars: Reassessing the role of astrocytes in brain edema

    PubMed Central

    Thrane, Alexander S.; Thrane, Vinita Rangroo; Nedergaard, Maiken

    2014-01-01

    Edema formation frequently complicates brain infarction, tumors and trauma. Despite the significant mortality of this condition, current treatment options are often ineffective or incompletely understood. Recent studies have revealed the existence of a brain-wide paravascular pathway for cerebrospinal (CSF) and interstitial fluid (ISF) exchange. The current review critically examines the contribution of this ‘glymphatic’ system to the main types of brain edema. We propose that in cytotoxic edema, energy depletion enhances glymphatic CSF influx, whilst suppressing ISF efflux. We also argue that paravascular inflammation or ‘paravasculitis’ plays a critical role in vasogenic edema. Finally, recent advances in diagnostic imaging of glymphatic function may hold the key to defining the edema profile of individual patients and thus enable more targeted therapy. PMID:25236348

  6. Dexamethasone intravitreal implant in the treatment of diabetic macular edema.

    PubMed

    Dugel, Pravin U; Bandello, Francesco; Loewenstein, Anat

    2015-01-01

    Diabetic macular edema (DME) resembles a chronic, low-grade inflammatory reaction, and is characterized by blood-retinal barrier (BRB) breakdown and retinal capillary leakage. Corticosteroids are of therapeutic benefit because of their anti-inflammatory, antiangiogenic, and BRB-stabilizing properties. Delivery modes include periocular and intravitreal (via pars plana) injection. To offset the short intravitreal half-life of corticosteroid solutions (~3 hours) and the need for frequent intravitreal injections, sustained-release intravitreal corticosteroid implants have been developed. Dexamethasone intravitreal implant provides retinal drug delivery for ≤6 months and recently has been approved for use in the treatment of DME. Pooled findings (n=1,048) from two large-scale, randomized Phase III trials indicated that dexamethasone intravitreal implant (0.35 mg and 0.7 mg) administered at ≥6-month intervals produced sustained improvements in best-corrected visual acuity (BCVA) and macular edema. Significantly more patients showed a ≥15-letter gain in BCVA at 3 years with dexamethasone intravitreal implant 0.35 mg and 0.7 mg than with sham injection (18.4% and 22.2% vs 12.0%). Anatomical assessments showed rapid and sustained reductions in macular edema and slowing of retinopathy progression. Phase II study findings suggest that dexamethasone intravitreal implant is effective in focal, cystoid, and diffuse DME, in vitrectomized eyes, and in combination with laser therapy. Ocular complications of dexamethasone intravitreal implant in Phase III trials included cataract-related events (66.0% in phakic patients), intraocular pressure elevation ≥25 mmHg (29.7%), conjunctival hemorrhage (23.5%), vitreous hemorrhage (10.0%), macular fibrosis (8.3%), conjunctival hyperemia (7.2%), eye pain (6.1%), vitreous detachment (5.8%), and dry eye (5.8%); injection-related complications (eg, retinal tear/detachment, vitreous loss, endophthalmitis) were infrequent (<2

  7. Pulmonary artery aneurysm in Behcet's disease: a case report.

    PubMed

    Kasikcioglu, Erdem; Akhan, Hulya; Cuhadaroglu, Caglar; Erkan, Feyza

    2004-05-01

    The pulmonary artery is the second most common site of arterial involvement in Behcet's disease. A 32-year-old man presented with bilateral ankle edema, abdominal discomfort, and hemoptysis. He had a history of recurrent oral and genital aphthous ulcerations for 1 year. The diagnosis of Behcet's disease was made on the basis of the criteria published by the International Study Group for Behcet's Disease. His chest X-ray revealed left hilar enlargement. A helical computed tomography (CT) scan showed a pulmonary aneurysm with intramural thrombosis in the left pulmonary artery and enlarged hepatic veins. Treatment with colchicine and cyclophosphamide was given for 24 months, and helical thoracic CT was performed again. Helical CT showed that the pulmonary aneurysm was reduced by treatment. Helical CT could be used in Behcet's disease for the diagnosis and follow-up of pulmonary involvement.

  8. Exposure to PM10 as a risk factor for the development of nasal obstruction and chronic obstructive pulmonary disease

    PubMed Central

    Sichletidis, Lazaros; Spyratos, Dionisios; Tsiotsios, Anastasios; Haidich, Anna-Bettina; Chloros, Diamantis; Ganidis, Ioannis; Michailidis, Dimitrios; Triantafyllou, Georgios; Kottakis, George; Melas, Dimitrios

    2014-01-01

    Objectives: To investigate whether air pollution is a potential risk factor for airways obstruction. Methods: A prospective cohort study (11.3±2.9 years) that took place in two areas (Eordea where concentration of PM10 was high and Grevena, Greece). We used the MRC questionnaire, spirometry, and anterior rhinomanometry at both visits. Results: Initially we examined 3046 subjects. After excluding chronic obstructive pulmonary disease (COPD) patients, we re-examined 872 subjects and 168 of them had developed COPD (Grevena: 24.3%, Eordea: 18.5%). Multivariable logistic regression analysis showed that the area of residence and thus exposure to air pollution was not a risk factor for the development of COPD (OR: 0.51, 95% CI: 0.18–1.46, P = 0.21). On the other hand, residence in Eordea was strongly related to the development of severe nasal obstruction (OR: 11.47, 95% CI: 6.15–21.40, P<0.001). Similar results were found after excluding patients with COPD stage I as well as in the subgroup of never smokers. Conclusion: Air pollution was associated with severe nasal obstruction but not with COPD development. PMID:24804336

  9. Endothelial HIF signaling regulates pulmonary fibrosis-associated pulmonary hypertension.

    PubMed

    Bryant, Andrew J; Carrick, Ryan P; McConaha, Melinda E; Jones, Brittany R; Shay, Sheila D; Moore, Christy S; Blackwell, Thomas R; Gladson, Santhi; Penner, Niki L; Burman, Ankita; Tanjore, Harikrishna; Hemnes, Anna R; Karwandyar, Ayub K; Polosukhin, Vasiliy V; Talati, Megha A; Dong, Hui-Jia; Gleaves, Linda A; Carrier, Erica J; Gaskill, Christa; Scott, Edward W; Majka, Susan M; Fessel, Joshua P; Haase, Volker H; West, James D; Blackwell, Timothy S; Lawson, William E

    2016-02-01

    Pulmonary hypertension (PH) complicating chronic parenchymal lung disease, such as idiopathic pulmonary fibrosis, results in significant morbidity and mortality. Since the hypoxia-inducible factor (HIF) signaling pathway is important for development of pulmonary hypertension in chronic hypoxia, we investigated whether HIF signaling in vascular endothelium regulates development of PH related to pulmonary fibrosis. We generated a transgenic model in which HIF is deleted within vascular endothelial cells and then exposed these mice to chronic intraperitoneal bleomycin to induce PH associated with lung fibrosis. Although no differences in the degree of fibrotic remodeling were observed, we found that endothelial HIF-deficient mice were protected against development of PH, including right ventricle and pulmonary vessel remodeling. Similarly, endothelial HIF-deficient mice were protected from PH after a 4-wk exposure to normobaric hypoxia. In vitro studies of pulmonary vascular endothelial cells isolated from the HIF-targeted mice and controls revealed that endothelial HIF signaling increases endothelial cell expression of connective tissue growth factor, enhances vascular permeability, and promotes pulmonary artery smooth muscle cell proliferation and wound healing ability, all of which have the potential to impact the development of PH in vivo. Taken together, these studies demonstrate that vascular endothelial cell HIF signaling is necessary for development of hypoxia and pulmonary fibrosis associated PH. As such, HIF and HIF-regulated targets represent a therapeutic target in these conditions.

  10. Macular Edema After Cataract Surgery In Eyes Without Pre-operative Central-involved Diabetic Macular Edema

    PubMed Central

    Baker, Carl W.; Almukhtar, Talat; Bressler, Neil M.; Glassman, Adam R.; Grover, Sandeep; Kim, Stephen J.; Murtha, Timothy J.; Rauser, Michael E.; Stockdale, Cynthia

    2014-01-01

    Objective To estimate the incidence of central-involved macular edema (ME)16 weeks following cataract surgery in eyes with diabetic retinopathy (DR) without definite central-involved diabetic macular edema (DME) preoperatively. Methods In a multicenter, prospective, observational study, participants (N = 293) with DR without definite OCT central subfield (CSF) thickening underwent cataract surgery. The primary outcome was development of central-involved ME defined as; (1) OCT CSF thickness ≥ 250μm (time domain) or ≥ 310μm (spectral domain) with ≥1 step increase in logOCT CSF thickness pre-operative to the 16-week visit; (2) ≥2-step increase in logOCT CSF pre-operative to 16-week visit; or (3) non-topical treatment for ME received before the 16-week visit with either of the OCT criteria met at the time of treatment. Results Median participant age was 64 years with median visual acuity letter score of 69 (Snellen equivalent 20/40). Forty-four percent of eyes had history of prior treatment for DME. Sixteen weeks postoperatively, central-involved ME was noted in 0% (95%CI: 0-20%) of 17 eyes with no pre-operative DME. Of eyes with non-central involved DME, 10% (95%CI: 5-18%) of 97 eyes without central involved DME and 12% (95%CI: 7-19%) of 147 eyes with possible central involved DME at baseline progressed to central-involved ME. History of DME treatment was significantly associated with central-involved ME development (P<0.001). Conclusion In eyes with DR without concurrent central-involved DME, presence of non-central DME immediately prior to cataract surgery, or history of DME treatment, may increase risk of developing central-involved ME 16 weeks after cataract extraction. PMID:23599174

  11. Direct effects of nitroprusside do not alter gas exchange in canine oleic acid edema.

    PubMed

    Angle, M; Ducas, J; Schick, U; Girling, L; Prewitt, R M

    1984-11-01

    The authors investigated why intrapulmonary shunt (QS/QT) increases with sodium nitroprusside (SNP) in canine oleic acid pulmonary edema. To determine the effects of flow alone on QS/QT, a peripheral arteriovenous fistula with a variable resistor was employed to increase cardiac output (Q) 26 and 52% above base line in a stepwise fashion (P less than 0.01). To examine the direct effects of SNP, distinct from changes in flow, the drug was given to produce matched increments in Q in each dog (P less than 0.01). To control for time, base-line measurements were obtained before and after each intervention, the sequence of which was alternated. At each increment in Q, SNP and the arteriovenous fistula increased QS/QT a similar amount. The mixed venous O2 tension (P-vO2) followed Q similarly in each group. Pulmonary vascular resistance (PVR) fell more (P less than 0.01) with SNP than with the arteriovenous fistula at identical Q and P-vO2. The authors conclude that, in this model, a direct pharmacological effect of SNP does not contribute to the deterioration in QS/QT. In fact, SNP exerts a pulmonary vasoactive effect that does not adversely affect gas exchange. PMID:6520043

  12. Post splenectomy related pulmonary hypertension

    PubMed Central

    Palkar, Atul V; Agrawal, Abhinav; Verma, Sameer; Iftikhar, Asma; Miller, Edmund J; Talwar, Arunabh

    2015-01-01

    Splenectomy predisposes patients to a slew of infectious and non-infectious complications including pulmonary vascular disease. Patients are at increased risk for venous thromboembolic events due to various mechanisms that may lead to chronic thromboembolic pulmonary hypertension (CTEPH). The development of CTEPH and pulmonary vasculopathy after splenectomy involves complex pathophysiologic mechanisms, some of which remain unclear. This review attempts congregate the current evidence behind our understanding about the etio-pathogenesis of pulmonary vascular disease related to splenectomy and highlight the controversies that surround its management. PMID:26949600

  13. Imaging of congenital pulmonary malformations.

    PubMed

    Praticò, Francesco Emanuele; Corrado, Michele; Della Casa, Giovanni; Parziale, Raffaele; Russo, Giuseppe; Gazzani, Silvia Eleonora; Rossi, Enrica; Borgia, Daniele; Mostardi, Maurizio; Bacchini, Emanuele; Cella, Simone; De Filippo, Massimo

    2016-01-01

    Congenital pulmonary malformations represent a broad spectrum of anomalies that may result in varied clinical and pathologic pictures, ranging from recurrent pulmonary infections and acute respiratory distress syndrome, which require timely drug therapy, up to large space-occupying lesions needing surgical treatment. This classification includes three distinct anatomical and pathological entities, represented by Congenital Cystic Adenomatoid Malformation, Bronchopulmonary Sequestration and Congenital Lobar Emphysema. The final result in terms of embryological and fetal development of these alterations is a Congenital Lung Hypoplasia. Since even Bronchial Atresia, Pulmonary Bronchogenic Cysts and Congenital Diaphragmatic Hernias are due to Pulmonary Hypoplasia, these diseases will be discussed in this review (1, 2). PMID:27467867

  14. Segmentation of tumor and edema along with healthy tissues of brain using wavelets and neural networks.

    PubMed

    Demirhan, Ayşe; Toru, Mustafa; Guler, Inan

    2015-07-01

    Robust brain magnetic resonance (MR) segmentation algorithms are critical to analyze tissues and diagnose tumor and edema in a quantitative way. In this study, we present a new tissue segmentation algorithm that segments brain MR images into tumor, edema, white matter (WM), gray matter (GM), and cerebrospinal fluid (CSF). The detection of the healthy tissues is performed simultaneously with the diseased tissues because examining the change caused by the spread of tumor and edema on healthy tissues is very important for treatment planning. We used T1, T2, and FLAIR MR images of 20 subjects suffering from glial tumor. We developed an algorithm for stripping the skull before the segmentation process. The segmentation is performed using self-organizing map (SOM) that is trained with unsupervised learning algorithm and fine-tuned with learning vector quantization (LVQ). Unlike other studies, we developed an algorithm for clustering the SOM instead of using an additional network. Input feature vector is constructed with the features obtained from stationary wavelet transform (SWT) coefficients. The results showed that average dice similarity indexes are 91% for WM, 87% for GM, 96% for CSF, 61% for tumor, and 77% for edema.

  15. Pulmonary hypertension

    MedlinePlus

    ... that damage the lungs, such as scleroderma and rheumatoid arthritis Birth defects of the heart Blood clots in the lung ( pulmonary embolism ) Heart failure Heart valve disease HIV infection Low oxygen levels in the blood ...

  16. Pulmonary aspergilloma

    MedlinePlus

    ... Coccidioidomycosis Cystic fibrosis Histoplasmosis Lung abscess Lung cancer Sarcoidosis See also: Aspergillosis Symptoms You may not have ... fibrosis Histoplasmosis Lung cancer - small cell Pulmonary tuberculosis Sarcoidosis Update Date 8/31/2014 Updated by: Jatin ...

  17. Secretory leukocyte protease inhibitor gene deletion alters bleomycin-induced lung injury, but not development of pulmonary fibrosis

    PubMed Central

    Habgood, Anthony N; Tatler, Amanda L; Porte, Joanne; Wahl, Sharon M; Laurent, Geoffrey J; John, Alison E; Johnson, Simon R; Jenkins, Gisli

    2016-01-01

    Idiopathic Pulmonary Fibrosis (IPF) is a progressive, fatal disease with limited treatment options. Protease mediated transforming growth factor-β (TGF-β) activation has been proposed as a pathogenic mechanism of lung fibrosis. Protease activity in the lung is tightly regulated by protease inhibitors, particularly secretory leukocyte protease inhibitor (SLPI). The bleomycin model of lung fibrosis was used to determine the effect of increased protease activity in the lungs of Slpi−/− mice following injury. Slpi−/−, and wild-type, mice received oropharyngeal administration of bleomycin (30 IU) and the development of pulmonary fibrosis was assessed. Pro and active forms of matrix metalloproteinase-2 (MMP-2) and MMP-9 were measured. Lung fibrosis was determined by collagen subtype specific gene expression, hydroxyproline concentration, and histological assessment. Alveolar TGF-β activation was measured using bronchoalveolar lavage cell pSmad2 levels and global TGF-β activity was assessed by pSmad2 immunohistochemistry. The active-MMP-9 to pro-MMP-9 ratio was significantly increased in Slpi−/− animals compared with wild-type animals, demonstrating enhanced metalloproteinase activity. Wild-type animals showed an increase in TGF-β activation following bleomycin, with a progressive and sustained increase in collagen type I, alpha 1 (Col1α1), III, alpha 1(Col3α1), IV, alpha 1(Col4α1) mRNA expression, and a significant increase in total lung collagen 28 days post-bleomycin. In contrast Slpi−/− mice showed no significant increase of alveolar TGF-β activity following bleomycin, above their already elevated levels, although global TGF-β activity did increase. Slpi−/− mice had impaired collagen gene expression but animals demonstrated minimal reduction in lung fibrosis compared with wild-type animals. These data suggest that enhanced proteolysis does not further enhance TGF-β activation, and inhibits sustained Col1α1, Col3α1 and Col4α1 gene

  18. Secretory leukocyte protease inhibitor gene deletion alters bleomycin-induced lung injury, but not development of pulmonary fibrosis.

    PubMed

    Habgood, Anthony N; Tatler, Amanda L; Porte, Joanne; Wahl, Sharon M; Laurent, Geoffrey J; John, Alison E; Johnson, Simon R; Jenkins, Gisli

    2016-06-01

    Idiopathic pulmonary fibrosis is a progressive, fatal disease with limited treatment options. Protease-mediated transforming growth factor-β (TGF-β) activation has been proposed as a pathogenic mechanism of lung fibrosis. Protease activity in the lung is tightly regulated by protease inhibitors, particularly secretory leukocyte protease inhibitor (SLPI). The bleomycin model of lung fibrosis was used to determine the effect of increased protease activity in the lungs of Slpi(-/-) mice following injury. Slpi(-/-), and wild-type, mice received oropharyngeal administration of bleomycin (30 IU) and the development of pulmonary fibrosis was assessed. Pro and active forms of matrix metalloproteinase (MMP)-2 and MMP-9 were measured. Lung fibrosis was determined by collagen subtype-specific gene expression, hydroxyproline concentration, and histological assessment. Alveolar TGF-β activation was measured using bronchoalveolar lavage cell pSmad2 levels and global TGF-β activity was assessed by pSmad2 immunohistochemistry. The active-MMP-9 to pro-MMP-9 ratio was significantly increased in Slpi(-/-) animals compared with wild-type animals, demonstrating enhanced metalloproteinase activity. Wild-type animals showed an increase in TGF-β activation following bleomycin, with a progressive and sustained increase in collagen type I, alpha 1 (Col1α1), III, alpha 1(Col3α1), IV, alpha 1(Col4α1) mRNA expression, and a significant increase in total lung collagen 28 days post bleomycin. In contrast Slpi(-/-) mice showed no significant increase of alveolar TGF-β activity following bleomycin, above their already elevated levels, although global TGF-β activity did increase. Slpi(-/-) mice had impaired collagen gene expression but animals demonstrated minimal reduction in lung fibrosis compared with wild-type animals. These data suggest that enhanced proteolysis does not further enhance TGF-β activation, and inhibits sustained Col1α1, Col3α1, and Col4α1 gene expression

  19. Estimating the effect of air pollution from a coal-fired power station on the development of children's pulmonary function

    SciTech Connect

    Dubnov, J.; Barchana, M.; Rishpon, S.; Leventhal, A.; Segal, I.; Carel, R.; Portnov, B.A.

