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Sample records for pulmonary edema developed

  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

    PubMed Central

    Tanser, Paul H.

    1980-01-01

    The physician who deals with pulmonary edema from a pathophysiologic basis will seldom make a diagnostic or therapeutic error. Recent additions to preload and afterload therapy have greatly helped in the emergency and ambulatory treatment of pulmonary edema due to left heart failure. Careful follow-up and patient self-monitoring are the most effective means of reducing hospitalization of chronic heart failure patients. PMID:21293700

  3. [Pulmonary circulation in embolic pulmonary edema].

    PubMed

    Sanotskaia, N V; Polikarpov, V V; Matsievskiĭ, D D

    1989-02-01

    The ultrasonic method was used in acute experiments on cats with open chest under artificial lung ventilation to obtain blood flow in low-lobar pulmonary artery and vein, the blood pressure in pulmonary artery, as well as the left atrial pressure in fat (olive oil) and mechanical (Lycopodium spores) pulmonary embolism. It is shown that pulmonary embolism produces the decrease in the blood flow in pulmonary artery and vein, the increase of the pressure in pulmonary artery and left atria, the increase of lung vessels resistance. The decrease is observed of systemic arterial pressure, bradycardia, and extrasystole. After 5-10 min the restoration of arterial pressure and heart rhythm occur and partial restoration of blood flow in pulmonary artery and vein. In many experiments the blood flow in vein outdoes that in the artery--it allows to suppose the increase of the blood flow in bronchial artery. After 60-90 min there occur sudden decrease of systemic arterial pressure, the decrease of the blood flow in pulmonary artery and vein. The pressure in pulmonary artery and resistance of pulmonary vessels remain high. Pulmonary edema developed in all animals. The death occurs in 60-100 min after the beginning of embolism. PMID:2923969

  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. [Neurogenic pulmonary edema. Report of 2 cases].

    PubMed

    Dragosavac, D; Falcão, A L; Araújo, S; Terzi, R G

    1997-06-01

    Neurogenic pulmonary edema is a rare and serious complication in patients with head injury. It also may develop after a variety of cerebral insults such as subarachnoid hemorrhage, brain tumors and after epileptic seizures. Thirty six patients with severe head injury and four patients with cerebrovascular insults treated in Intensive Care Unit of HC-UNICAMP from January to September 1995 were evaluated. In this period there were two patients with neurogenic pulmonary edema, one with head injury and other with intracerebral hemorrhage. Diagnosis was made by rapid onset of pulmonary edema, severe hypoxemia, decrease of pulmonary complacence and diffuse pulmonary infiltrations, without previous history of tracheal aspiration or any other risk factor for development of adult respiratory distress syndrome. In the first case, with severe head trauma, neurogenic pulmonary edema was diagnosed at admission one hour after trauma, associated with severe systemic inflammatory reaction, and good outcome in three days. The second case, with hemorrhagic vascular insult, developed neurogenic pulmonary edema the fourth day after drainage of intracerebral hematoma and died. PMID:9629392

  6. Hyskon-induced pulmonary edema.

    PubMed

    Mangar, D

    1993-12-01

    Hyskon (32 percent dextran-70) (Hyskon Division, Pharmacia) is used during hysteroscopy to help visualization of the uterine surfaces. Pulmonary edema of an uncertain cause has occurred in many patients. Because this study could not be conducted in humans, we determined if Hyskon caused cardiogenic or non-cardiogenic pulmonary edema in a dog model. Dogs were randomly assigned to receive an infusion of Hyskon or whole blood to sustain left ventricular end-diastolic pressure between 20 and 23 millimeters of mercury for 60 minutes. In dogs receiving blood, there was no protein in the bronchoalveolar lavage before or after blood was given. In the Hyskon group, there was no protein in the bronchoalveolar lavage before Hyskon and 0.6 +/- 1.4 milligrams per deciliter (range of 0.1 to 3.7 milligram per deciliter) after Hyskon. The ratio of bronchoalveolar lavage protein to plasma protein after Hyskon was 8.0 +/- 18.0 percent compared with zero percent in the blood group. Hyskon altered pulmonary microvascular membrane permeability, causing alveolar flooding with plasma proteins and possibly accounting for the deterioration of oxygenation and pulmonary compliance seen in patients. These results suggest a significant noncardiogenic component of Hyskon induced pulmonary edema. PMID:7505487

  7. 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

  8. 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

  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. Amiodarone-induced pulmonary toxicity mimicking acute pulmonary edema.