    2007-01-15

    Using geographical information systems (GIS) tools, the present study analyzed the association between children's lung function development and their long-term exposure to air pollution. The study covered the cohort of 1492 schoolchildren living in the vicinity of a major coal-fired power station in the Hadera sub-district of Israel. In 1996 and 1999, the children underwent subsequent pulmonary function tests (PFT) (forced vital capacity (FVC) and forced expiratory volume during the first second (FEV1)), and the children's parents completed a detailed questionnaire on their health status and household characteristics. A negative association was found between changes in the results of PFT and the estimated individual levels of air pollution. A sensitivity test revealed a FEV1 decline from -4.3% for the average pollution level to -10.2% for the high air pollution level. The results of a sensitivity test for FVC were found to be similar. Association with the reported health status was found to be insignificant. As we conclude, air pollution from a coal-fired power station, although not exceeding local pollution standards, had a negative effect on children's lung function development. As argued, previous studies carried out in the region failed to show the above association because they were based on zone approaches that assign average concentration levels of air pollutants to all individuals in each zone, leading to a misclassification bias of individual exposure.

  20. Neuronal damage in pericontusional edema zone.

    PubMed

    Kushi, H; Saito, T; Makino, K; Hayashi, N

    2003-01-01

    In this study, we investigated the molecular biological and histopathological aspects of the etiological mechanisms for pericontusional edema zone (PEZ). The subjects were 5 patients with traumatic brain injury who underwent surgery to evacuate the resulting hematoma. The average age of the subjects was 52 +/- 27.5 years. The GCS at the time of admission was 5-9. At operation apart from evacuating the hematoma, the PEZ was also excised and then examined histopathologically. Cerebrospinal fluid (CSF) levels of IL-6, IL-8, and IL-10 were measured at the time of admission and at 24 and 72 hours. Histological examination revealed large numbers of neutrophils accumulating within blood vessels in the PEZ, with some focal migration. IL-6: CSF levels at the time of admission and at 24, 72, and 72 hours were 550, 4350, and 878000 pg/ml, respectively (median values). IL-8: CSF levels were 715, 804, and 24900 pg/ml, respectively. IL-10: CSF levels were 15, 4, and 5 pg/ml, respectively. High levels of IL-6 and IL-8 were seen from an early stage, and became markedly higher with enlargement of the PEZ. The PEZ is thought to be due to microvascular disturbance by neutrophils stimulated by inflammatory cytokines, and neuronal damage from migrated neutrophils. PMID:14753464

  1. Measurement of regional pulmonary blood volume in patients with increased pulmonary blood flow or pulmonary arterial hypertension

    SciTech Connect

    Wollmer, P.; Rozcovek, A.; Rhodes, C.G.; Allan, R.M.; Maseri, A.

    1984-01-01

    The effects of chronic increase in pulmonary blood flow and chronic pulmonary hypertension on regional pulmonary blood volume was measured in two groups of patients. One group of patients had intracardiac, left-to-right shunts without appreciable pulmonary hypertension, and the other consisted of patients with Eisenmenger's syndrome or primary pulmonary hypertension, i.e. patients with normal or reduced blood flow and severe pulmonary hypertension. A technique based on positron tomography was used to measure lung density (by transmission scanning) and regional pulmonary blood volume (after inhalation of /sup 11/CO). The distribution of pulmonary blood volume was more uniform in patients with chronic increase in pulmonary blood flow than in normal subjects. There were also indications of an absolute increase in intrapulmonary blood volume by about 15%. In patients with chronic pulmonary arterial hypertension, the distribution of pulmonary blood volume was also abnormally uniform. There was, however, no indication that overall intrapulmonary blood volume was substantially different from normal subjects. The abnormally uniform distribution of pulmonary blood volume can be explained by recruitment and/or dilatation of vascular beds. Intrapulmonary blood volume appears to be increased in patients with intracardiac, left-to-right shunts. With the development of pulmonary hypertension, intrapulmonary blood volume falls, which may be explained by reactive changes in the vasculature and/or obliteration of capillaries.

  2. Pulmonary hyalinizing granuloma in HIV/AIDS.

    PubMed

    Liu, Theresa; Kyrollos, Maggy; Kravcik, Stephen

    2007-09-01

    A 55-year-old man who was recently diagnosed with HIV/AIDS developed multiple bilateral pulmonary nodules after starting highly active antiretroviral therapy. Workup confirmed the diagnosis of pulmonary hyalinizing granuloma. This is the first described case of pulmonary hyalinizing granuloma in HIV/AIDS, and may represent a rare form of immune reconstitution inflammatory syndrome. PMID:18923729

  3. Pulmonary hyalinizing granuloma in HIV/AIDS

    PubMed Central

    Liu, Theresa; Kyrollos, Maggy; Kravcik, Stephen

    2007-01-01

    A 55-year-old man who was recently diagnosed with HIV/AIDS developed multiple bilateral pulmonary nodules after starting highly active antiretroviral therapy. Workup confirmed the diagnosis of pulmonary hyalinizing granuloma. This is the first described case of pulmonary hyalinizing granuloma in HIV/AIDS, and may represent a rare form of immune reconstitution inflammatory syndrome. PMID:18923729

  4. Vascular endothelial growth factor A protein level and gene expression in intracranial meningiomas with brain edema.

    PubMed

    Nassehi, Damoun; Dyrbye, Henrik; Andresen, Morten; Thomsen, Carsten; Juhler, Marianne; Laursen, Henning; Broholm, Helle

    2011-12-01

    Meningiomas are the second most common primary intracranial tumors in adults. Although meningiomas are mostly benign, more than 50% of patients with meningioma develop peritumoral brain edema (PTBE), which may be fatal because of increased intracranial pressure. Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen and angiogen. VEGF-A protein, which is identical to vascular permeability factor, is a regulator of angiogenesis. In this study, 101 patients with meningiomas, and possible co-factors to PTBE, such as meningioma subtypes and tumor location, were examined. Forty-three patients had primary, solitary, supratentorial meningiomas with PTBE. In these, correlations in PTBE, edema index, VEGF-A protein, VEGF gene expression, capillary length, and tumor water content were investigated. DNA-branched hybridization was used for measuring VEGF gene expression in tissue homogenates prepared from frozen tissue samples. The method for VEGF-A analysis resembled an ELISA assay, but was based on chemiluminescence. The edema index was positively correlated to VEGF-A protein (p = 0.014) and VEGF gene expression (p < 0.05). The capillary length in the meningiomas was positively correlated to the PTBE (p = 0.038). If VEGF is responsible for the formation of PTBE, the edema may be treated with the anti-VEGF drug Bevacizumab (Avastin), which has been shown to reduce PTBE in patients with glioblastoma multiforme. PMID:22085359

  5. Types of Pulmonary Hypertension

    MedlinePlus

    ... from the NHLBI on Twitter. Types of Pulmonary Hypertension The World Health Organization divides pulmonary hypertension (PH) ... are called pulmonary hypertension.) Group 1 Pulmonary Arterial Hypertension Group 1 PAH includes: PAH that has no ...

  6. New Perspectives in Edema Control via Electrical Stimulation

    PubMed Central

    Mendel, Frank C.; Fish, Dale R.

    1993-01-01

    Clinicians commonly use electrical stimulation (ES) to control acute edema. But, except for anecdotal reports, there is little evidence to support that practice. We recently conducted a series of controlled, blinded studies on several nonhuman animal models to determine the efficacy of several forms of ES, but high-voltage pulsed current (HVPC) in particular, in controlling acute posttraumatic edema. We observed that acute posttraumatic edema is curbed by HVPC when certain protocols are used. Results of these studies suggest to us that wave form, polarity, treatment schedule, intensity and frequency of pulses all influence ES, and that clinical protocols need revision. PMID:16558209

  7. Probability of developing proximal deep-vein thrombosis and/or pulmonary embolism after distal deep-vein thrombosis.

    PubMed

    Brateanu, Andrei; Patel, Krishna; Chagin, Kevin; Tunsupon, Pichapong; Yampikulsakul, Pojchawan; Shah, Gautam V; Wangsiricharoen, Sintawat; Amah, Linda; Allen, Joshua; Shapiro, Aryeh; Gupta, Neha; Morgan, Lillie; Kumar, Rahul; Nielsen, Craig; Rothberg, Michael B

    2016-03-01

    Isolated distal deep-vein thrombosis (DDVT) of the lower extremities can be associated with subsequent proximal deep-vein thrombosis (PDVT) and/or acute pulmonary embolism (PE). We aimed to develop a model predicting the probability of developing PDVT and/or PE within three months after an isolated episode of DDVT. We conducted a retrospective cohort study of patients with symptomatic DDVT confirmed by lower extremity vein ultrasounds between 2001-2012 in the Cleveland Clinic Health System. We reviewed all the ultrasounds, chest ventilation/perfusion and computed tomography scans ordered within three months after the initial DDVT to determine the incidence of PDVT and/or PE. A multiple logistic regression model was built to predict the rate of developing these complications. The final model included 450 patients with isolated DDVT. Within three months, 30 (7 %) patients developed an episode of PDVT and/or PE. Only two factors predicted subsequent thromboembolic complications: inpatient status (OR, 6.38; 95 % CI, 2.17 to 18.78) and age (OR, 1.02 per year; 95 % CI, 0.99 to 1.05). The final model had a bootstrap bias-corrected c-statistic of 0.72 with a 95 % CI (0.64 to 0.79). Outpatients were at low risk (< 4 %) of developing PDVT/PE. Inpatients aged ≥ 60 years were at high risk (> 10 %). Inpatients aged < 60 were at intermediate risk. We created a simple model that can be used to risk stratify patients with isolated DDVT based on inpatient status and age. The model might be used to choose between anticoagulation and monitoring with serial ultrasounds.

  8. Pulmonary embolism

    SciTech Connect

    Dunnick, N.R.; Newman, G.E.; Perlmutt, L.M.; Braun, S.D.

    1988-11-01

    Pulmonary embolism is a common medical problem whose incidence is likely to increase in our aging population. Although it is life-threatening, effective therapy exists. The treatment is not, however, without significant complications. Thus, accurate diagnosis is important. Unfortunately, the clinical manifestations of pulmonary embolism are nonspecific. Furthermore, in many patients the symptoms of an acute embolism are superimposed on underlying chronic heart or lung disease. Thus, a high index of suspicion is needed to identify pulmonary emboli. Laboratory parameters, including arterial oxygen tensions and electrocardiography, are as nonspecific as the clinical signs. They may be more useful in excluding another process than in diagnosing pulmonary embolism. The first radiologic examination is the chest radiograph, but the clinical symptoms are frequently out of proportion to the findings on the chest films. Classic manifestations of pulmonary embolism on the chest radiograph include a wedge-shaped peripheral opacity and a segmental or lobar diminution in vascularity with prominent central arteries. However, these findings are not commonly seen and, even when present, are not specific. Even less specific findings include cardiomegaly, pulmonary infiltrate, elevation of a hemidiaphragm, and pleural effusion. Many patients with pulmonary embolism may have a normal chest radiograph. The chest radiograph is essential, however, for two purposes. First, it may identify another cause of the patient's symptoms, such as a rib fracture, dissecting aortic aneurysm, or pneumothorax. Second, a chest radiograph is essential to interpretation of the radionuclide V/Q scan. The perfusion scan accurately reflects the perfusion of the lung. However, a perfusion defect may result from a variety of etiologies. Any process such as vascular stenosis or compression by tumor may restrict blood flow. 84 references.

  9. Interrelation between Alterations in Pulmonary Mechanics and hemodynamics in Acute Myocardial Infarction

    PubMed Central

    Interiano, Benjamin; Hyde, Richard W.; Hodges, Morrison; Yu, Paul N.

    1973-01-01

    major factor. Frequency dependence of RT accompanied by elevated pulmonary vascular pressures and extravascular water volume indicates that pulmonary congestion causes the development of uneven time constants in the airways. Vascular engorgement and interstitial edema from elevated vascular pressures causing narrowing of the peripheral airways and closure of collateral airways could account for the above findings. Images PMID:4719674

  10. Hantavirus Fever without Pulmonary Syndrome in Panama

    PubMed Central

    Armien, Blas; Pascale, Juan M.; Muñoz, Carlos; Mariñas, Jamileth; Núñez, Heydy; Herrera, Milagro; Trujillo, José; Sánchez, Deyanira; Mendoza, Yaxelis; Hjelle, Brian; Koster, Frederick

    2013-01-01

    In Panama, hantavirus pulmonary syndrome (HPS) is caused by Choclo virus, a species phylogenetically related to Andes and Maporal viruses. Up to 60% of the population has been positive for specific serum antibody in community-based surveys, but mortality is very uncommon. In four western Panama clinics, we tested individuals presenting with a severe febrile prodrome for acute hantavirus (HV) infection by immunoglobulin M enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction as well as clinically similar infections, such as dengue and leptospirosis. From 2006 to 2009, at least 21% of 117 patients diagnosed with HV infection had HV Fever (HF) with no evidence of pulmonary edema (no respiratory distress or radiographic lung infiltrates), and 44% of patients had very mild HPS (radiographic pulmonary edema but no respiratory insufficiency). HV infection caused by Choclo virus in Panama presents often as HF, which contrasts with HV in the Americas but is consistent with the high seroprevalence in endemic regions. PMID:23836565

  11. Multiple bilateral pulmonary nodules masquerading as pulmonary metastasis; a case of nodular sarcoidosis

    PubMed Central

    Jafari, Mostafa; Farrokh, Donya; Mohammadpanah, Najmeh

    2016-01-01

    Sarcoidosis is a multi-system inflammatory disorder of unknown etiology that is manifested by the presence of non-caseating granulomas. Multiple pulmonary nodules are rare presentations of sarcoidosis. We report a case of nodular sarcoidosis in a young male of Middle-East origin who had initially presented with bilateral painful ankle edema. His chest X-ray showed multiple bilateral pulmonary nodules. A high resolution computed tomography scan of the chest demonstrated multiple pulmonary nodular lesions and also mediastinal and hilar lymphadenopathy. Subsequent biopsies revealed non-necrotizing granuloma with multi-nucleated giant cells indicative of sarcoidosis. An appropriate work-up was done to confirm the true nature of the nodules and facilitate treatment. PMID:27757192

  12. Ulinastatin attenuates brain edema after traumatic brain injury in rats.

    PubMed

    Cui, Tao; Zhu, Gangyi

    2015-03-01

    Traumatic brain injury (TBI) remains the leading cause of injury-related death and disability. Brain edema, one of the most major complications of TBI, contributes to elevated intracranial pressure, and poor prognosis following TBI. The objective of this study was to evaluate whether Ulinastatin (UTI), a serine protease inhibitor, attenuates brain edema following TBI. Our results showed that treatment with UTI at a dose of 50,000 U/kg attenuated the brain edema, as assayed by water content 24 h after TBI induction. This attenuation was associated with a significant decrease of the expression level of aquaporin-4. In addition, we showed that UTI treatment also markedly inhibited the expression of pro-inflammatory cytokines including IL-1β and TNF-α as well as activity of NF-κB. Collectively, our findings suggested that UTI may be a promising strategy to treat brain edema following TBI.

  13. Scalp edema: don't forget sunburn in children.

    PubMed

    Shah, Binod; Yavuz, Süleyman Tolga; Tekşam, Ozlem

    2012-01-01

    Scalp edema is an uncommon and striking finding in children that may alarm both parents and physicians. The objectives of this case report were to raise awareness among pediatric emergency physicians of the unusual presentation of sunburn as scalp edema. We present the case of an eight-year-old boy with sunburn of the head, presenting with scalp and face edema. Pitting edema and erythema were dominant on the forehead. Shaving of the boy's head the day before the symptoms was the most striking issue, and the sunburn healed gradually without any complications. Healthcare professionals should be aware of this condition, and the diagnosis of sunburn must be kept in mind in otherwise healthy-looking patients with a unique history.

  14. Mathematical modelling of blood-brain barrier failure and edema

    NASA Astrophysics Data System (ADS)

    Waters, Sarah; Lang, Georgina; Vella, Dominic; Goriely, Alain

    2015-11-01

    Injuries such as traumatic brain injury and stroke can result in increased blood-brain barrier permeability. This increase may lead to water accumulation in the brain tissue resulting in vasogenic edema. Although the initial injury may be localised, the resulting edema causes mechanical damage and compression of the vasculature beyond the original injury site. We employ a biphasic mixture model to investigate the consequences of blood-brain barrier permeability changes within a region of brain tissue and the onset of vasogenic edema. We find that such localised changes can indeed result in brain tissue swelling and that the type of damage that results (stress damage or strain damage) depends on the ability of the brain to clear edema fluid.

  15. Effects of metformin treatment on glioma-induced brain edema.

    PubMed

    Zhao, Bin; Wang, Xiaoke; Zheng, Jun; Wang, Hailiang; Liu, Jun

    2016-01-01

    Considerable evidence has demonstrated that metformin can activate 5'-AMP-activated protein kinase (AMPK) signaling pathway, which plays a critical role in protection of endothelial cell permeability. Hence, the present study evaluated the effects of metformin on blood brain barrier permeability and AQP4 expression in vitro, and assessed the effects of metformin treatment on tumor-induced brain edema in vivo. Hypoxia or VEGF exposure enhanced bEnd3 endothelial cell monolayer permeability and attenuated the expression of tight junction proteins including Occludin, Claudin-5, ZO-1, and ZO-2. However, 0.5 mM metformin treatment protected bEnd3 endothelial cell monolayer from hypoxia or VEGF-induced permeability, which was correlated with increased expression of tight junction proteins. Furthermore, metformin treatment attenuated AQP4 protein expression in cultured astrocytes. Such an effect involved the activation of AMPK and inhibition of NF-κB. Finally, metformin treatment dose-dependently reduced glioma induced vascular permeability and cerebral edema in vivo in rats. Thus, our results suggested that metformin may protect endothelial cell tight junction, prevent damage to the blood brain barrier induced by brain tumor growth, and alleviate the formation of cerebral edema. Furthermore, since the formation of cytotoxic edema and AQP4 expression was positively correlated, our results indicated that metformin may reduce the formation of cytotoxic edema. However, given that AQP4 plays a key role in the elimination of cerebral edema, attenuation of AQP4 expression by metformin may reduce the elimination of cerebral edema. Hence, future studies will be necessary to dissect the specific mechanisms of metformin underlying the dynamics of tumor-induced brain edema in vivo.

  16. Effects of metformin treatment on glioma-induced brain edema

    PubMed Central

    Zhao, Bin; Wang, Xiaoke; Zheng, Jun; Wang, Hailiang; Liu, Jun

    2016-01-01

    Considerable evidence has demonstrated that metformin can activate 5’-AMP-activated protein kinase (AMPK) signaling pathway, which plays a critical role in protection of endothelial cell permeability. Hence, the present study evaluated the effects of metformin on blood brain barrier permeability and AQP4 expression in vitro, and assessed the effects of metformin treatment on tumor-induced brain edema in vivo. Hypoxia or VEGF exposure enhanced bEnd3 endothelial cell monolayer permeability and attenuated the expression of tight junction proteins including Occludin, Claudin-5, ZO-1, and ZO-2. However, 0.5 mM metformin treatment protected bEnd3 endothelial cell monolayer from hypoxia or VEGF-induced permeability, which was correlated with increased expression of tight junction proteins. Furthermore, metformin treatment attenuated AQP4 protein expression in cultured astrocytes. Such an effect involved the activation of AMPK and inhibition of NF-κB. Finally, metformin treatment dose-dependently reduced glioma induced vascular permeability and cerebral edema in vivo in rats. Thus, our results suggested that metformin may protect endothelial cell tight junction, prevent damage to the blood brain barrier induced by brain tumor growth, and alleviate the formation of cerebral edema. Furthermore, since the formation of cytotoxic edema and AQP4 expression was positively correlated, our results indicated that metformin may reduce the formation of cytotoxic edema. However, given that AQP4 plays a key role in the elimination of cerebral edema, attenuation of AQP4 expression by metformin may reduce the elimination of cerebral edema. Hence, future studies will be necessary to dissect the specific mechanisms of metformin underlying the dynamics of tumor-induced brain edema in vivo. PMID:27648126

  17. Effects of metformin treatment on glioma-induced brain edema

    PubMed Central

    Zhao, Bin; Wang, Xiaoke; Zheng, Jun; Wang, Hailiang; Liu, Jun

    2016-01-01

    Considerable evidence has demonstrated that metformin can activate 5’-AMP-activated protein kinase (AMPK) signaling pathway, which plays a critical role in protection of endothelial cell permeability. Hence, the present study evaluated the effects of metformin on blood brain barrier permeability and AQP4 expression in vitro, and assessed the effects of metformin treatment on tumor-induced brain edema in vivo. Hypoxia or VEGF exposure enhanced bEnd3 endothelial cell monolayer permeability and attenuated the expression of tight junction proteins including Occludin, Claudin-5, ZO-1, and ZO-2. However, 0.5 mM metformin treatment protected bEnd3 endothelial cell monolayer from hypoxia or VEGF-induced permeability, which was correlated with increased expression of tight junction proteins. Furthermore, metformin treatment attenuated AQP4 protein expression in cultured astrocytes. Such an effect involved the activation of AMPK and inhibition of NF-κB. Finally, metformin treatment dose-dependently reduced glioma induced vascular permeability and cerebral edema in vivo in rats. Thus, our results suggested that metformin may protect endothelial cell tight junction, prevent damage to the blood brain barrier induced by brain tumor growth, and alleviate the formation of cerebral edema. Furthermore, since the formation of cytotoxic edema and AQP4 expression was positively correlated, our results indicated that metformin may reduce the formation of cytotoxic edema. However, given that AQP4 plays a key role in the elimination of cerebral edema, attenuation of AQP4 expression by metformin may reduce the elimination of cerebral edema. Hence, future studies will be necessary to dissect the specific mechanisms of metformin underlying the dynamics of tumor-induced brain edema in vivo.

  18. Effects of metformin treatment on glioma-induced brain edema.

    PubMed

    Zhao, Bin; Wang, Xiaoke; Zheng, Jun; Wang, Hailiang; Liu, Jun

    2016-01-01

    Considerable evidence has demonstrated that metformin can activate 5'-AMP-activated protein kinase (AMPK) signaling pathway, which plays a critical role in protection of endothelial cell permeability. Hence, the present study evaluated the effects of metformin on blood brain barrier permeability and AQP4 expression in vitro, and assessed the effects of metformin treatment on tumor-induced brain edema in vivo. Hypoxia or VEGF exposure enhanced bEnd3 endothelial cell monolayer permeability and attenuated the expression of tight junction proteins including Occludin, Claudin-5, ZO-1, and ZO-2. However, 0.5 mM metformin treatment protected bEnd3 endothelial cell monolayer from hypoxia or VEGF-induced permeability, which was correlated with increased expression of tight junction proteins. Furthermore, metformin treatment attenuated AQP4 protein expression in cultured astrocytes. Such an effect involved the activation of AMPK and inhibition of NF-κB. Finally, metformin treatment dose-dependently reduced glioma induced vascular permeability and cerebral edema in vivo in rats. Thus, our results suggested that metformin may protect endothelial cell tight junction, prevent damage to the blood brain barrier induced by brain tumor growth, and alleviate the formation of cerebral edema. Furthermore, since the formation of cytotoxic edema and AQP4 expression was positively correlated, our results indicated that metformin may reduce the formation of cytotoxic edema. However, given that AQP4 plays a key role in the elimination of cerebral edema, attenuation of AQP4 expression by metformin may reduce the elimination of cerebral edema. Hence, future studies will be necessary to dissect the specific mechanisms of metformin underlying the dynamics of tumor-induced brain edema in vivo. PMID:27648126

  19. Angioneurotic edema: a rare case of hypersensitivity to metoclopramide

    PubMed Central

    Zakrzewski, Aleksander; Matuszewski, Tomasz; Kruszewski, Jerzy

    2013-01-01

    The case of a 30-year-old woman who had already experienced two incidents of angioneurotic edema and urticaria caused by drugs during the acute gastroenteritis. The allergological workup revealed hypersensitivity to metoclopramide. This case documents that metoclopramide, a drug commonly used to inhibit the vomiting, may cause not only bronchospastic reaction in an asthmatic patient but also angioneurotic edema of the tongue and larynx as well as urticaria. No similar cases in the literature were found. PMID:24278059

  20. Local fluid shifts and edema in humans during simulated microgravity

    NASA Technical Reports Server (NTRS)

    Hargens, Alan R.

    1991-01-01

    Local fluid shifts and edema in humans during simulated microgravity is studied. Recent results and significance and future plans on the following research topics are discussed: mechanisms of headward edema formation during head-down tilt; postural responses of head and foot microcirculations and their sensitivity to bed rest; and transcapillary fluid transport associated with lower body negative pressure (LBNP) with and without saline ingestion.

  1. Current concept of chronic mountain sickness: pulmonary hypertension-related high-altitude heart disease.

    PubMed

    Ge, R L; Helun, G

    2001-01-01

    High-altitude heart disease, a form of chronic mountain sickness, has been well established in both Tibet and Qinghai provinces of China, although little is known regarding this syndrome in other countries, particularly in the West. This review presents a general overview of high-altitude heart disease in China and briefly summarizes the existing data with regard to the prevalence, clinical features, and pathophysiology of the illness. The definition of high-altitude heart disease is right ventricular enlargement that develops primarily (by high-altitude exposure) to pulmonary hypertension without excessive polycythemia. The prevalence is higher in children than adults and in men than women, but is lower in both sexes of Tibetan high-altitude residents compared with acclimatized newcomers, such as Han Chinese. Clinical symptoms consist of headache, dyspnea, cough, irritability, and sleeplessness. Physical findings include a marked cyanosis, rapid heart and respiratory rates, edema of the face, liver enlargement, and rales. Most patients have complete recovery on descent to a lower altitude, but symptoms recur with a return to high altitude. Right ventricular enlargement, pulmonary hypertension, and remodeling of pulmonary arterioles are hallmarks of high-altitude heart disease. It is hoped that this information will assist in understanding this type of chronic mountain sickness, facilitate international exchange of data, and stimulate further research into this poorly understood condition.

  2. Blood pressure, edema and proteinuria in pregnancy. 7. Edema-plus-proteinuria relationships.

    PubMed

    Sellmann, A H

    1976-01-01

    1. A total of 488 pregnancies had the combination of two-plus or more proteinuria and edema of the hands and face. Of these, 208 were white and 280 were black gravidas. In the white gravidas, 8 fetal and neonatal deaths occurred with a perinatal mortality of 38.5 per 1,000. There were 13 perinatal deaths in the black subgroup with a perinatal mortality rate of 46.4 per 1,000. The overall perinatal mortality rate was 43.0 per 1,000, which could be compared to the overall perinatal mortality rate of 32.8 per 1,000 for the segment of the study population without edema or proteinuria. This underscored the implication of increased hazard to fetal outcome of these clinical signs in combination. 2. The analysis of the matrix data showed scattered rates throughout gestation in white median-age nulliparas. Their black counterparts had comparable increased mortality rates. In the white multiparas of ages 20 to 34 years, the highest rates were found at relatively low blood pressure levels. The black median-age multiparas had rates associated with higher pressure readings, especially at or above 125/75. In teenage mulliparas with edema and proteinuria, perinatal mortality rates were similar for both subgroups and were found in somewhat lower blood pressures. 3. The incremental analysis was remarkable in that rates were scattered widely in the white subgroups, but tightly clustered in the black subgroups. The black median-age nulliparas had perinatal mortality concentrated about 115 to 134 mm. Hg systolic and 65 to 84 mm. Hg diastolic. The overall mortality rates of this subgroup were the highest of the subgroups studied. The black 20 to 34 year old multiparas had highest coassociated deaths in the 134-154 mm. Hg systolic levels throughout pregnancy. The clustering effect was most pronounced in black teenage nulliparas in both systolic and diastolic blood pressure groups at much lower levels. 4. The use of a critical cut-off blood pressure level of 125 mm. Hg systolic and 75 mm

  3. Smoking and smoking cessation in relation to the development of co-existing non-small cell lung cancer with chronic obstructive pulmonary disease.

    PubMed

    Zhai, Rihong; Yu, Xiaojin; Wei, Yongyue; Su, Li; Christiani, David C

    2014-02-15

    Previous studies have identified a mixed-phenotype of non-small cell lung cancer (NSCLC) with co-existing chronic obstructive pulmonary disease (COPD). Although NSCLC and COPD share a common risk factor in smoking, whether and how smoking may contribute to the coexistence of NSCLC with COPD (NSCLC-COPD) is unclear. Our study suggests that cigarette smoking is the major risk factor for the development of NSCLC-COPD, especially in females and among patients with squamous cell carcinoma subtype.

  4. Pulmonary hyalinizing granuloma.

    PubMed

    Yousem, S A; Hochholzer, L

    1987-01-01

    Pulmonary hyalinizing granulomas are distinct fibrosing lesions of lung, having central whorled deposits of lamellar collagen. Twenty-four cases of this unusual pulmonary lesion are reported herein. Hyalinizing granulomas occur in middle-aged persons and are frequently mistaken for metastatic carcinoma radiographically. More than half of the patients had autoimmune phenomena or previous exposures to mycobacterial or fungal antigens. Four patients had sclerosing mediastinitis develop. A progressive debilitating clinical course was related to increasing dyspnea and bilateral disease on chest radiographs. A discussion of the histogenesis and histologic differential diagnosis is presented. PMID:3799538

  5. Modelling pulmonary blood flow

    PubMed Central

    Tawhai, Merryn H.; Burrowes, Kelly S.

    2008-01-01

    Computational model analysis is a method that has been used widely to understand and interpret complexity of interactions in the pulmonary system. Pulmonary blood transport is a multi-scale phenomenon that involves scale-dependent structure and function, therefore requiring different model assumptions for the microcirculation and the arterial or venous flows. The blood transport systems interact with the surrounding lung tissue, and are dependent on hydrostatic pressure gradients, control of vasoconstriction, and the topology and material composition of the vascular trees. This review focuses on computational models that have been developed to study the different mechanisms contributing to regional perfusion of the lung. Different models for the microcirculation and the pulmonary arteries are considered, including fractal approaches and anatomically-based methods. The studies that are reviewed illustrate the different complementary approaches that can be used to address the same physiological question of flow heterogeneity. PMID:18434260

  6. Treatment of pulmonary hypertension

    PubMed Central

    Patel, Rajendrakumar; Aronow, Wilbert S.; Patel, Laxeshkumar; Gandhi, Kaushang; Desai, Harit; Kaul, Dhiraj; Sahgal, Sumir P.

    2012-01-01

    Summary Pulmonary arterial hypertension (PAH) is a chronic progressive disease of the pulmonary vasculature characterized by elevated pulmonary arterial pressure and secondary right ventricular failure. PAH is considered a life-threatening condition unless treated. This article provides a comprehensive review of controlled and uncontrolled trials to define the risk-benefit for different therapeutic options of this clinical disorder. Relevant published articles were identified through searches of the National Center for Biotechnology PubMed database. All therapeutic measures for PAH were discussed. Six drugs have been approved in the United States for the treatment of PAH. Extensive medical advancement has been achieved in treatment of PAH. However, none of the approved therapies have shown ability to cure the disease. New research should be performed to develop promising new therapies. PMID:22460104

  7. Evaluation of brain edema using magnetic resonance proton relaxation times

    SciTech Connect

    Fu, Y.; Tanaka, K.; Nishimura, S. )

    1990-01-01

    Experimental and clinical studies on the evaluation of water content in cases of brain edema were performed in vivo, using MR proton relaxation times (longitudinal relaxation time, T1; transverse relaxation time, T2). Brain edema was produced in the white matter of cats by the direct infusion method. The correlations between proton relaxation times obtained from MR images and the water content of white matter were studied both in autoserum-infused cats and in saline-infused cats. The correlations between T1 as well as T2 and the water content in human vasogenic brain edema were also examined and compared with the data obtained from the serum group. T1 and T2 showed good correlations with the water content of white matter not only in the experimental animals but also in the clinical cases. The quality of the edema fluid did not influence relaxation time and T1 seemed to represent almost solely the water content of the tissue. T2, however, was affected by the nature of existence of water and was more sensitive than T1 in detecting extravasated edema fluid. It seems feasible therefore to evaluate the water content of brain edema on the basis of T1 values.

  8. Pathophysiology, Evaluation, and Management of Edema in Childhood Nephrotic Syndrome

    PubMed Central

    Ellis, Demetrius

    2016-01-01

    Generalized edema is a major presenting clinical feature of children with nephrotic syndrome (NS) exemplified by such primary conditions as minimal change disease (MCD). In these children with classical NS and marked proteinuria and hypoalbuminemia, the ensuing tendency to hypovolemia triggers compensatory physiological mechanisms, which enhance renal sodium (Na+) and water retention; this is known as the “underfill hypothesis.” Edema can also occur in secondary forms of NS and several other glomerulonephritides, in which the degree of proteinuria and hypoalbuminemia, are variable. In contrast to MCD, in these latter conditions, the predominant mechanism of edema formation is “primary” or “pathophysiological,” Na+ and water retention; this is known as the “overfill hypothesis.” A major clinical challenge in children with these disorders is to distinguish the predominant mechanism of edema formation, identify other potential contributing factors, and prevent the deleterious effects of diuretic regimens in those with unsuspected reduced effective circulatory volume (i.e., underfill). This article reviews the Starling forces that become altered in NS so as to tip the balance of fluid movement in favor of edema formation. An understanding of these pathomechanisms then serves to formulate a more rational approach to prevention, evaluation, and management of such edema. PMID:26793696

  9. [Migraine with prolonged eyelid edema: a series of 10 cases].

    PubMed

    Toribio-Díaz, M E; Cuadrado-Pérez, M L; Peláez, A; Aledo-Serrano, Angel; Pedraza, M Isabel; Porta-Etessam, Jesús; Guerrero-Peral, Angel L

    2014-05-01

    Introduccion. La migraña puede cursar con sintomas autonomicos craneales propios de las cefaleas trigeminoautonomicas, lo que plantea dificultades en el diagnostico. Objetivo. Describir una serie de diez pacientes con edema palpebral asociado a la migraña. Pacientes y metodos. Diez pacientes atendidos en la consulta de cefaleas de tres hospitales (nueve mujeres, un varon; edad: 26-53 años), con edema palpebral recurrente asociado a la migraña. Resultados. Segun los criterios diagnosticos de la Clasificacion Internacional de las Cefaleas (ICHD-III, version beta), ocho pacientes presentaban migraña sin aura, una tenia migraña con aura y otra, migraña cronica. El edema palpebral aparecia durante las crisis de migraña mas intensas, y tenia mayor duracion que la cefalea. Se descartaron causas farmacologicas o sistemicas del edema en todos los casos. Otros sintomas autonomicos asociados fueron la inyeccion conjuntival (n = 3), el lagrimeo (n = 2) y la rinorrea (n = 1). Tanto el dolor como el edema asociado respondieron a los tratamientos sintomaticos y preventivos de la migraña. Conclusiones. El edema palpebral es un posible acompañante de la migraña. Aparece en algunos pacientes con los episodios de mayor intensidad, y responde al tratamiento sintomatico y preventivo de la migraña.

  10. Aquaporin-4: A Potential Therapeutic Target for Cerebral Edema

    PubMed Central

    Tang, Guanghui; Yang, Guo-Yuan

    2016-01-01

    Aquaporin-4 (AQP4) is a family member of water-channel proteins and is dominantly expressed in the foot process of glial cells surrounding capillaries. The predominant expression at the boundaries between cerebral parenchyma and major fluid compartments suggests the function of aquaporin-4 in water transfer into and out of the brain parenchyma. Accumulating evidences have suggested that the dysregulation of aquaporin-4 relates to the brain edema resulting from a variety of neuro-disorders, such as ischemic or hemorrhagic stroke, trauma, etc. During edema formation in the brain, aquaporin-4 has been shown to contribute to the astrocytic swelling, while in the resolution phase, it has been seen to facilitate the reabsorption of extracellular fluid. In addition, aquaporin-4-deficient mice are protected from cytotoxic edema produced by water intoxication and brain ischemia. However, aquaporin-4 deletion exacerbates vasogenic edema in the brain of different pathological disorders. Recently, our published data showed that the upregulation of aquaporin-4 in astrocytes probably contributes to the transition from cytotoxic edema to vasogenic edema. In this review, apart from the traditional knowledge, we also introduce our latest findings about the effects of mesenchymal stem cells (MSCs) and microRNA-29b on aquaporin-4, which could provide powerful intervention tools targeting aquaporin-4. PMID:27690011

  11. [Pulmonary complications of acute myocardial infarct. Therapeutic orientation].