    PubMed

    Fabiani, Iacopo; Tacconi, Danilo; Grotti, Simone; Brandini, Rossella; Salvadori, Claudia; Caremani, Marcello; Bolognese, Leonardo

    2011-05-01

    Amiodarone is a highly effective antiarrhythmic drug. Its long-term use may, however, lead to several adverse effects, with pulmonary toxicity being the most serious. The article presents the case of a 78-year-old woman with a history of cardiac surgery, who after 2 years of amiodarone therapy for prophylactic treatment of atrial fibrillation developed amiodarone pneumonitis mimicking an acute pulmonary edema. The patient failed to respond to diuretic therapy and several courses of anti-infective therapy. Differential diagnosis of different causes of pulmonary infiltrates did not demonstrate any other abnormality. Lung biopsy findings were consistent with the diagnosis of amiodarone pneumonitis. Given the widespread use of amiodarone as an antiarrhythmic agent, pneumologists and cardiologists should consider this important adverse effect as a differential diagnosis of pulmonary distress refractory to therapy in all patients treated with amiodarone who present with respiratory symptoms and pneumonia-like illness. PMID:19924000

  12. Acute pulmonary edema caused by quinine.

    PubMed

    Everts, Richard J; Hayhurst, Michael D; Nona, Basim P

    2004-09-01

    A 57-year-old man who had been intermittently taking one 300-mg tablet of quinine sulfate orally for leg cramps experienced transient acute pulmonary edema and hypotension 30-40 minutes after ingestion on two consecutive occasions. He was not taking any concomitant drugs, and there was no alternative explanation for either event. Serial troponin T tests and electrocardiograms, obtained on admission to the hospital, followed by an outpatient echocardiogram and a coronary angiogram, were essentially normal. We compared this case with one previously published and nine previously unpublished reports of quinine-associated pulmonary edema and conclude that some cases of pulmonary edema or adult respiratory distress syndrome in patients with malaria may be caused by an adverse reaction to quinine. Although infrequent, clinicians should be aware of this potentially serious and costly adverse reaction. PMID:15460183

  13. 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.

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

    PubMed

    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. PMID:3284867

  15. 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

  16. Serotonin syndrome presenting as pulmonary edema.

    PubMed

    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

  17. 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

  18. 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. PMID:26785085

  19. Pulmonary edema: a complication following dental treatment under general anesthesia.

    PubMed Central

    Yanko, R.; Garfunkel, A. A.; Kaufman, E.

    1996-01-01

    This article describes pulmonary edema in two young, physically healthy individuals following routine intensive dental treatment under general anesthesia. The etiology, diagnosis, prognosis, and treatment are discussed. This paper demonstrates that young, healthy patients may develop pulmonary edema in the perianesthesia period or even during anesthesia itself. Obstructive events, which occur especially in the post extubation period, may trigger this condition, as may other well-known phenomena. Early diagnosis and intensive treatment are mandatory in order to effectively resolve the situation. PMID:10323128

  20. 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

  1. 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

  2. An unusual cause of pulmonary edema.

    PubMed

    Chong, Adrian; Wahi, Sudhir; Harvey, Ryan; Finn, Chris; Shah, Pallav; Gould, Paul

    2014-03-01

    Primary cardiac tumors are rare malignancies. Patients may present with congestive cardiac failure due to intracavitary obstruction to blood flow, valvular dysfunction, embolic phenomena, local invasion resulting in arrhythmias, pericardial involvement, constitutional symptoms, or paraneoplastic syndromes. We describe the case of a previously fit 79-year-old woman who presented with acute pulmonary edema due to a large left atrial pleomorphic sarcoma causing severe functional mitral stenosis. She underwent palliative debulking surgery with good symptomatic relief. PMID:24585913

  3. 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. PMID:25291181

  4. Fatal reexpansion pulmonary edema in a kitten following surgical correction of pectus excavatum.

    PubMed

    Soderstrom, M J; Gilson, S D; Gulbas, N

    1995-01-01

    Fulminant, fatal pulmonary edema developed in an eight-week-old kitten following external splint correction of severe pectus excavatum. History, signalment, onset of clinical signs, and gross pathological findings were most compatible with a diagnosis of reexpansion pulmonary edema (RPE). This report presents case findings and a literature review of RPE. PMID:7773758

  5. Effect of melengestrol acetate on development of 3-methylindole-induced pulmonary edema and emphysema in sheep.

    PubMed Central

    Popp, J D; McAllister, T A; Kastelic, J P; Majak, W; Ayroud, M; VanderKop, M A; Karren, D; Yost, G S; Cheng, K J