    PubMed

    Cano, A E; Meaney, E

    1975-01-01

    The heart and the lung make up an inseparable anatomic and functional unit. The changes in one affect the other and vice versa. In acute myocardial infarction a heart failure syndrome develops. This syndrome is characterized by passive pulmonary congestion, which leads to hypoxemia. This hypoxemia indicate the functional disturbance of the lung, and the hemodinamic evolution of the disease. Arterial gases determination is the best way to assess the sickness progression. A certain paralelism exists among the central venous saturation, cardiac insufficiency and the degree of pulmonary disfunction. Such a procedure is not very appreciable and does not substitute the direct analysis of the arterial PO2. The pulmonary complications in the myocardial infarction shock are directly responsable of death in 50% of the patients. To heart failure and shock, hipperfusion and hypoxia are added. Many vessels close due to the decrease in the pulmonary flow. This brings about the release of substances that are toxic to the vessel causing an inflammatory vascular reaction. The decrease in the flow harms the lung cell and for this reason atelectasia or alveolar colapse occur; besides inducing the formation of shunts. Under these conditions the lung compliance decreases. The areas that are badly ventilated and hypoperfused can easily become infected and pneumonitis and abscesses cause even more harm to the tissue. The decrease in the speed of circulation and hematologic changes of shock, induce a diseminated intravascular coagulation. What was stated before leads to an important reduction of the lung as a depurating organ and makes the shock irreversible. As far as therapy is concerned in the prevention of vascular colaps and the improvement of the oxemia, oxygen is very useful when there is a venous congestion (clinically, X rays, and oxemia). When the concentration of O2 is lower than 50% in the cases with slight cardiac failure; do not use oxygen in higher concentrations unless the

  12. Proteases and oxidants in experimental pulmonary inflammatory injury.

    PubMed

    Schraufstätter, I U; Revak, S D; Cochrane, C G

    1984-04-01

    We have examined various biochemical parameters of pulmonary inflammation in experimental animals. Intrabronchial instillation of glucose oxidase-glucose (GO/G) to produce oxidants or formylated norleu-leu-phe (FNLP) or phorbol myristate acetate (PMA) as leukocytic stimuli induced severe acute pulmonary injury in New Zealand white rabbits. PMA also induced inflammation when administered intravenously. Each stimulus induced transudation of protein from the vascular space into the pulmonary tissues, and an influx of leukocytes during the 4-6 h period of the experiment. Pathophysiologic changes were measured by edema formation (transudation of 125I-bovine serum albumin), and histologic examination. Biochemical analysis was performed by measuring concentrations of potentially injurious agents in bronchoalveolar lavage (BAL) fluid. Increased acid protease and myeloperoxidase levels were found in the BAL fluid after administration of either of the stimuli. Evidence of oxidant generation in vivo was obtained in two different ways. In the first, specific activities for catalase were measured in the BAL fluid in the presence or absence of 3-amino, 1,2,4 triazole (AT), injected at intervals before obtaining BAL fluid. In the presence of AT, specific activities for catalase dropped to 0.22 after a double instillation of FNLP and to 0.15 in the presence of GO/G. In neutrophil-depleted FNLP animals, catalase was not greatly inhibited by AT (sp act 0.90). In the second, intracellular levels of total glutathione (GSH + GSSG) in whole lung tissue and alveolar macrophages decreased when stimuli of neutrophils were administered. Intrabronchially instilled PMA, e.g., caused a drop of glutathione in whole lung tissue from the control value of 2.3 mumol GSH equivalent/100 mg dry wt to 0.54 mumol GSH equivalent/100 mg dry wt at 4 h. Neutrophil depletion and superoxide dismutase protected from this effect. From these results, we conclude that O-2 or its metabolites can initiate severe

  13. Microarray analysis in pulmonary hypertension.

    PubMed

    Hoffmann, Julia; Wilhelm, Jochen; Olschewski, Andrea; Kwapiszewska, Grazyna

    2016-07-01

    Microarrays are a powerful and effective tool that allows the detection of genome-wide gene expression differences between controls and disease conditions. They have been broadly applied to investigate the pathobiology of diverse forms of pulmonary hypertension, namely group 1, including patients with idiopathic pulmonary arterial hypertension, and group 3, including pulmonary hypertension associated with chronic lung diseases such as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. To date, numerous human microarray studies have been conducted to analyse global (lung homogenate samples), compartment-specific (laser capture microdissection), cell type-specific (isolated primary cells) and circulating cell (peripheral blood) expression profiles. Combined, they provide important information on development, progression and the end-stage disease. In the future, system biology approaches, expression of noncoding RNAs that regulate coding RNAs, and direct comparison between animal models and human disease might be of importance. PMID:27076594

  14. Microarray analysis in pulmonary hypertension

    PubMed Central

    Hoffmann, Julia; Wilhelm, Jochen; Olschewski, Andrea

    2016-01-01

    Microarrays are a powerful and effective tool that allows the detection of genome-wide gene expression differences between controls and disease conditions. They have been broadly applied to investigate the pathobiology of diverse forms of pulmonary hypertension, namely group 1, including patients with idiopathic pulmonary arterial hypertension, and group 3, including pulmonary hypertension associated with chronic lung diseases such as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. To date, numerous human microarray studies have been conducted to analyse global (lung homogenate samples), compartment-specific (laser capture microdissection), cell type-specific (isolated primary cells) and circulating cell (peripheral blood) expression profiles. Combined, they provide important information on development, progression and the end-stage disease. In the future, system biology approaches, expression of noncoding RNAs that regulate coding RNAs, and direct comparison between animal models and human disease might be of importance. PMID:27076594

  15. Cocaine-induced pulmonary changes: HRCT findings *

    PubMed Central

    de Almeida, Renata Rocha; Zanetti, Gláucia; Souza, Arthur Soares; de Souza, Luciana Soares; Silva, Jorge Luiz Pereira e; Escuissato, Dante Luiz; Irion, Klaus Loureiro; Mançano, Alexandre Dias; Nobre, Luiz Felipe; Hochhegger, Bruno; Marchiori, Edson

    2015-01-01

    Abstract Objective: To evaluate HRCT scans of the chest in 22 patients with cocaine-induced pulmonary disease. Methods: We included patients between 19 and 52 years of age. The HRCT scans were evaluated by two radiologists independently, discordant results being resolved by consensus. The inclusion criterion was an HRCT scan showing abnormalities that were temporally related to cocaine use, with no other apparent causal factors. Results: In 8 patients (36.4%), the clinical and tomographic findings were consistent with "crack lung", those cases being studied separately. The major HRCT findings in that subgroup of patients included ground-glass opacities, in 100% of the cases; consolidations, in 50%; and the halo sign, in 25%. In 12.5% of the cases, smooth septal thickening, paraseptal emphysema, centrilobular nodules, and the tree-in-bud pattern were identified. Among the remaining 14 patients (63.6%), barotrauma was identified in 3 cases, presenting as pneumomediastinum, pneumothorax, and hemopneumothorax, respectively. Talcosis, characterized as perihilar conglomerate masses, architectural distortion, and emphysema, was diagnosed in 3 patients. Other patterns were found less frequently: organizing pneumonia and bullous emphysema, in 2 patients each; and pulmonary infarction, septic embolism, eosinophilic pneumonia, and cardiogenic pulmonary edema, in 1 patient each. Conclusions: Pulmonary changes induced by cocaine use are varied and nonspecific. The diagnostic suspicion of cocaine-induced pulmonary disease depends, in most of the cases, on a careful drawing of correlations between clinical and radiological findings. PMID:26398752

  16. Intratracheal instillation of ethyl pyruvate nanoparticles prevents the development of shunt-flow-induced pulmonary arterial hypertension in a rat model

    PubMed Central

    Liu, Kai; Zhang, Xiquan; Cao, Guangqing; Liu, Yongjun; Liu, Chuanzhen; Sun, Hourong; Pang, Xinyan

    2016-01-01

    Purpose To investigate whether inhalation of ethyl pyruvate (EP) encapsulated with poly(ethylene glycol)-block-lactide/glycolide copolymer nanoparticles (EP-NPs) can prevent the development of shunt-flow-induced hyperkinetic pulmonary arterial hypertension (PAH) in a rat model. Materials and methods Rats were separated into five groups: blank (ie, no treatment after shunt flow), normal control (ie, no shunt flow or treatment), EP-NP instillation, EP-only instillation, and vehicle. The animals received intratracheal instillation of EP-NPs or other treatments immediately after a shunt flow, and treatment continued weekly until the end of the experiment. Hemodynamic data were recorded, pulmonary arterial remodeling was assessed, and levels of inflammatory mediators and ET1 expression in the lung and serum were analyzed. In addition, retention of EP in the lungs of rats in the EP-NP and EP-only groups was measured using high-performance liquid chromatography. Results After 12 weeks, hemodynamic abnormalities and pulmonary arterial remodeling were improved in the EP-NP instillation group, compared with the blank, EP-only, and vehicle groups (P<0.05). In addition, the EP-NP group showed significantly decreased levels of HMGB1, IL-6, TNFα, reactive oxygen species, and ET1 in the lung during PAH development (P<0.05). Furthermore, EP-NP instillation was associated with reduced serum levels of inflammatory factors and ET1. High-performance liquid-chromatography measurement indicated that EP retention was greater in the lungs of the EP-NP group than in the EP-only group. Conclusion EP-NP instillation attenuated inflammation and prevented pulmonary arterial remodeling during the development of PAH induced by shunt flow. In the future, EP-NP delivery into the lung might provide a novel approach for preventing PAH. PMID:27354791

  17. Macular edema in underserved diabetic patients: Improving detection by enhancing the optical signature and data analysis techniques

    NASA Astrophysics Data System (ADS)

    Alhamami, Mastour Abdullah

    Diabetic retinopathy and diabetic macular edema are chief causes of vision loss in working adults. Thus, retinal screening of patients with diabetes has become standard practice in some countries to prevent visual impairment and blindness from diabetic retinopathy. One goal is to improve techniques currently used to diagnose diabetic retinopathy. Another goal is to probe pathophysiological changes seen with imaging methods. Analysis was performed on a novel dataset from more than 2000 underserved adult diabetic patients, who were recruited for a screening study for diabetic eye disease. Data were collected from four county clinics at Alameda Health, Alameda County, CA. Over 90% of patients self-identified as a racial/ethnic identity other than non-Hispanic white. We investigated the prevalence and optical properties of macular edema. In the first study, a retrospective cohort study was performed to compare macular thickness in diabetic patients with and without macular edema to determine the presence of damage to the external limiting membrane or and the relation of damage to the ELM to damage to photoreceptors. In the second study, we investigated whether the information in red light better visualizes cysts in diabetic macular edema, as compared to green light. In the third study, we investigated whether the demographic and blood glucose information predict diabetic macular edema. Three logistic regression analyses were compared. In the fourth study, we examined how different outcome measures of retinal thickness vary with demographic and blood glucose measures, using a trichotomous variable for retinal thickness. The findings point strongly to large individual differences in the development of macular edema, which is difficult to diagnose with the most common methods in dark eyes. Further, while blood glucose was found to be important, there are additional differences in the potential for macular edema that are associated with ethnic group and gender.

  18. Making pulmonary rehabilitation a success in COPD.

    PubMed

    Bourbeau, J

    2010-01-01

    A truly successful pulmonary rehabilitation entails implementing physical activity maintenance. This article reviews the current knowledge on pulmonary rehabilitation and the expected benefits, the setting, the relationship between self-management and pulmonary rehabilitation, in order to develop and implement clinically-effective physical activity maintenance interventions. The effectiveness of pulmonary rehabilitation is well-established. However, access to pulmonary rehabilitation is limited. Home-based pulmonary rehabilitation has been shown to be an effective, equivalent alternative to outpatient pulmonary rehabilitation in COPD patients. The opportunity to offer different pulmonary rehabilitation settings tailored to individual needs should improve accessibility to this intervention. Sustained long-term physical activity remains the most important challenge for COPD patients. We need a dependable system of coordinated health care interventions and communication, and components that include self-management support. Self-management should be an integrated part of pulmonary rehabilitation and remain long after the pulmonary rehabilitation is completed. By early identification of patients who may have difficulty maintaining exercise and implementing appropriate self-management interventions during and after the rehabilitation program, it may be possible to promote better long-term involvement in physical activity. Pulmonary rehabilitation should not stand alone; the best program is that which can be maintained to translate into a continuous increase in the activities of daily living. Future research should evaluate the effect of self-management interventions combined with pulmonary rehabilitation to improve long-term activity and exercise maintenance. PMID:20809435

  19. Unusual Development of Pulmonary Tumor Embolism from Controlled Liver Metastases of Transitional Cell Carcinoma: An Autopsy Case.

    PubMed

    Kitayama, Hiromitsu; Yokota, Taro; Kondo, Tomohiro; Sugiyama, Junko; Hirayama, Michiaki; Oyamada, Yumiko; Tsuji, Yasushi

    2016-01-01

    Clinicians generally suspect pulmonary tumor embolism (PTE) with uncontrolled carcinomas which often spread to lungs. We, however, experienced an autopsy case of diffuse microscopic PTE despite controlled liver metastases of transitional cell carcinoma (TCC). A 66-year-old man with progressing respiratory symptoms showed almost normal chest findings on computed tomography. Although liver metastases were successfully shrunk by chemotherapy, the patient died from aggressive respiratory failure. An autopsy revealed small pulmonary vessels showing diffuse tumor emboli. TCC can cause PTE even if liver metastases are controlled. We must therefore be aware that PTE can manifest as respiratory symptoms without any computed tomography findings. PMID:27580549

  20. PULMONARY TOXICOLOGY

    EPA Science Inventory

    Pulmonary disease and dysfunction exact a tremendous health burden on society. In a recent survey of lung disease published by the American Lung Association in 2012, upwards of 10 million Americans were diagnosed with chronic bronchitis while over 4 million Americans had emphysem...

  1. Pulmonary ascariasis.

    PubMed

    Mukerjee, C M; Thompson, J E

    1979-07-28

    A case of pulmonary ascariasis is reported for the first time in Australia. Because of increasing immigration from countries which have a high incidence of ascariasis (especially those of South-East Asia), and increasing travel to Asian countries, the awareness of this infestation as a cause of respiratory disease may be of great importance. PMID:40103

  2. Pulmonary schistosomiasis.

    PubMed

    Hill, I R; Turk, E P

    1980-09-01

    Two cases are reported of the incidental finding of pulmonary schistosomiasis in the victims of a fatal aircraft accident. The presence of this disease had no bearing on the causation of the accident, but it gives insight into the potential hazards of dissemination of diseases by travellers. The finding also emphasises the value of routine postmortems and histology in all aircraft accident victims.

  3. A global view of pulmonary hypertension.

    PubMed

    Hoeper, Marius M; Humbert, Marc; Souza, Rogerio; Idrees, Majdy; Kawut, Steven M; Sliwa-Hahnle, Karen; Jing, Zhi-Cheng; Gibbs, J Simon R

    2016-04-01

    Pulmonary hypertension is a substantial global health issue. All age groups are affected with rapidly growing importance in elderly people, particularly in countries with ageing populations. Present estimates suggest a pulmonary hypertension prevalence of about 1% of the global population, which increases up to 10% in individuals aged more than 65 years. In almost all parts of the world, left-sided heart and lung diseases have become the most frequent causes of pulmonary hypertension. About 80% of affected patients live in developing countries, where pulmonary hypertension is frequently associated with congenital heart disease and various infectious disorders, including schistosomiasis, HIV, and rheumatic heart disease. These forms of pulmonary hypertension occur predominantly in those younger than 65 years. Independently of the underlying disease, the development of pulmonary hypertension is associated with clinical deterioration and a substantially increased mortality risk. Global research efforts are needed to establish preventive strategies and treatments for the various types of pulmonary hypertension. PMID:26975810

  4. Right Pulmonary Artery Distensibility Index (RPAD Index). A field study of an echocardiographic method to detect early development of pulmonary hypertension and its severity even in the absence of regurgitant jets for Doppler evaluation in heartworm-infected dogs.

    PubMed

    Venco, Luigi; Mihaylova, Liliya; Boon, June A

    2014-11-15

    Despite the term "heartworm disease" Dirofilaria immitis infection in dogs should be considered a pulmonary arterial disease that might only involve the right heart structures in its late stage. Chronic infection by adult heartworms in dogs results in proliferative endoarteritis leading to progressively increasing pulmonary artery pressure due to reduced elasticity. Elasticity allows the pulmonary arteries to stretch in response to each pulse and helps maintain a relatively constant pressure in the arteries despite the pulsating nature of the blood flow. Pulmonary artery distensibility for both acute and chronic pulmonary hypertension has been investigated in humans using MRI and has been correlated with the severity of hypertension and its outcome and treatment response. The aim of the present study was to investigate whether echocardiographic measurement of the percentage change in diameter of the right pulmonary artery in systole and diastole (distensibility) may be of value in assessing the presence and severity of pulmonary hypertension in heartworm-infected dogs. The Right Pulmonary Artery Distensibility Index (RPAD Index) (which is calculated as the difference in diameter of the right pulmonary artery in systole and diastole) was calculated in healthy and naturally infected heartworm-positive dogs. The right pulmonary artery was chosen because it is usually affected earlier and to a greater degree. Data were obtained from healthy heartworm-free dogs without any clinical, radiographic, or echocardiographic signs of pulmonary hypertension; naturally infected heartworm-positive dogs in different stages of the disease in which pulmonary pressure could be measured by Doppler echocardiography (using tricuspid and or pulmonary regurgitation velocity and pressure gradient); and naturally infected heartworm-positive dogs in different stages of the disease (with or without tricuspid and or pulmonary regurgitation) in which the pulmonary pressure was measured

  5. Tumor necrosis factor alpha-induced pulmonary vascular endothelial injury.

    PubMed Central

    Goldblum, S E; Hennig, B; Jay, M; Yoneda, K; McClain, C J

    1989-01-01

    Tumor necrosis factor alpha (TNF-alpha) mediates components of the acute-phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied whether human recombinant TNF-alpha (rTNF-alpha) could increase pulmonary edema formation and pulmonary vascular permeability. Rabbits preinfused with 125I-albumin were administered rTNF-alpha or saline. Animals were sacrificed, and lung wet/dry weight ratios as well as bronchoalveolar lavage fluid and plasma 125I activities were determined. rTNF-alpha increased lung wet/dry weight ratios by 151% (P less than 0.02) and bronchoalveolar lavage fluid/plasma 125I activity ratios by 376% (P less than 0.01) compared with values for saline controls. Electron microscopy of lung sections demonstrated endothelial injury, perivascular edema, and extravasation of an ultrastructural permeability tracer. To demonstrate that rTNF-alpha could directly increase pulmonary vascular endothelial permeability in vitro, we studied albumin transfer across cultured porcine pulmonary artery endothelial cell monolayers. rTNF-alpha induced time-dependent dose-response increments in transendothelial albumin flux in the absence of granulocyte effector cells. These observations suggest that rTNF-alpha can provoke acute pulmonary vascular endothelial injury in vivo as well as in vitro. Images PMID:2925247

  6. [Surgical treatment of chronic thromboembolic pulmonary hypertension].

    PubMed

    Mercier, Olaf; Fadel, Elie; Mussot, Sacha; Fabre, Dominique; Ladurie, François-Leroy; Angel, Claude; Brenot, Philippe; Riou, Jean-Yves; Bourkaib, Riad; Lehouerou, Daniel; Musat, Andy; Stephan, François; Rohnean, Adéla; Jaïs, Xavier; Humbert, Marc; Sitbon, Olivier; Simonneau, Gérald; Dartevelle, Philippe

    2014-09-01

    Chronic thromboembolic pulmonary hypertension is a rare but underdiagnosed disease. The development of imaging played a crucial role for the screening and the decision of operability over the past few years. Indeed, chronic thromboembolic pulmonary hypertension is the only type of pulmonary hypertension with a potential curative treatment: pulmonary endarterectomy. It is a complexe surgical procedure performed under cardiopulmonary bypass with deep hypothermia and circulatory arrest. The aim of the procedure is to completely remove the scar tissue inside the pulmonary arteries down to the segmental and sub-segmental levels. Compared to lung transplantation, which carries a postoperative mortality of 15-20% and a 5-year survival of 50%, pulmonary endarterectomy is a curative treatment with a postoperative mortality of less than 3%. However, lung transplantation remains an option for young patients with inoperable distal disease or after pulmonary endarterectomy failure. Considering that medical history of deep venous thrombosis or pulmonary embolism is lacking in 25 to 50%, the diagnosis of chronic thromboembolic pulmonary hypertension remains challenging. The lung V/Q scan is useful for the diagnosis showing ventilation and perfusion mismatches. Lesions located at the level of the pulmonary artery, the lobar or segmental arteries may be accessible to surgical removal. The pulmonary angiogram with the lateral view and the pulmonary CT scan help to determine the level of the intravascular lesions. If there is a correlation between the vascular obstruction assessed by imaging and the pulmonary resistance, pulmonary endarterectomy carries a postoperative mortality of less than 3% and has a high rate of success. If the surgery is performed at a later stage of the disease, pulmonary arteriolitis developed mainly in unobstructed territories and participated in the elevated vascular resistance. At this stage, postoperative risk is higher. PMID:25154908

  7. Temporal correlation of optical coherence tomography in-vivo images of rabbit airway for the diagnosis of edema

    NASA Astrophysics Data System (ADS)

    Kang, DongYel; Wang, Alex; Tjoa, Tjoson; Volgger, Veronika; Hamamoto, Ashley; Su, Erica; Jing, Joseph; Chen, Zhongping; Wong, Brian J. F.

    2014-03-01

    Recently, full-range optical coherence tomography (OCT) systems have been developed to image the human airway. These novel systems utilize a fiber-based OCT probe which acquires three-dimensional (3-D) images with micrometer resolution. Following an airway injury, mucosal edema is the first step in the body's inflammatory response, which occasionally leads to airway stenosis, a life-threatening condition for critically ill newborns. Therefore, early detection of edema is vital for airway management and prevention of stenosis. In order to examine the potential of the full-range OCT to diagnose edema, we investigated temporal correlation of OCT images obtained from the subglottic airway of live rabbits. Temporally correlated OCT images were acquired at fixed locations in the rabbit subglottis of either artificially induced edema or normal tissues. Edematous tissue was experimentally modeled by injecting saline beneath the epithelial layer of the subglottic mucosa. The calculated cross temporal correlations between OCT images of normal airway regions show periodicity that correlates with the respiratory motion of the airway. However, the temporal correlation functions calculated from OCT images of the edematous regions show randomness without the periodic characteristic. These in-vivo experimental results of temporal correlations between OCT images show the potential of a computer-based or -aided diagnosis of edema in the human respiratory mucosa with a full-range OCT system.

  8. Diabetic Macular Edema: From Old Concepts to New Therapeutic Avenues

    PubMed Central

    Mansour, Ahmad M; Pulido, Jose S; Arevalo, J Fernando

    2015-01-01

    Diabetic macular edema (DME) is a significant cause of blindness in the working population and is currently challenging to treat. Current interventions include focal laser or intravitreal injections. This article outlines a new treatment protocol based on the theory that peripheral ischemia is the precursor to angiogenesis, which will ultimately gather its momentum at the fovea. Extreme peripheral light laser panretinal photocoagulation (PRP) back to the equator reduces excessive production of the vascular endothelial growth factor (VEGF) in the eye. This decreases VEGF-induced DME and provides long-term protection against the development of neovascularization. Initial exacerbation of DME often accompanies PRP. Therefore, injections of anti-VEGF agents (with or without dexamethasone implants) initially can forestall worsening of DME and prevent loss of vision. However, on the other hand, applying peripheral PRP and intraocular injections can induce posterior vitreous detachment (PVD). This could help release vitreomacular adhesions (VMA) and vitreomacular traction (VMT), thereby decreasing DME severity and improving the response to intravitreal injections. In the current approach, peripheral retinal photocoagulation should stop the drive for VEGF release; moreover, laser ablation should produce secondary, accidental, and beneficial PVD. This approach precludes focal laser therapy and paves the path for prolonged intervals between anti-VEGF therapy. PMID:27800500

  9. Acute hemorrhagic edema of infancy and common mimics.

    PubMed

    Homme, James L; Block, Jason M

    2016-05-01

    Acute hemorrhagic edema of infancy (AHEI) is a rare acute benign cutaneous leukocytoclastic vasculitis affecting children younger than 24 months of age. Its presentation can be confused with those of urticaria, erythema multiforme, Henoch-Schönlein purpura, idiopathic thrombocytopenia,meningococcemia, Kawasaki disease, and drug rash. We present 2 cases of acute hemorrhagic edema of infancy, discuss the characteristics of AHEI, and compare and contrast AHEI with similar dermatologic presentations. This review provides emergency physicians with the basic knowledge necessary to easily recognize AHEI as a distinct clinical entity. The patients were 19- and 23-month-old females who presented to the pediatric emergency department at St Mary's Hospital,Mayo Clinic in Rochester, Minnesota, with impressive purpuric rashes and edema of the hands and feet after preceding upper respiratory tract infections. Both children had benign courses with complete resolution of clinical findings. These 2 cases typify the presentation of AHEI.Acute hemorrhagic edema of infancy presents with characteristic purpuric lesions and extremity edema. The emergency physician's recognition of these presenting characteristics will help diagnose AHEI, avoid unnecessary procedures and tests, and aid in counseling the patient's parents.

  10. Finger stiffness or edema as presenting symptoms of eosinophilic fasciitis.

    PubMed

    Suzuki, Shingo; Noda, Kazutaka; Ohira, Yoshiyuki; Shikino, Kiyoshi; Ikusaka, Masatomi

    2015-10-01

    To investigate the clinical features and finger symptoms of eosinophilic fasciitis (EF), we reviewed five patients with EF. The chief complaint was pain, edema and/or stiffness of the extremities. The distal extremities were affected in all patients, and there was also proximal involvement in one patient. One patient had asymmetrical symptoms. All four patients with upper limb involvement had limited range of motion of the wrist joints, and three of them complained of finger symptoms. Two of these three patients showed slight non-pitting edema of the hands, and the other one had subcutaneous induration of the forearm. All four patients with lower limb symptoms had limited range of motion of the ankle joints, and two showed edema or induration of the legs. Inflammatory changes in the joints were not detected in any of the patients. Two patients displayed neither objective induration nor edema, and two patients had muscle tenderness. In conclusion, finger symptoms of patients with EF might be caused by fasciitis of the forearms, which leads to dysfunction of the long finger flexors and extensors as well as slight edema of hands. Limited range of motion of wrist and/or ankle joints indicates sensitively distal muscle dysfunction caused by fasciitis.

  11. Sox18 preserves the pulmonary endothelial barrier under conditions of increased shear stress.

    PubMed

    Gross, Christine M; Aggarwal, Saurabh; Kumar, Sanjiv; Tian, Jing; Kasa, Anita; Bogatcheva, Natalia; Datar, Sanjeev A; Verin, Alexander D; Fineman, Jeffrey R; Black, Stephen M

    2014-11-01

    Shear stress secondary to increased pulmonary blood flow (PBF) is elevated in some children born with congenital cardiac abnormalities. However, the majority of these patients do not develop pulmonary edema, despite high levels of permeability inducing factors. Previous studies have suggested that laminar fluid shear stress can enhance pulmonary vascular barrier integrity. However, little is known about the mechanisms by which this occurs. Using microarray analysis, we have previously shown that Sox18, a transcription factor involved in blood vessel development and endothelial barrier integrity, is up-regulated in an ovine model of congenital heart disease with increased PBF (shunt). By subjecting ovine pulmonary arterial endothelial cells (PAEC) to laminar flow (20 dyn/cm(2) ), we identified an increase in trans-endothelial resistance (TER) across the PAEC monolayer that correlated with an increase in Sox18 expression. Further, the TER was also enhanced when Sox18 was over-expressed and attenuated when Sox18 expression was reduced, suggesting that Sox18 maintains the endothelial barrier integrity in response to shear stress. Further, we found that shear stress up-regulates the cellular tight junction protein, Claudin-5, in a Sox18 dependent manner, and Claudin-5 depletion abolished the Sox18 mediated increase in TER in response to shear stress. Finally, utilizing peripheral lung tissue of 4 week old shunt lambs with increased PBF, we found that both Sox18 and Claudin-5 mRNA and protein levels were elevated. In conclusion, these novel findings suggest that increased laminar flow protects endothelial barrier function via Sox18 dependent up-regulation of Claudin-5 expression. PMID:24677020

  12. Sox18 preserves the pulmonary endothelial barrier under conditions of increased shear stress

    PubMed Central

    Gross, Christine M.; Aggarwal, Saurabh; Kumar, Sanjiv; Tian, Jing; Kasa, Anita; Bogatcheva, Natalia; Datar, Sanjeev A.; Verin, Alexander D.; Fineman, Jeffrey R.; Black, Stephen M.

    2014-01-01

    Shear stress secondary to increased pulmonary blood flow (PBF) is elevated in some children born with congenital cardiac abnormalities. However, the majority of these patients do not develop pulmonary edema, despite high levels of permeability inducing factors. Previous studies have suggested that laminar fluid shear stress can enhance pulmonary vascular barrier integrity. However, little is known about the mechanisms by which this occurs. Using microarray analysis, we have previously shown that Sox18, a transcription factor involved in blood vessel development and endothelial barrier integrity, is up-regulated in an ovine model of congenital heart disease with increased PBF (shunt). By subjecting ovine pulmonary arterial endothelial cells (PAEC) to laminar flow (20 dyn/cm2), we identified an increase in trans-endothelial resistance (TER) across the PAEC monolayer that correlated with an increase in Sox18 expression. Further, the TER was also enhanced when Sox18 was over-expressed and attenuated when Sox18 expression was reduced, suggesting that Sox18 maintains the endothelial barrier integrity in response to shear stress. Further, we found that shear stress up-regulates the cellular tight junction protein, Claudin-5, in a Sox18 dependent manner, and Claudin-5 depletion abolished the Sox18 mediated increase in TER in response to shear stress. Finally, utilizing peripheral lung tissue of 4 week old shunt lambs with increased PBF, we found that both Sox18 and Claudin-5 mRNA and protein levels were elevated. In conclusion, these novel findings suggest that increased laminar flow protects endothelial barrier function via Sox18 dependent up-regulation of Claudin-5 expression. PMID:24677020

  13. Spectral Domain Optical Coherence Tomography Features and Classification Systems for Diabetic Macular Edema: A Review.

    PubMed

    Ruia, Surabhi; Saxena, Sandeep; Gemmy Cheung, Chui Ming; Gilhotra, Jagjit S; Lai, Timothy Y Y

    2016-01-01

    Spectral domain optical coherence tomography (SD-OCT) is fast becoming the current standard of care for the detection and assessment of diabetic macular edema. With the application of SD-OCT for imaging of retinal microstructure and measurement of retinal thickness, new information regarding disease characteristics has been gathered, which was unrecognized previously. Retinal thickness measurements on SD-OCT have also been used for deciding the management and monitoring of the disease. Since its development, OCT has enhanced the understanding of retinal anatomical changes in diabetic retinopathy. Several authors have used SD-OCT to classify diabetic macular edema with the purpose of correlating the pathophysiology with disease severity. The classification systems have helped monitor the treatment efficacy and provide prognostic information on the treatment outcome. The following review article summarizes these classifications. PMID:27632028

  14. Bilateral Bone Marrow Edema Syndrome of the Femoral Head with a Unique Onset: A Case Report.

    PubMed

    Yi, Seung Rim; Lee, Ye Hyun; Kim, Hae Min

    2015-12-01

    Bone marrow edema syndrome (BMES) is a rare condition which mainly affects the hip area. The etiology and pathogenesis of BMES is still unclear. Pain near the affected area, regional osteoporosis, bone marrow edema (identified using magnetic resonance imaging) and spontaneous regression within 6-12 months are the main characteristics of BMES. In this case, a 52-year-old male was diagnosed with BMES of the right hip followed by spontaneous subsiding of symptoms. After 3 years, and under nearly the same social and physical conditions, he was admitted again with newly developed left hip pain and again diagnosed with BMES. We report this rare case since a similar one has not been previously reported in the domestic literature and may be considered valuable for basic research relating to the pathogenesis of BMES. PMID:27536636

  15. Bilateral Bone Marrow Edema Syndrome of the Femoral Head with a Unique Onset: A Case Report

    PubMed Central

    Yi, Seung Rim; Kim, Hae Min

    2015-01-01

    Bone marrow edema syndrome (BMES) is a rare condition which mainly affects the hip area. The etiology and pathogenesis of BMES is still unclear. Pain near the affected area, regional osteoporosis, bone marrow edema (identified using magnetic resonance imaging) and spontaneous regression within 6-12 months are the main characteristics of BMES. In this case, a 52-year-old male was diagnosed with BMES of the right hip followed by spontaneous subsiding of symptoms. After 3 years, and under nearly the same social and physical conditions, he was admitted again with newly developed left hip pain and again diagnosed with BMES. We report this rare case since a similar one has not been previously reported in the domestic literature and may be considered valuable for basic research relating to the pathogenesis of BMES. PMID:27536636

  16. Pulmonary Hypertension Secondary to COPD.

    PubMed

    Shujaat, Adil; Bajwa, Abubakr A; Cury, James D

    2012-01-01

    The development of pulmonary hypertension in COPD adversely affects survival and exercise capacity and is associated with an increased risk of severe acute exacerbations. Unfortunately not all patients with COPD who meet criteria for long term oxygen therapy benefit from it. Even in those who benefit from long term oxygen therapy, such therapy may reverse the elevated pulmonary artery pressure but cannot normalize it. Moreover, the recent discovery of the key roles of endothelial dysfunction and inflammation in the pathogenesis of PH provides the rationale for considering specific pulmonary vasodilators that also possess antiproliferative properties and statins.

  17. Postmortem pulmonary CT in hypothermia.

    PubMed

    Schweitzer, Wolf; Thali, Michael; Giugni, Giannina; Winklhofer, Sebastian

    2014-12-01

    Fatal hypothermia has been associated with pulmonary edema. With postmortem full body computed tomography scanning (PMCT), the lungs can also be examined for CT attenuation. In fatal hypothermia cases low CT attenuation appeared to prevail in the lungs. We compared 14 cases of fatal hypothermia with an age-sex matched control group. Additionally, 4 cases of carbon monoxide (CO) poisoning were examined. Furthermore, 10 test cases were examined to test predictability based on PMCT. Two readers measured CT attenuation on four different axial slices across the lungs (blinded to case group and other reader's results). Hypothermia was associated with statistically significantly lower lung PMCT attenuation and lower lung weights than controls, and there was a dose-effect relationship at an environmental temperature cutoff of 2 °C. CO poisoning yielded low pulmonary attenuation but higher lung weights. General model based prediction yielded a 94% probability for fatal hypothermia deaths and a 21% probability for non-hypothermia deaths in the test group. Increased breathing rate is known to accompany both CO poisoning and hypothermia, so this could partly explain the low PMCT lung attenuation due to an oxygen dissociation curve left shift. A more marked distension in fatal hypothermia, compared to CO poisoning, indicates that further, possibly different mechanisms, are involved in these cases. Increased dead space and increased stiffness to deflation (but not inflation) appear to be effects of inhaling cold air (but not CO) that may explain the difference in low PMCT attenuation seen in hypothermia cases. PMID:25326676

  18. Postmortem pulmonary CT in hypothermia.

    PubMed

    Schweitzer, Wolf; Thali, Michael; Giugni, Giannina; Winklhofer, Sebastian

    2014-12-01

    Fatal hypothermia has been associated with pulmonary edema. With postmortem full body computed tomography scanning (PMCT), the lungs can also be examined for CT attenuation. In fatal hypothermia cases low CT attenuation appeared to prevail in the lungs. We compared 14 cases of fatal hypothermia with an age-sex matched control group. Additionally, 4 cases of carbon monoxide (CO) poisoning were examined. Furthermore, 10 test cases were examined to test predictability based on PMCT. Two readers measured CT attenuation on four different axial slices across the lungs (blinded to case group and other reader's results). Hypothermia was associated with statistically significantly lower lung PMCT attenuation and lower lung weights than controls, and there was a dose-effect relationship at an environmental temperature cutoff of 2 °C. CO poisoning yielded low pulmonary attenuation but higher lung weights. General model based prediction yielded a 94% probability for fatal hypothermia deaths and a 21% probability for non-hypothermia deaths in the test group. Increased breathing rate is known to accompany both CO poisoning and hypothermia, so this could partly explain the low PMCT lung attenuation due to an oxygen dissociation curve left shift. A more marked distension in fatal hypothermia, compared to CO poisoning, indicates that further, possibly different mechanisms, are involved in these cases. Increased dead space and increased stiffness to deflation (but not inflation) appear to be effects of inhaling cold air (but not CO) that may explain the difference in low PMCT attenuation seen in hypothermia cases.

  19. A fatal adverse effect of cefazolin administration: severe brain edema in a patient with multiple meningiomas.

    PubMed

    Tribuddharat, Sirirat; Sathitkarnmanee, Thepakorn; Kitkhuandee, Amnat; Theerapongpakdee, Sunchai; Ngamsaengsirisup, Kriangsak; Chanthawong, Sarinya

    2016-01-01

    Cefazolin is commonly administered before surgery as a prophylactic antibiotic. Hypersensitivity to cefazolin is not uncommon, and the symptoms mostly include urticaria, skin reaction, diarrhea, vomiting, and transient neutropenia, which are rarely life threatening. We present a rare case of fatal cefazolin hypersensitivity in a female who was diagnosed with multiple meningiomas and scheduled for craniotomy and tumor removal. Immediately after cefazolin IV administration, the patient developed acute hypertensive crisis, which resolved within 10 minutes after the treatment. This was followed by unexplained metabolic acidosis. The patient then developed severe brain edema 100 minutes later. The patient had facial edema when her face was exposed for the next 30 minutes. A computed tomography scan revealed global brain edema with herniation. She was admitted to the intensive care unit for symptomatic treatment and died 10 days after surgery from multiorgan failure. The serum IgE level was very high (734 IU/mL). Single-dose administration of cefazolin for surgical prophylaxis may lead to rare, fatal adverse reaction. The warning signs are sudden, unexplained metabolic acidosis, hypertensive crisis, tachycardia, and facial angioedema predominating with or without cutaneous symptoms like urticaria. PMID:26929668

  20. Alleviation of ischemia-induced brain edema by activation of the central histaminergic system in rats.

    PubMed

    Irisawa, Yumi; Adachi, Naoto; Liu, Keyue; Arai, Tatsuru; Nagaro, Takumi

    2008-09-01

    We have reported that facilitation of central histaminergic activity prevents the development of ischemia-induced brain injury. Since cerebral edema is a major cause of brain damage, we studied effects on brain edema of postischemic administration of L-histidine, a precursor of histamine, and thioperamide, a histamine H(3)-receptor antagonist, both of which enhance central histaminergic activity. Focal cerebral ischemia for 2 h was provoked by transient occlusion of the right middle cerebral artery in rats, and the water content and infarct size were determined 24 h after reperfusion. Changes in the extracellular concentration of histamine were examined in the striatum by a microdialysis procedure, and effects of these compounds were evaluated. Repeated administration of L-histidine (1000 mg/kg x 2, i.p.), immediately and 6 h after reperfusion, reduced the increase in the water contents in ischemic regions. Simultaneous administration of thioperamide (5 mg/kg, s.c.) with L-histidine (1000 mg/kg, i.p.) completely prevented edema formation and alleviated brain infarction, although a single dose of L-histidine, immediately after reperfusion, showed no benefits. The striatal histamine level was gradually increased after reperfusion as well as during ischemia. Simultaneous administration of thioperamide with L-histidine markedly increased the brain histamine concentration, and the value increased up to 230% of that in the saline group 5 - 6 h after reperfusion. L-Histidine alone did not affect the increase in the histamine output after ischemia. These findings suggest that further activation of the central histaminergic system after initiation of cerebral ischemia prevents development of ischemia-induced brain edema.

  1. [Pulmonary melioidosis].

    PubMed

    Perret, J L; Vidal, D; Thibault, F

    1998-12-01

    Melioidosis is most frequently encountered in pulmonary localization. Melioidosis is an infectious disease caused by Burkholderia pseudomallei first described by Whitmore in 1912 in Burma. B. pseudomallei is a Gram negative rod belonging to the Pseudomonadaceae family. Soil and water are the natural reservoirs for the germ which is a specific pathogen for several mammal species. Long endemic in Southeast Asia and several tropical zones, B. pseudomallei has recently been found in temperate zones, including France. Human contamination occurs via the transcutaneous route and often leads to dormant inapparent infection. Many conditions, such as diabetes, renal lithiasis, various circumstances of immunodepression or stress, facilitate clinical manifestations which vary greatly. Pulmonary manifestations may be acute and extensive, producing a torpid pseudo-tuberculous condition or a variety of clinical and radiological features mimicking other diseases. Bacteriological and serological tests may be negative. Exposure in an endemic zone, the notion of a favorable context, weight loss, cavitary images on successive chest x-rays and the presence of extra-pulmonary localizations may be suggestive. Ceftazidime or the amoxicillin-clavulanic acid combination are indicated, but mortality in acute forms still reaches 40%. Relapse can be expected if the treatment duration is too short. PMID:10100350

  2. Bone marrow edema syndrome in postpartal women: treatment with iloprost.

    PubMed

    Aigner, Nicholas; Meizer, Roland; Meraner, Dominik; Becker, Stephan; Meizer, Elizabeth; Landsiedl, Franz

    2009-04-01

    Bone marrow edema syndrome of the femoral head in pregnant women is a rare disease resulting in disabling coxalgia, beginning in the last 3 months of pregnancy and persisting for several months after parturition. The parenteral administration of the vasoactive drug iloprost constitutes a new approach to the treatment of painful bone marrow edema syndrome of the hip of pregnant women. Six postpartal women (8 hips) with bone marrow edema syndrome of the femoral head were treated with iloprost followed by 3 weeks of partial weight-bearing. Relief from pain, restoration of functional capacity, and normalization of the MRI signal pattern were rapidly achieved, thus avoiding the need for surgical intervention. As the substance is contraindicated in pregnancy, therapy may begin only some days after parturition, with a short discontinuation in breastfeeding.

  3. [Literature review: Diabetic macular edema. Repercussions and treatment].

    PubMed

    Carmona-Moxica, Luis Roberto; Hernández-Núñez, Fabiola

    2015-01-01

    In our country there is a report of prevalence of Diabetes Mellitus in the adult population of a 10%, occupying one of the first causes of morbidity-mortality, also visual and labor incapacity. Macular edema is the first cause of lost vision in the diabetic patient. There are classic methods to detect it, as the examination with biomicroscope, indirect ophthalmoscopy, fluorangiography (FAR), and the new and gold standard method for diagnostic and sequence examination, Ocular Coherence Tomography (OCT). With OCT had been possible the study of distinct types of macular edema, that could represent distinct clinical states, with specific treatments. The protocol of treatment of macular edema, continues changing. The traditional methods as metabolic control and fotocoagulation with Laser now have more options as intravitreal injection of triamcinolone, or antiangiogenic substances, even surgical treatment with vitrectomy. There are many prospective and randomized studies evaluating this methods, so until now is difficult to determine which treatment is the best.

  4. Prediction of visual acuity recovery in cystoid macular edema.

    PubMed

    McDonnell, P J; Ryan, S J; Walonker, A F; Miller-Scholte, A

    1992-05-01

    Three consecutive patients participated in a prospective evaluation of pseudophakic cystoid macular edema. The duration of the macular edema ranged from 6 to 8 months. On the initial visit, the best corrected acuity with spectacles was determined and a potential acuity meter reading was obtained; this test suggested potential for visual recovery in two of the three patients. Sub-tenon's injections of methylprednisolone acetate (20 mg) were administered along with topical 1% prednisolone acetate and 1% atropine. One month later, visual acuity was improved by more than 2 Snellen lines in all three of the patients. A visual acuity measurement with the potential acuity meter that is better than the best corrected acuity with spectacles may reflect the presence of intact, but dysfunctional photoreceptors that are capable of restoring visual acuity upon resolution of the edema.

  5. Pulmonary Arterial Hypertension

    MedlinePlus

    ... What Is Pulmonary Hypertension? To understand pulmonary hypertension (PH) it helps to understand how blood ows throughout ... is too high, it is called pulmonary hypertension (PH). How the pressure in the right side of ...

  6. What Causes Pulmonary Hypertension?

    MedlinePlus

    ... from the NHLBI on Twitter. What Causes Pulmonary Hypertension? Pulmonary hypertension (PH) begins with inflammation and changes in the ... different types of PH. Group 1 pulmonary arterial hypertension (PAH) may have no known cause, or the ...

  7. Iris angiography in cystoid macular edema after cataract extraction.

    PubMed

    Kottow, M; Hendrickson, P

    1975-07-01

    Iris angiography was performed on eight patients (nine eyes), who had cystoid macular edema postcataract extraction. The fundus fluorescein angiographies showed typical star-shaped, multiloculated staining of the macular area. The iris angiographies demonstrated moderate to massive leakage of dye from the iris, and possibly leakage of ciliary body vessels into the anterior chamber, thus evidencing the until now suspected but undocumented fact that fluorescein leakage is not restricted to the fundus vessels. These data tend to support the idea that this type of macular edema is due to a vascular abnormality, and not to altered vitreous mechanics.

  8. Discrimination between different types of white matter edema with diffusion-weighted MR imaging.

    PubMed

    Ebisu, T; Naruse, S; Horikawa, Y; Ueda, S; Tanaka, C; Uto, M; Umeda, M; Higuchi, T

    1993-01-01

    Brain edema can be classified into three categories: vasogenic, cytotoxic, and interstitial. The mechanism of edema is thought to be different in each type. The authors studied the movement of water molecules in each type of white matter edema in a rat model by using diffusion-weighted magnetic resonance imaging. Conventional T2-weighted imaging did not allow distinction between the three types of white matter edema; the three types of edema were, however, distinguished by using diffusion-weighted imaging. The apparent diffusion coefficient (ADC) of water was different in each type of edema. Water molecules in cytotoxic edema induced by triethyl-tin intoxication showed a smaller and less anisotropic ADC than in normal white matter. In contrast, water in vasogenic edema induced by cold injury had a larger and more anisotropic ADC than in normal white matter. Water in interstitial edema due to kaolin-induced hydrocephalus had an anisotropic and very large ADC. PMID:8280975

  9. [Immune complex glomerulonephritis associated with pulmonary tuberculosis].

    PubMed

    Villar, I; Hernández, E; Cozzi, J; Paletta, C; Mathurín, S

    1994-01-01

    A 32 year old man was admitted for dyspnea, hemoptysis, macroscopic hematuria, hypertension (140/100), peripheral edema and hemodynamic decompensation. Lung Xrays revealed pulmonary edema and a cavity in the left apex. Laboratory determinations revealed an altered renal function with increased creatinine and urea levels and nephrotic syndrome. There was leucocyturia, hematuria and cylindruria. The sputum showed a large number of acid-fast bacilli. The patient began anti-tuberculosis treatment with three drugs (isoniacid, rifampicin, pirazinamide). On ultrasonography, both kidneys revealed ecogenic lesions with size, shape and cortico-medular relationship preserved. The patient persisted with altered renal function, steady levels of urea nitrogen, creatinine and potassium, preserved diuresis and hypertension. Bidimensional echocardiogram: LVDD 55 mm, hypoquinetic septum, pericardic effusion, thickened pericardium, pleural effusion, shortening fraction decreased. He received treatment for this congestive cardiac failure and hypertension with enalapril, nifedipine and fursemide. A percutaneous renal biopsy was performed with anatomopathologic diagnosis of diffuse encocapillar proliferative glomerulonephritis with crescents (15%) and total glomerular sclerosis (33%). Immunofluorescence: positive, immune-complexes with IgM and C3. The patient gradually recovered his normal renal function, improved his pleural effusions and normalized his cardiac function. He was discharged in good clinical condition on the 69th day of anti-tuberculosis treatment. An association between pulmonary tuberculosis and glomerulonephritis is discussed. It is proposed that renal lesions might be the consequence of the tuberculosis due to the sedimentation of circulating immune-complexes. PMID:7854090

  10. Acute respiratory distress syndrome caused by Mycoplasma pneumoniae without elevated pulmonary vascular permeability: a case report

    PubMed Central

    Takahashi, Naoki; Oi, Rie; Ota, Muneyuki; Toriumi, Shinichi; Ogushi, Fumitaka

    2016-01-01

    Sporadic patients with acute respiratory distress syndrome (ARDS) caused by Mycoplasma pneumoniae have been reported. However, knowledge about the pathophysiology and pharmacological treatment of this condition is insufficient. Moreover, the pulmonary vascular permeability in ARDS related to M. pneumoniae infection has not been reported. We report a case of ARDS caused by Mycoplasma pneumoniae without elevated pulmonary vascular permeability, which was successfully treated using low-dose short-term hydrocortisone, suggesting that pulmonary infiltration in ARDS caused by Mycoplasma pneumoniae does not match the criteria of permeability edema observed in typical ARDS. PMID:27162691

  11. Effect of Vandetanib on Andes virus survival in the hamster model of Hantavirus pulmonary syndrome.

    PubMed

    Bird, Brian H; Shrivastava-Ranjan, Punya; Dodd, Kimberly A; Erickson, Bobbie R; Spiropoulou, Christina F

    2016-08-01

    Hantavirus pulmonary syndrome (HPS) is a severe disease caused by hantavirus infection of pulmonary microvascular endothelial cells leading to microvascular leakage, pulmonary edema, pleural effusion and high case fatality. Previously, we demonstrated that Andes virus (ANDV) infection caused up-regulation of vascular endothelial growth factor (VEGF) and concomitant downregulation of the cellular adhesion molecule VE-cadherin leading to increased permeability. Analyses of human HPS-patient sera have further demonstrated increased circulating levels of VEGF. Here we investigate the impact of a small molecule antagonist of the VEGF receptor 2 (VEGFR-2) activation in vitro, and overall impact on survival in the Syrian hamster model of HPS. PMID:27233645

  12. Pulmonary pathology in pediatric cerebral malaria.

    PubMed

    Milner, Danny; Factor, Rachel; Whitten, Rich; Carr, Richard A; Kamiza, Steve; Pinkus, Geraldine; Molyneux, Malcolm; Taylor, Terrie

    2013-12-01

    Respiratory signs are common in African children where malaria is highly endemic, and thus, parsing the role of pulmonary pathology in illness is challenging. We examined the lungs of 100 children from an autopsy series in Blantyre, Malawi, many of whom death was attributed to Plasmodium falciparum malaria. Our aim was to describe the pathologic manifestations of fatal malaria; to understand the role of parasites, pigment, and macrophages; and to catalog comorbidities. From available patients, which included 55 patients with cerebral malaria and 45 controls, we obtained 4 cores of lung tissue for immunohistochemistry and morphological evaluation. We found that, in patients with cerebral malaria, large numbers of malaria parasites were present in pulmonary alveolar capillaries, together with extensive deposits of malaria pigment (hemozoin). The number of pulmonary macrophages in this vascular bed did not differ between patients with cerebral malaria, noncerebral malaria, and nonmalarial diagnoses. Comorbidities found in some cerebral malaria patients included pneumonia, pulmonary edema, hemorrhage, and systemic activation of coagulation. We conclude that the respiratory distress seen in patients with cerebral malaria does not appear to be anatomic in origin but that increasing malaria pigment is strongly associated with cerebral malaria at autopsy.

  13. Simple pulmonary eosinophilia

    MedlinePlus

    Pulmonary infiltrates with eosinophilia; Loffler syndrome; Eosinophilic pneumonia; Pneumonia - eosinophilic ... simple pulmonary eosinophilia is a severe type of pneumonia called acute idiopathic eosinophilic pneumonia.

  14. Localization of potential binding sites for the edema disease verotoxin (VT2e) in pigs.

    PubMed Central

    Waddell, T E; Coomber, B L; Gyles, C L

    1998-01-01

    The purpose of this study was to identify organs and cells to which the edema disease verotoxin (VT2e) could bind in pigs. Frozen 4-5 microns thick sections of organs usually affected in edema disease (colon, spinal cord, cerebellum and eyelid) and organs not usually affected (liver, ileum) from two 5- to 6-week-old weaned pigs were permeabilized with acetone, then exposed to VT2e. Unbound VT2e was removed by washing and bound VT2e was detected by immunohistochemistry. In the eyelid, double-label immunofluorescence was used to identify the cells to which VT2e bound. VT2e was shown to bind to all six organs that were examined. The toxin bound to arteries in all organs, to veins in all organs except the liver, and to enterocytes in the ileal crypts. Double labelling of eyelid with monoclonal antibodies specific for von Willebrand factor or alpha-smooth actin and VT2e showed that the toxin bound to endothelial and vascular smooth muscle cells. The binding of VT2e to endothelium is consistent with findings for other verotoxins but binding to vascular smooth muscle has not been reported for other verotoxins. It is concluded that i) factors other than the presence of receptors for VT2e influence the development of lesions in edema disease, and ii) smooth muscle necrosis, which is characteristic of the vascular lesions in edema disease, may be due to a direct action of toxin on smooth muscle cells. Images Figure 1. Figure 2. PMID:9553705

  15. Aquaporin-4 Deletion in Mice Reduces Encephalopathy and Brain Edema in Experimental Acute Liver Failure

    PubMed Central

    Rama Rao, Kakulavarapu V.; Verkman, A. S.; Curtis, Kevin M.; Norenberg, Michael D.

    2014-01-01

    Brain edema and associated astrocyte swelling leading to increased intracranial pressure are hallmarks of acute liver failure (ALF). Elevated blood and brain levels of ammonia have been implicated in the development of brain edema in ALF. Cultured astrocytes treated with ammonia have been shown to undergo cell swelling and such swelling was associated with an increase in the plasma membrane expression of aquaporin-4 (AQP4) protein. Further, silencing the AQP4 gene in cultured astrocytes was shown to prevent the ammonia-induced cell swelling. Here, we examined the evolution of brain edema in AQP4-null mice and their wild type counterparts (WT-mice) in different models of ALF induced by thioacetamide (TAA) or acetaminophen (APAP). Induction of ALF with TAA or APAP significantly increased brain water content in WT mice (by 1.6 ± 0.3 and 2.3 ± 0.4 %, respectively). AQP4 protein was significantly increased in brain plasma membranes of WT mice with ALF induced by either TAA or APAP. In contrast to WT-mice, brain water content did not increase in AQP4-null mice. Additionally, AQP4-null mice treated with either TAA or APAP showed a remarkably lesser degree of neurological deficits as compared to WT mice; the latter displayed an inability to maintain proper gait, and demonstrated a markedly reduced exploratory behavior, with the mice remaining in one corner of the cage with its head tilted downwards. These results support a central role of AQP4 in the brain edema associated with ALF. PMID:24321433

  16. Edema surrounding calcified intracranial cysticerci: clinical manifestations, natural history, and treatment

    PubMed Central

    Nash, Theodore

    2012-01-01

    Calcified granulomas are the most common radiological finding in neurocysticercosis (10–20% of endemic populations). A small proportion serves as foci of seizure activity, which results in large numbers of persons with epilepsy. Calcified granulomas are not all the same. Some demonstrate blood–brain barrier dysfunction (magnetic resonance imaging enhancement) most likely due to the presence of inflammation, visualizable scolices, and/or gliosis. About half the patients with a recent history of seizures, positive serology, and only calcified lesions develop perilesional edema at the time of a seizure recurrence. The natural history, treatment, and pathophysiology of this phenomenon are not well studied. Episodes are usually associated with seizures or other neurological manifestations, resolve by 4–6 weeks, sometimes occur repeatedly, and usually involve a subset of the same calcifications. Treatment is supportive. Histopathological examination of one calcification associated with multiple perilesional edema episodes revealed significant inflammation and supports the concept that perilesional edema is inflammatory in nature. This most likely is due to host responses to released or newly recognized parasite antigen and/or upregulation of the host immune response. Immunosuppressive and anti-inflammatory agents may be useful in prevention and/or treatment of this phenomenon. PMID:23265551

  17. Sjogren's syndrome presenting as remitting seronegative symmetric synovitis with pitting edema (RS3PE).

    PubMed

    Choi, Young Mi; Sheen, Dong Hyuk; Lee, Yun Jong; Lee, Eun Bong; Song, Yeong Wook

    2003-08-01

    Remitting seronegative symmetric synovitis with pitting edema (RS3PE) syndrome is characterized by symmetrical and acute synovitis, pitting edema, the absence of rheumatoid factor, increased acute phase reactants, lack of bony erosions on radiography, and benign and short clinical course. Half of all patients with Sjogren's syndrome experience arthritis during the disease course. We here describe the first case of Sjogren's syndrome presenting as RS3PE. She had swelling in knees, ankles, and wrists. After then the swelling spread to her lower legs, feet, face, and both hands. She was admitted to another hospital and was suspected of lupus or rheumatoid arthritis. Three months later, she had dry mouth and had lower lip biopsy. She was admitted to this hospital due to development of swelling in face and lower legs for 3 days. On physical examination, she had pitting edema in both hands and feet dorsum. Laboratory test showed elevated erythrocyte sedimentation rate, positivity of rheumatoid factor, anti-nuclear antibody, and anti-Ro antibody. There was no erosion in the hands radiography. Schirmer's test and lip biopsy was compatible with Sjogren's syndrome. She was diagnosed RS3PE and Sjogren's syndrome. She was begun with prednisolone and her symptoms improved gradually.

  18. High lung volume increases stress failure in pulmonary capillaries

    NASA Technical Reports Server (NTRS)

    Fu, Z.; Costello, M. L.; Tsukimoto, K.; Prediletto, R.; Elliott, A. R.; Mathieu-Costello, O.; West, J. B.

    1992-01-01

    We previously showed that when pulmonary capillaries in anesthetized rabbits are exposed to a transmural pressure (Ptm) of approximately 40 mmHg, stress failure of the walls occurs with disruption of the capillary endothelium, alveolar epithelium, or sometimes all layers. The present study was designed to test whether stress failure occurred more frequently at high than at low lung volumes for the same Ptm. Lungs of anesthetized rabbits were inflated to a transpulmonary pressure of 20 cmH2O, perfused with autologous blood at 32.5 or 2.5 cmH2O Ptm, and fixed by intravascular perfusion. Samples were examined by both transmission and scanning electron microscopy. The results were compared with those of a previous study in which the lung was inflated to a transpulmonary pressure of 5 cmH2O. There was a large increase in the frequency of stress failure of the capillary walls at the higher lung volume. For example, at 32.5 cmH2O Ptm, the number of endothelial breaks per millimeter cell lining was 7.1 +/- 2.2 at the high lung volume compared with 0.7 +/- 0.4 at the low lung volume. The corresponding values for epithelium were 8.5 +/- 1.6 and 0.9 +/- 0.6. Both differences were significant (P less than 0.05). At 52.5 cmH2O Ptm, the results for endothelium were 20.7 +/- 7.6 (high volume) and 7.1 +/- 2.1 (low volume), and the corresponding results for epithelium were 32.8 +/- 11.9 and 11.4 +/- 3.7. At 32.5 cmH2O Ptm, the thickness of the blood-gas barrier was greater at the higher lung volume, consistent with the development of more interstitial edema. Ballooning of the epithelium caused by accumulation of edema fluid between the epithelial cell and its basement membrane was seen at 32.5 and 52.5 cmH2O Ptm. At high lung volume, the breaks tended to be narrower and fewer were oriented perpendicular to the axis of the pulmonary capillaries than at low lung volumes. Transmission and scanning electron microscopy measurements agreed well. Our findings provide a physiological

  19. Factors influencing development and mortality of acute respiratory failure in hospitalized patient with active pulmonary tuberculosis: a 10-year retrospective review

    PubMed Central

    Maneenil, Kunlatida

    2016-01-01

    Background Pulmonary tuberculosis with acute respiratory failure is fatal and is a burden in the intensive care units and leads to mortality. This retrospective study identifies the factors influencing the development of pulmonary tuberculosis requiring mechanical ventilation (TBMV) and mortality in the hospitalized patients with pulmonary tuberculosis. Methods The medical records of hospitalized adult patients with pulmonary tuberculosis were retrospectively reviewed. Demographic data, clinical presentations, radiographic findings, biochemical tests, and clinical outcomes were collected. Data were compared by Student’s t-test and Chi-square test between groups. Select variables that were statistically significant with P values <0.1 were introduced into a forward, stepwise, logistic regression model. Odds ratios (ORs) and their 95% confidence intervals (CIs) identified the independent influencing factors in the development of TBMV and mortality. Results Of 268 enrolled patients, 185 (69.0%) were male. The patients were equally divided between the TBMV and non-TBMV groups. The shorter duration of illness (OR, 0.99; 95% CI, 0.98–0.99), underlying disease of AIDS (OR, 14.55; 95% CI, 1.71–123.91), presentation of fever (OR, 2.11; 95% CI, 1.20–3.71) and dyspnea (OR, 3.51; 95% CI, 2.02–6.11), large amount of acid fast bacilli on sputum smear (OR, 3.76; 95% CI, 1.90–7.47), lower serum albumin level (OR, 0.39; 95% CI, 0.26–0.59), and delayed initiation of anti-tuberculosis agents (OR, 1.06; 95% CI, 1.00–1.12) were independent factors to develop TBMV. Male gender (OR, 2.16; 95% CI, 1.01–4.61), consolidation pattern on chest X-ray (OR, 2.41; 95% CI, 1.17–4.98), and lower serum albumin (OR, 0.39; 95% CI, 0.21–0.71) were correlated to mortality. Conclusions The incidence and mortality rate of TBMV patients were high. Acute tuberculous pneumonia, underlying disease of AIDS, amount of acid fast bacilli, and delayed administration of anti-tuberculosis agents

  20. Saddle pulmonary embolus and bronchiolitis obliterans with organizing pneumonia develop simultaneously after first cyclophosphamide, methotrexate, 5FU chemotherapy for breast cancer.

    PubMed

    Al-Hameed, Fahad M

    2015-06-01

    A 62-year-old woman underwent a right mastectomy with axillary node dissection for a poorly differentiated ductal carcinoma. One month later, she underwent a left nephrectomy for a renal cell carcinoma. Two weeks after, she received her first cycle of cyclophosphamide, methotrexate, and 5FU (CMF) as a part of her breast cancer treatment. We describe an unusual case of non-occlusive saddle pulmonary embolus with extensive bilateral deep vein thrombosis and severe bronchiolitis obliterans with organizing pneumonia developing simultaneously after the first CMF chemotherapy for breast cancer. PMID:25987120

  1. Microscopic polyangiitis associated with pleuropericarditis, pulmonary embolism and pulmonary hemorrhage as a complication of silicosis

    PubMed Central

    Al-Rajhi, Amjad; Brega, Elisa Ferreira; Colman, Neil C.

    2015-01-01

    Silica (silicon dioxide) occupational exposure has been linked to both pulmonary and extra-pulmonary toxicity. Silicosis is the major pulmonary toxicity, which has also been associated with the development of collagen-vascular disease and with anti-neutrophil cytoplasmic antibody (ANCA)-positive vasculitis, especially perinuclear anti-neutrophil cytoplasmic antibodies (P-ANCA). The most common pulmonary manifestations of microscopic polyangitis (MPA) are interstitial fibrosis and alveolar hemorrhage. We describe a patient who had unusual presentation of microscopic polyangitis, characterized by lung hemorrhage, rapidly progressive glomerulonephritis, pleuropericarditis and pulmonary embolism that was associated with a history of silica exposure and radiologic evidence for silicosis. PMID:26236617

  2. Pulmonary Edema and Plasma Volume Changes in Dysbarism. M.S. Thesis - Texas Univ.

    NASA Technical Reports Server (NTRS)

    Joki, J. A.

    1972-01-01

    Two groups of anesthetized, fasted pigs were utilized. One group of 13 animals (8.5 to 16.6 kilograms) was exposed to a high-pressure environment, and the other group of eight animals (6.9 to 20.0 kilograms) constituted the control group. The experimental group was subjected to an atmosphere of 90 percent nitrogen and 10 percent oxygen at a pressure of 50 psig for 30 minutes and then decompressed at a rate 10 psi/min. Plasma volumes, using both iodine-125-tagged-albumin and chromium-51-tagged-cell dilution techniques, were measured before, immediately after, and at 30 and 60 minutes after decompression. Aortic and right-ventricular systolic pressures were also recorded. At 60 minutes after decompression, blood samples were taken, the animals were sacrificed, and the water content of the lungs, kidneys, livers, and spleens was estimated by measuring tissue wet weight and dry weight. Protein extravasation and tissue blood volumes were determined by measuring the iodine-125-tagged-albumin and chromium-51-tagged-cell spaces in homo-genates of the organs under investigation.

  3. Cardiovascular dysfunction and pulmonary edema secondary to severe envenoming by Tityus pachyurus sting. Case report.

    PubMed

    Izquierdo, Ledys María; Rodríguez Buitrago, Javier R

    2012-09-15

    The scorpion envenomation is considered the second event by poisonous animals in importance around the world according to the World Health Organization. In Colombia there are 35 species of clinical significance, among them, the genus Tityus, which contains the most deadly scorpions in South America and is represented by 29 species of wide distribution in Colombia, which include Tityus pachyurus causing life-threatening events, especially in children. The present work shows the case of a 12 years old boy, from Tolemaida to 2 h of Bogotá D.C., who was stung by a scorpion on his right thigh, with the onset of intense signs and symptoms of local effect rapidly progressing to severe systemic involvement causing myocardial dysfunction, cardiovascular collapse and heart arrest, and his favorable response to adequate basic and advanced life support and use of scorpion-specific F(ab')2 antivenom. PMID:22683677

  4. Pulmonary hypertension and pulmonary artery dissection

    PubMed Central

    Corrêa, Ricardo de Amorim; Silva, Luciana Cristina dos Santos; Rezende, Cláudia Juliana; Bernardes, Rodrigo Castro; Prata, Tarciane Aline; Silva, Henrique Lima

    2013-01-01

    Pulmonary artery dissection is a fatal complication of long-standing pulmonary hypertension, manifesting as acute, stabbing chest pain, progressive dyspnea, cardiogenic shock, or sudden death. Its incidence has been underestimated, and therapeutic options are still scarce. In patients with pulmonary hypertension, new chest pain, acute chest pain, or cardiogenic shock should raise the suspicion of pulmonary artery dissection, which can result in sudden death. PMID:23670510

  5. [Pulmonary hyalinizing granuloma mimicking pulmonary carcinoma].

    PubMed

    Uçvet, Ahmet; Tözüm, Halil; Gürsoy, Soner; Gülle, Ali Alper; Yaldiz, Sadik; Aydoğdu Dinç, Zekiye

    2006-01-01

    Pulmonary hyalinizing granuloma is a rare fibrosing nodular disease of the lung characterized by solitary or multiple pulmonary nodules. They can occur after inflammatory or post-inflammatory changes. A 60 years old asymptomatic patient admitted to our clinic because of a solid mass of 6 cm in his routine chest radiography. A lobectomy was performed and the histological diagnosis was reported as pulmonary hyalinizing granuloma. This case, mimicking pulmonary carcinoma, is rarely found in the literature. PMID:16615022

  6. Diagnostics for pulmonary tuberculosis

    PubMed Central

    Cudahy, Patrick

    2016-01-01

    Tuberculosis (TB) remains a leading cause of human suffering and mortality despite decades of effective treatment being available. Accurate and timely diagnosis remains an unmet goal. The HIV epidemic has also led to new challenges in the diagnosis of TB. Several new developments in TB diagnostics have the potential to positively influence the global campaign against TB. We aim to review the performance of both established as well as new diagnostics for pulmonary TB in adults, and discuss the ongoing challenges. PMID:27005271

  7. Balanoposthitis and Penile Edema: Atypical Manifestations of Primary Syphilis.

    PubMed

    Rovira-López, Roger; García-Martínez, Pablo; Martín-Ezquerra, Gemma; Pujol, Ramon M; Aventín, Daniel López

    2015-09-01

    The typical finding in primary syphilis stage is a unique, painless chancre with indurated borders. We report a case of primary syphilis presenting as erosive and crusted balanoposthitis with an underlying chancre, penile edema, and bilateral inguinal lymphadenopathy in a heterosexual man.

  8. Water entry into astrocytes during brain edema formation.

    PubMed

    Nase, Gabriele; Helm, P Johannes; Enger, Rune; Ottersen, Ole P

    2008-06-01

    The process of brain edema formation has been studied extensively at the macroscopic level. In contrast, little is known about water fluxes and volume changes at the cellular level in the initial phase of brain edema. Insight in these "microscopic" events could pave the way for more efficient prevention and therapy. Here, we report measurements of brain cell volume responses recorded in vivo in a model of systemic hyponatremia. Transgenic mice expressing fluorescent proteins in astrocytes were subjected to hypo-osmotic stress and two photon laser scanning microscopy. Volume measurements of glial cells in the cerebellum and the visual cortex indicate that individual astrocytes undergo a position-dependent increase in cell volume by a factor of two or more during edema formation. Our data are the first to show that volume changes can be monitored at the cellular level in vivo and demonstrate that astrocytes are sites of water entry in the initial phase of brain edema formation. The uptake of water in astrocytes is likely to reflect the strong expression of aquaporin-4 in these cells.

  9. Continuous IV Infusion is the Choice Treatment Route for Arginine-vasopressin Receptor Blocker Conivaptan in Mice to Study Stroke-evoked Brain Edema.

    PubMed

    Zeynalov, Emil; Jones, Susan M; Elliott, J Paul

    2016-01-01

    Stroke is one of the major causes of morbidity and mortality in the world. Stroke is complicated by brain edema and other pathophysiological events. Among the most important players in the development and evolution of stroke-evoked brain edema is the hormone arginine-vasopressin and its receptors, V1a and V2. Recently, the V1a and V2 receptor blocker conivaptan has been attracting attention as a potential drug to reduce brain edema after stroke. However, animal models which involve conivaptan applications in stroke research need to be modified based on feasible routes of administration. Here the outcomes of 48 hr continuous intravenous (IV) are compared with intraperitoneal (IP) conivaptan treatments after experimental stroke in mice. We developed a protocol in which middle cerebral artery occlusion was combined with catheter installation into the jugular vein for IV treatment of conivaptan (0.2 mg) or vehicle. Different cohorts of animals were treated with 0.2 mg bolus of conivaptan or vehicle IP daily. Experimental stroke-evoked brain edema was evaluated in mice after continuous IV and IP treatments. Comparison of the results revealed that the continuous IV administration of conivaptan alleviates post-ischemic brain edema in mice, unlike the IP administration of conivaptan. We conclude that our model can be used for future studies of conivaptan applications in the context of stroke and brain edema. PMID:27684044

  10. Postmortem diagnosis of acute myocardial infarction in patients with acute respiratory failure - demographics, etiologic and pulmonary histologic analysis

    PubMed Central

    de Matos Soeiro, Alexandre; Ruppert, Aline D; Canzian, Mauro; Capelozzi, Vera L; Serrano, Carlos V

    2012-01-01

    OBJECTIVES: Acute respiratory failure is present in 5% of patients with acute myocardial infarction and is responsible for 20% to 30% of the fatal post-acute myocardial infarction. The role of inflammation associated with pulmonary edema as a cause of acute respiratory failure post-acute myocardial infarction remains to be determined. We aimed to describe the demographics, etiologic data and histological pulmonary findings obtained through autopsies of patients who died during the period from 1990 to 2008 due to acute respiratory failure with no diagnosis of acute myocardial infarction during life. METHODS: This study considers 4,223 autopsies of patients who died of acute respiratory failure that was not preceded by any particular diagnosis while they were alive. The diagnosis of acute myocardial infarction was given in 218 (4.63%) patients. The age, sex and major associated diseases were recorded for each patient. Pulmonary histopathology was categorized as follows: diffuse alveolar damage, pulmonary edema, alveolar hemorrhage and lymphoplasmacytic interstitial pneumonia. The odds ratio of acute myocardial infarction associated with specific histopathology was determined by logistic regression. RESULTS: In total, 147 men were included in the study. The mean age at the time of death was 64 years. Pulmonary histopathology revealed pulmonary edema as well as the presence of diffuse alveolar damage in 72.9% of patients. Bacterial bronchopneumonia was present in 11.9% of patients, systemic arterial hypertension in 10.1% and dilated cardiomyopathy in 6.9%. A multivariate analysis demonstrated a significant positive association between acute myocardial infarction with diffuse alveolar damage and pulmonary edema. CONCLUSIONS: For the first time, we demonstrated that in autopsies of patients with acute respiratory failure as the cause of death, 5% were diagnosed with acute myocardial infarction. Pulmonary histology revealed a significant inflammatory response, which has

  11. Understanding and treating pulmonary hypertension in congenital diaphragmatic hernia.

    PubMed

    Pierro, M; Thébaud, B

    2014-12-01

    Lung hypoplasia and pulmonary hypertension are classical features of congenital diaphragmatic hernia (CDH) and represent the main determinants of survival. The mechanisms leading to pulmonary hypertension in this malformation are still poorly understood, but may combine altered vasoreactivity, pulmonary artery remodeling, and a hypoplastic pulmonary vascular bed. Efforts have been directed at correcting the "reversible" component of pulmonary hypertension of CDH. However, pulmonary hypertension in CDH is often refractory to pulmonary vasodilators. A new emerging pattern of late (months after birth) and chronic (months to years after birth) pulmonary hypertension are described in CDH survivors. The true incidence and implications for outcome and management need to be confirmed by follow-up studies from referral centers with high patient output. In order to develop more efficient strategies to treat pulmonary hypertension and improve survival in most severe cases, the ultimate therapeutic goal would be to promote lung and vascular growth. PMID:25456753

  12. Depot delivery of dexamethasone and cediranib for the treatment of brain tumor associated edema in an intracranial rat glioma model.

    PubMed

    Ong, Qunya; Hochberg, Fred H; Cima, Michael J

    2015-11-10

    Treatments of brain tumor associated edema with systemically delivered dexamethasone, the standard of care, and cediranib, a novel anti-edema agent, are associated with systemic toxicities in brain tumor patients. A tunable, reservoir-based drug delivery device was developed to investigate the effects of delivering dexamethasone and cediranib locally in the brain in an intracranial 9L gliosarcoma rat model. Reproducible, sustained releases of both dexamethasone and solid dispersion of cediranib in polyvinylpyrrolidone (AZD/PVP) from these devices were achieved. The water-soluble AZD/PVP, which exhibited similar bioactivity as cediranib, was developed to enhance the release of cediranib from the device. Local and systemic administration of both dexamethasone and cediranib was equally efficacious in alleviating edema but had no effect on tumor growth. Edema reduction led to modest but significant improvement in survival. Local delivery of dexamethasone prevented dexamethasone-induced weight loss, an adverse effect seen in animals treated with systemic dexamethasone. Local deliveries of dexamethasone and cediranib via these devices used only 2.36% and 0.21% of the systemic doses respectively, but achieved similar efficacy as systemic drug deliveries without the side effects associated with systemic administration. Other therapeutic agents targeting brain tumor can be delivered locally in the brain to provide similar improved treatment outcomes.

  13. Postoperative Acute Pulmonary Embolism Following Pulmonary Resections

    PubMed Central

    Shonyela, Felix Samuel; Liu, Bo; Jiao, Jia

    2015-01-01

    Postoperative acute pulmonary embolism after pulmonary resections is highly fatal complication. Many literatures have documented cancer to be the highest risk factor for acute pulmonary embolism after pulmonary resections. Early diagnosis of acute pulmonary embolism is highly recommended and computed tomographic pulmonary angiography is the gold standard in diagnosis of acute pulmonary embolism. Anticoagulants and thrombolytic therapy have shown a great success in treatment of acute pulmonary embolism. Surgical therapies (embolectomy and inferior vena cava filter replacement) proved to be lifesaving but many literatures favored medical therapy as the first choice. Prophylaxis pre and post operation is highly recommended, because there were statistical significant results in different studies which supported the use of prophylaxis in prevention of acute pulmonary embolism. Having reviewed satisfactory number of literatures, it is suggested that thoroughly preoperative assessment of patient conditions, determining their risk factors complicating to pulmonary embolism and the use of appropriate prophylaxis measures are the key options to the successful minimization or eradication of acute pulmonary embolism after lung resections. PMID:26354232

  14. Presurgical Pulmonary Evaluation in Renal Transplant Patients

    PubMed Central

    Sahni, Sonu; Molmenti, Ernesto; Bhaskaran, Madhu C.; Ali, Nicole; Basu, Amit; Talwar, Arunabh

    2014-01-01

    Patients with chronic renal failure (CRF) due to various mechanisms are prone to significant pulmonary comorbidities. With the improvements in renal replacement therapy (RRT), patients with CRF are now expected to live longer, and thus may develop complications in the lung from these processes. The preferred treatment of CRF is kidney transplantation and patients who are selected to undergo transplant must have a thorough preoperative pulmonary evaluation to assess pulmonary status and to determine risk of postoperative pulmonary complications. A MEDLINE®/PubMed® search was performed to identify all articles outlining the course of pre-surgical pulmonary evaluation with an emphasis on patients with CRF who have been selected for renal transplant. Literature review concluded that in addition to generic pre-surgical evaluation, renal transplant patients must also undergo a full cardiopulmonary and sleep evaluation to investigate possible existing pulmonary pathologies. Presence of any risk factor should then be aggressively managed or treated prior to surgery. PMID:25599047

  15. Idiopathic pulmonary fibrosis - clinical management guided by the evidence-based GRADE approach: what arguments can be made against transparency in guideline development?

    PubMed

    Rochwerg, Bram; Schünemann, Holger J; Raghu, Ganesh

    2016-02-10

    Evidence-based guidelines have undergone an incredible transformation over the last number of years. Significant advances include explicit linkages of systematic evidence summaries to the strength and direction of recommendations, consideration of all patient-important factors, transparent reporting of the recommendation generation process including conflict of interest management strategies and the production of clinical practice guidelines which use simple and clear language. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology provides a framework for guideline development and was employed to produce the recently published ATS/ERS/JRS/ALAT update on treatment for idiopathic pulmonary fibrosis (IPF). Herein we discuss the advantages of using an evidence-based approach for guideline development using the IPF process and resultant document as an example.

  16. Self-limiting Atypical Antipsychotics-induced Edema: Clinical Cases and Systematic Review

    PubMed Central

    Umar, Musa Usman; Abdullahi, Aminu Taura

    2016-01-01

    A number of atypical antipsychotics have been associated with peripheral edema. The exact cause is not known. We report two cases of olanzapine-induced edema and a brief review of atypical antipsychotic-induced edema, possible risk factors, etiology, and clinical features. The recommendation is given on different methods of managing this side effect. PMID:27335511

  17. 9 CFR 311.8 - Cattle carcasses affected with anasarca or generalized edema.

    Code of Federal Regulations, 2011 CFR

    2011-01-01

    ... anasarca or generalized edema. 311.8 Section 311.8 Animals and Animal Products FOOD SAFETY AND INSPECTION... ADULTERATED CARCASSES AND PARTS § 311.8 Cattle carcasses affected with anasarca or generalized edema. (a... characterized by an extensive or well-marked generalized edema shall be condemned. (b) Carcasses of...

  18. 9 CFR 311.8 - Cattle carcasses affected with anasarca or generalized edema.

    Code of Federal Regulations, 2014 CFR

    2014-01-01

    ... anasarca or generalized edema. 311.8 Section 311.8 Animals and Animal Products FOOD SAFETY AND INSPECTION... ADULTERATED CARCASSES AND PARTS § 311.8 Cattle carcasses affected with anasarca or generalized edema. (a... characterized by an extensive or well-marked generalized edema shall be condemned. (b) Carcasses of...

  19. 9 CFR 311.8 - Cattle carcasses affected with anasarca or generalized edema.

    Code of Federal Regulations, 2012 CFR

    2012-01-01

    ... anasarca or generalized edema. 311.8 Section 311.8 Animals and Animal Products FOOD SAFETY AND INSPECTION... ADULTERATED CARCASSES AND PARTS § 311.8 Cattle carcasses affected with anasarca or generalized edema. (a... characterized by an extensive or well-marked generalized edema shall be condemned. (b) Carcasses of...

  20. 9 CFR 309.8 - Cattle affected with anasarca and generalized edema.

    Code of Federal Regulations, 2014 CFR

    2014-01-01

    ... generalized edema. 309.8 Section 309.8 Animals and Animal Products FOOD SAFETY AND INSPECTION SERVICE... anasarca and generalized edema. All cattle found on ante-mortem inspection to be affected with anasarca in advanced stages and characterized by an extensive and generalized edema shall be identified as...

  1. 9 CFR 309.8 - Cattle affected with anasarca and generalized edema.

    Code of Federal Regulations, 2013 CFR

    2013-01-01

    ... generalized edema. 309.8 Section 309.8 Animals and Animal Products FOOD SAFETY AND INSPECTION SERVICE... anasarca and generalized edema. All cattle found on ante-mortem inspection to be affected with anasarca in advanced stages and characterized by an extensive and generalized edema shall be identified as...

  2. 9 CFR 311.8 - Cattle carcasses affected with anasarca or generalized edema.

    Code of Federal Regulations, 2010 CFR

    2010-01-01

    ... anasarca or generalized edema. 311.8 Section 311.8 Animals and Animal Products FOOD SAFETY AND INSPECTION... ADULTERATED CARCASSES AND PARTS § 311.8 Cattle carcasses affected with anasarca or generalized edema. (a... characterized by an extensive or well-marked generalized edema shall be condemned. (b) Carcasses of...

  3. 9 CFR 311.8 - Cattle carcasses affected with anasarca or generalized edema.

    Code of Federal Regulations, 2013 CFR

    2013-01-01

    ... anasarca or generalized edema. 311.8 Section 311.8 Animals and Animal Products FOOD SAFETY AND INSPECTION... ADULTERATED CARCASSES AND PARTS § 311.8 Cattle carcasses affected with anasarca or generalized edema. (a... characterized by an extensive or well-marked generalized edema shall be condemned. (b) Carcasses of...

  4. 9 CFR 309.8 - Cattle affected with anasarca and generalized edema.

    Code of Federal Regulations, 2012 CFR

    2012-01-01

    ... generalized edema. 309.8 Section 309.8 Animals and Animal Products FOOD SAFETY AND INSPECTION SERVICE... anasarca and generalized edema. All cattle found on ante-mortem inspection to be affected with anasarca in advanced stages and characterized by an extensive and generalized edema shall be identified as...

  5. 9 CFR 309.8 - Cattle affected with anasarca and generalized edema.

    Code of Federal Regulations, 2011 CFR

    2011-01-01

    ... generalized edema. 309.8 Section 309.8 Animals and Animal Products FOOD SAFETY AND INSPECTION SERVICE... anasarca and generalized edema. All cattle found on ante-mortem inspection to be affected with anasarca in advanced stages and characterized by an extensive and generalized edema shall be identified as...

  6. Well-Known and Less Well-Known Functions of Alpha-1 Antitrypsin. Its Role in Chronic Obstructive Pulmonary Disease and Other Disease Developments.

    PubMed

    Janciauskiene, Sabina; Welte, Tobias

    2016-08-01

    Alpha-1 antitrypsin (A1AT) is an acute-phase protein, and is best known as an inhibitor of the serine proteases, specifically, neutrophil elastase, proteinase 3, and cathepsin G. The discovery of the connection between inherited A1AT deficiency and emphysema resulted in the concept of a proteinase-antiproteinase imbalance to explain the pathogenic mechanisms of chronic obstructive pulmonary disease, as well as the concomitant development of augmentation therapy with plasma-purified human A1AT. This proteinase-antiproteinase imbalance concept has been difficult to prove, as no single mechanism can account for the complex pathology of chronic obstructive pulmonary disease. New studies have begun to characterize A1AT as an antiinflammatory and an immunoregulatory protein, independent of its antiprotease activity. We recently found that A1AT binds to free fatty acids, and it is this form of A1AT that induces the expression and release of angiopoietin-like protein 4, a protein associated with dyslipidemia and inflammation. This latter finding further strengthens the idea that describing A1AT therapy as antiserine protease is perhaps an oversimplification. The preliminary findings suggest that A1AT could be used for the management of diseases not necessarily related to inherited A1ATD, and points toward a need for more detailed investigations into the relationships between the concentration, structure, and function of A1AT protein. PMID:27564662

  7. Electron microscopic features of brain edema in rodent cerebral malaria in relation to glial fibrillary acidic protein expression.

    PubMed

    Ampawong, Sumate; Chaisri, Urai; Viriyavejakul, Parnpen; Nontprasert, Apichart; Grau, Georges E; Pongponratn, Emsri

    2014-01-01

    The mechanisms leading to cerebral malaria (CM) are not completely understood. Brain edema has been suggested as having an important role in experimental CM. In this study, CBA/CaH mice were infected with Plasmodium berghei ANKA blood-stage and when typical symptoms of CM developed on day 7, brain tissues were processed for electron-microscopic and immunohistochemical studies. The study demonstrated ultrastructural hallmarks of cerebral edema by perivascular edema and astroglial dilatation confirming existing evidence of vasogenic and cytogenic edema. This correlates closely with the clinical features of CM. An adaptive response of astrocytic activity, represented by increasing glial fibrillary acidic protein (GFAP) expression in the perivascular area and increasing numbers of large astrocyte clusters were predominately found in the CM mice. The presence of multivesicular and lamellar bodies indicates the severity of cerebral damage in experimental CM. Congestion of the microvessels with occluded white blood cells (WBCs), parasitized red blood cells (PRBCs) and platelets is also a crucial covariate role for CM pathogenesis.

  8. Thrombin exacerbates brain edema in focal cerebral ischemia.

    PubMed

    Hua, Y; Wu, J; Keep, R F; Hoff, J T; Xi, G

    2003-01-01

    Thrombin contributes to edema formation after intracerebral hemorrhage. Recent studies suggest that thrombin may also play a role in ischemic brain damage. In the present study, adult male Sprague-Dawley rats were anesthetized with pentobarbital. Middle cerebral artery (MCA) was occluded using the suture method. We found that brain thrombin activity was elevated after permanent MCA occlusion as was prothrombin messenger RNA expression. Intracerebral injection of a thrombin inhibitor, hirudin, reduced neurological deficits following cerebral ischemia. In contrast, intracerebral administration of exogenous thrombin (at a dose that is non-toxic to normal brain), markedly exacerbated brain edema after transient focal cerebral ischemia. These results indicate that extravascular thrombin inhibition may be a new therapeutic target for cerebral ischemia.

  9. Emma Kohman and the early history of nutritional edema.

    PubMed

    Bing, F C

    1983-06-01

    Nutritional edema is a generalized edematous condition that afflicted whole populations of central European countries during World War 1--and other areas since that time--with a mortality rate of about 50%. An analogous condition in white rats was produced by Emma Kohman as a graduate student in Chicago (1916 to 1919). She fed the rats a diet similar to that consumed by human subjects but prevented or cured nutritional edema in the animals by feeding them good quality protein in suitable amounts. Her work, verified by others, was of immense practical significance and helped establish the value of animal experiments in the study of human diseases. Ms. Kohman gave up a scientific career to be a homemaker when she married in 1919.

  10. Particulate air pollution and susceptibility to the development of pulmonary tuberculosis disease in North Carolina: an ecological study

    PubMed Central

    Schoenbach, Victor J.; Richardson, David B.; Gammon, Marilie D.

    2015-01-01

    Although Mycobacterium tuberculosis is the causative agent of pulmonary tuberculosis (PTB), environmental factors may influence disease progression. Ecologic studies conducted in countries outside the USA with high levels of air pollution and PTB have suggested a link between active disease and ambient air pollution. The present investigation is the first to examine the ambient air pollution/PTB association in a country, where air pollution levels are comparatively lower. We used Poisson regression models to examine the association of outdoor air pollutants, PM10 and PM2.5 with rates of PTB in North Carolina residents during 1993–2007. Results suggest a potential association between long-term exposure to particulate matter (PM) and PTB disease. In view of the high levels of air pollution and high rates of PTB worldwide, a potential association between ambient air pollution and tuberculosis warrants further study. PMID:24387197

  11. Particulate air pollution and susceptibility to the development of pulmonary tuberculosis disease in North Carolina: an ecological study.

    PubMed

    Smith, Genee S; Schoenbach, Victor J; Richardson, David B; Gammon, Marilie D

    2014-04-01

    Although Mycobacterium tuberculosis is the causative agent of pulmonary tuberculosis (PTB), environmental factors may influence disease progression. Ecologic studies conducted in countries outside the USA with high levels of air pollution and PTB have suggested a link between active disease and ambient air pollution. The present investigation is the first to examine the ambient air pollution-PTB association in a country, where air pollution levels are comparatively lower. We used Poisson regression models to examine the association of outdoor air pollutants, PM10 and PM2.5 with rates of PTB in North Carolina residents during 1993-2007. Results suggest a potential association between long-term exposure to particulate matter (PM) and PTB disease. In view of the high levels of air pollution and high rates of PTB worldwide, a potential association between ambient air pollution and tuberculosis warrants further study.

  12. Reduction of endoplasmic reticulum stress by 4-phenylbutyric acid prevents the development of hypoxia-induced pulmonary arterial hypertension.

    PubMed

    Koyama, Masayuki; Furuhashi, Masato; Ishimura, Shutaro; Mita, Tomohiro; Fuseya, Takahiro; Okazaki, Yusuke; Yoshida, Hideaki; Tsuchihashi, Kazufumi; Miura, Tetsuji

    2014-05-01

    Pulmonary arterial hypertension (PAH) is characterized by vasoconstriction and vascular remodeling of the pulmonary artery (PA). Recently, endoplasmic reticulum (ER) stress and inappropriate adaptation through the unfolded protein response (UPR) have been disclosed in various types of diseases. Here we examined whether ER stress is involved in the pathogenesis of PAH. Four weeks of chronic normobaric hypoxia increased right ventricular (RV) systolic pressure by 63% compared with that in normoxic controls and induced RV hypertrophy and medial thickening of the PA in C57BL/6J mice. Treatment with 4-phenylbutyric acid (4-PBA), a chemical chaperone, significantly reduced RV systolic pressure by 30%, attenuated RV hypertrophy and PA muscularization, and increased total running distance in a treadmill test by 70% in hypoxic mice. The beneficial effects of 4-PBA were associated with suppressed expression of inflammatory cytokines and ER stress markers, including Grp78 and Grp94 in the activating transcription factor-6 branch, sXbp1 and Pdi in the inositol-requiring enzyme-1 branch and Atf4 in the PKR-like ER kinase branch, and reduced phosphorylation of c-Jun NH2-terminal kinase and eukaryotic translation initiation factor-2α in the lung. The pattern of changes in ER stress and inflammatory markers by 4-PBA in the lung of the PAH model was reproduced in PA smooth muscle cells by chronic stimulation of platelet-derived growth factor-BB or hypoxia. Furthermore, knockdown of each UPR branch sensor activated other branches and promoted proliferation of PA smooth muscle cells. The findings indicate that activation of all branches of the UPR and accompanying inflammation play a major role in the pathogenesis of PAH, and that chemical chaperones are potentially therapeutic agents for PAH.

  13. Acute hemorrhagic edema of infancy after MMR vaccine.

    PubMed

    Binamer, Yousef

    2015-01-01

    Acute hemorrhagic edema of infancy (AHEI) is a rare type of leuckocytoclastic vasculitis. It affects mainly children less than two years of age. Many precipitating factors have been reported, including infectious etiology and vaccination. We are reporting a two-year-old boy with AHEI after measles, mumps, and rubella (MMR) vaccine. To our knowledge this is the second reported case after an MMR vaccine.

  14. Intractable bone marrow edema syndrome of the hip.

    PubMed

    Gao, Fuqiang; Sun, Wei; Li, Zirong; Guo, Wanshou; Kush, Nepali; Ozaki, Koji

    2015-04-01

    There is a need for an effective and noninvasive treatment for intractable bone marrow edema syndrome of the hip. Forty-six patients with intractable bone marrow edema syndrome of the hip were retrospectively studied to compare the short-term clinical effects of treatment with high-energy extracorporeal shock wave therapy vs femoral head core decompression. The postoperative visual analog scale score decreased significantly more in the extracorporeal shock wave therapy group compared with the femoral head core decompression group (P<.05). For unilateral lesions, postoperative Harris Hip Scores for all hips in the extracorporeal shock wave therapy group were more significantly improved than Harris Hip Scores for all hips in the femoral head core decompression group (P<.05). Patients who underwent extracorporeal shock wave therapy also resumed daily activities significantly earlier. Average overall operative time was similar in both groups. Symptoms disappeared significantly sooner in the extracorporeal shock wave therapy group in patients with both unilateral (P<.01) and bilateral lesions (P<.05). Hospital costs were significantly lower with extracorporeal shock wave therapy compared with femoral head core decompression. The intraoperative fluoroscopy radiation dose was lower in extracorporeal shock wave therapy than in femoral head core decompression for both unilateral (P<.05) and bilateral lesions (P<.01). On magnetic resonance imaging (MRI), bone marrow edema improved in all patients during the follow-up period. After extracorporeal shock wave therapy, all patients remained pain-free and had normal findings on posttreatment radiographs and MRI scans. Extracorporeal shock wave therapy appears to be a valid, reliable, and noninvasive tool for rapidly resolving intractable bone marrow edema syndrome of the hip, and it has a low complication rate and relatively low cost compared with other conservative and surgical treatment approaches.

  15. Acute hemorrhagic edema of infancy after MMR vaccine.

    PubMed

    Binamer, Yousef

    2015-01-01

    Acute hemorrhagic edema of infancy (AHEI) is a rare type of leuckocytoclastic vasculitis. It affects mainly children less than two years of age. Many precipitating factors have been reported, including infectious etiology and vaccination. We are reporting a two-year-old boy with AHEI after measles, mumps, and rubella (MMR) vaccine. To our knowledge this is the second reported case after an MMR vaccine. PMID:26409801

  16. Vascular structure determines pulmonary blood flow distribution.

    PubMed

    Hlastala, M P; Glenny, R W

    1999-10-01

    Scientific knowledge develops through the evolution of new concepts. This process is usually driven by new methodologies that provide observations not previously available. Understanding of pulmonary blood flow determinants advanced significantly in the 1960s and is now changing rapidly again, because of increased spatial resolution of regional pulmonary blood flow measurements.

  17. Pulmonary Tuberculosis and Lepromatous Leprosy Coinfection

    PubMed Central

    Sendrasoa, F. A.; Ranaivo, I. M.; Raharolahy, O.; Andrianarison, M.; Ramarozatovo, L. S.; Rapelanoro Rabenja, F.

    2015-01-01

    Simultaneous occurrence of leprosy and pulmonary tuberculosis is reported infrequently in the modern era. We report a case of pulmonary tuberculosis diagnosed in patient being treated with glucocorticoids for complications of leprosy (type II reaction). Physicians should recognize that the leprosy patients treated with glucocorticoid may develop tuberculosis. PMID:26504603

  18. Abnormal neutrophil-pulmonary interaction in the adult respiratory distress syndrome. Qualitative and quantitative assessment of pulmonary neutrophil kinetics in humans with in vivo /sup 111/indium neutrophil scintigraphy

    SciTech Connect

    Warshawski, F.J.; Sibbald, W.J.; Driedger, A.A.; Cheung, H.

    1986-05-01

    In the absence of direct toxins, the majority of evidence from animal models suggests that neutrophils (PMN) are necessary for the full expression of the abnormal pulmonary permeability accompanying acute microvascular lung injury. We therefore studied the role of the PMN in the human correlate of this disease, the adult respiratory distress syndrome (ARDS), by assessing the pulmonary retention of infused autologous /sup 111/Indium-labeled PMN (PMN-In). We evaluated 79 patients, prospectively categorized as: active ARDS (Aa; n = 30), active ARDS and concurrent corticosteroid therapy (As; n = 11), resolving ARDS (Ar; n = 13), sepsis without pulmonary edema (S; n = 7), and cardiac pulmonary edema (C; n = 18). This clinical separation was confirmed by retrospective analysis of associated measures of hemodynamic and respiratory dysfunction. We found that both analog scintigrams (positive/negative for diffuse pulmonary PMN-In sequestration) and computer-assisted quantitative analysis in 46 patients (T 1/2 of first hour demargination and percentage of peak activity/pixel/second remaining at 17 to 20 h) showed a significant rank order decrease in the pulmonary retention of labeled PMN-In through the Groups Aa----As----S----Ar----C. Our findings recognized aspects of in vivo PMN-In behavior that implied pathophysiologic differences between groups of critically ill patients in either the PMN themselves or in PMN-pulmonary endothelial interaction. This demonstrates the possibility of abnormal in vivo PMN-endothelial interaction in ARDS by virtue of the greater pulmonary localization of PMN in active ARDS versus resolving disease, septic non-ARDS states, and cardiac pulmonary edema.

  19. An accurate and simple method for measurement of paw edema.

    PubMed

    Fereidoni, M; Ahmadiani, A; Semnanian, S; Javan, M

    2000-01-01

    Several methods for measuring inflammation are available that rely on the parameters changing during inflammation. The most commonly used methods estimate the volume of edema formed. In this study, we present a novel method for measuring the volume of pathologically or artificially induced edema. In this model, a liquid column is placed on a balance. When an object is immersed, the liquid applies a force F to attempt its expulsion. Physically, F is the weight (W) of the volume of liquid displaced by that part of the object inserted into the liquid. A balance is used to measure this force (F=W).Therefore, the partial or entire volume of any object, for example, the inflamed hind paw of a rat, can be calculated thus, using the specific gravity of the immersion liquid, at equilibrium mass/specific gravity=volume (V). The extent of edema at time t (measured as V) will be V(t)-V(o). This method is easy to use, materials are of low cost and readily available. It is important that the rat paw (or any object whose volume is being measured) is kept from contacting the wall of the column containing the fluid whilst the value on the balance is read.

  20. [Retinal vein occlusion management algorithm. Part 2. Macular edema].

    PubMed

    Budzinskaya, M V; Mazurina, N K; Egorov, A E; Kuroedov, A V; Loskutov, I A; Plyukhova, A A; Razik, S; Ryabtseva, A A; Simonova, S V

    2015-01-01

    Macular edema (ME) is the most common complication of both ischemic and nonischemic retinal vein occlusion (RVO). If the main trunk of the central retinal vein is involved, ME occurs in 100% of cases. According to the Central Vein Occlusion Study, in 65% of RVO and ME patients with baseline visual acuity (VA) of at least 0.5 (Golovin-Sivtsev chart) or higher, ME may resolve itself without treatment with subsequent VA improvement. Therefore, we recommend a 3-month treatment-free follow-up of nonischemic central RVO (CRVO) and ME patients with VA of 0.5 or higher. If no improvement is noted within this period, treatment is initiated. Immediate treatment is required in patients with cystic ME revealed by optical coherence tomography (OCT) and VA below 0.5. Ischemic maculopathy is extremely unpromising. Modified grid laser photocoagulation should not be used as monotherapy for macular edema. Repeated corticosteroid (Ozurdex) and/or anti-VEGF (ranibizumab, aflibercept) intravitreal injections are considered the first choice treatment for ME in CRVO patients. Efficiency assessments should include monthly OCT. For persistent ME, intravitreal therapy can be supplemented by laser retinal photocoagulation (panretinal or modified grid). Anti-VEGF treatment schemes should be adjusted in BRVO patients as most of their edemas are self-limiting. Of laser photocoagulation techniques, only modified grid is used. PMID:26977728