    1998-01-01

    The involvement of melengestrol acetate (MGA) in susceptibility to developing pulmonary edema and emphysema following oral administration of 3-methylindole (3MI) was investigated using 10 Suffolk ewes receiving 0 or 0.15 mg of MGA daily (n = 5). Blood, urine and ruminal fluid were collected immediately prior to 3MI dosing (0.2 g/kg BW) and 1, 2, 3, 4, 5, 6, 12 and 24 h (blood); 3, 6, 9, 12 and 15 h (urine) and 1, 2, 3 and 12 h (ruminal fluid) afterward. Ewes receiving MGA experienced earlier (P < 0.05) onset of respiratory distress than the control ewes (2.5 vs 4 h), and upon euthanasia at 96 h, their lung weight relative to body weight tended (P < 0.10) to be lower. Ruminal 3MI concentrations did not differ between treatments (P > 0.05). Ewes receiving MGA had higher (P < 0.05) concentrations of 3MI metabolites in plasma prior to dosing than did control ewes, and these values tended to remain higher throughout the sampling period. Immunoreactivity assays indicated more pneumotoxin present in the lungs of MGA-treated ewes than controls. Lung damage was apparently more acute and accelerated in the MGA-treated ewes than in the controls. Urinary 3MI mercapturate concentrations differed (control > MGA-treated, P < 0.05) at 9, 12, and 15 h, but this difference was not apparent when urinary production (as estimated by creatinine concentration) was considered. The implications of these findings for MGA-treated feedlot heifers are currently under investigation. Images Figure 1. PMID:9798092

  6. Increased lung vasoreactivity in children from Leadville, Colorado, after recovery from high-altitude pulmonary edema.

    PubMed

    Fasules, J W; Wiggins, J W; Wolfe, R R

    1985-11-01

    Cardiac catheterization was performed on seven children after recovery from high-altitude pulmonary edema. All were life-long residents at elevations above 10,000 feet. Three of the seven had developed pulmonary edema without antecedent travel to low altitude but had an upper respiratory infection. Response of pulmonary arterial pressure to 16% inspired oxygen in all seven was compared with that in six well children who resided at a similar altitude and had no history of high-altitude pulmonary edema. With hypoxia the susceptible patients had a greater mean pulmonary arterial pressure (56.3 +/- 23.8) than the nonsusceptible children (18.8 +/- 3.9, p less than .05). Comparison with historical hemodynamic responses in children at high altitudes showed a similar greater mean pulmonary arterial pressure in the susceptible children. Thus, in children from high altitudes, increased pulmonary vasoreactivity to hypoxia may play a role in the pathogenesis of high-altitude pulmonary edema. The development of pulmonary edema in high-altitude residents with upper respiratory infections and no antecedent low-altitude journey is consistent with the presence of other factors such as inflammation, which may play a role in the pathogenesis of the edema. The finding of right ventricular hypertrophy on an electrocardiogram in children from high altitudes may be predictive of their susceptibility to high-altitude pulmonary edema. PMID:4042303

  7. 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.

  8. Postobstructive pulmonary edema after biopsy of a nasopharyngeal mass

    PubMed Central

    Mehta, Keyur Kamlesh; Ahmad, Sabina Qureshi; Shah, Vikas; Lee, Haesoon

    2015-01-01

    We describe a case of 17 year-old male with a nasopharyngeal rhabdomyosarcoma who developed postobstructive pulmonary edema (POPE) after removing the endotracheal tube following biopsy. He developed muffled voice, rhinorrhea, dysphagia, odynophagia, and difficulty breathing through nose and weight loss of 20 pounds in the preceding 2 months. A nasopharyngoscopy revealed a fleshy nasopharyngeal mass compressing the soft and hard palate. Head and neck MRI revealed a large mass in the nasopharynx extending into the bilateral choana and oropharynx. Biopsy of the mass was taken under general anesthesia with endotracheal intubation. Immediately after extubation he developed oxygen desaturation, which did not improve with bag mask ventilation with 100% of oxygen, but improved after a dose of succinylcholine. He was re-intubated and pink, frothy fluid was suctioned from the endotracheal tube. Chest radiograph (CXR) was suggestive of an acute pulmonary edema. He improved with mechanical ventilation and intravenous furosemide. His pulmonary edema resolved over the next 24 h. POPE is a rare but serious complication associated with upper airway obstruction. The pathophysiology of POPE involves hemodynamic changes occurring in the lung and the heart during forceful inspiration against a closed airway due to an acute or chronic airway obstruction. This case illustrates the importance of considering the development of POPE with general anesthesia, laryngospasm and removal of endotracheal tube to make prompt diagnosis and to initiate appropriate management. PMID:26744691

  9. Postobstructive pulmonary edema after biopsy of a nasopharyngeal mass.

    PubMed

    Mehta, Keyur Kamlesh; Ahmad, Sabina Qureshi; Shah, Vikas; Lee, Haesoon

    2015-01-01

    We describe a case of 17 year-old male with a nasopharyngeal rhabdomyosarcoma who developed postobstructive pulmonary edema (POPE) after removing the endotracheal tube following biopsy. He developed muffled voice, rhinorrhea, dysphagia, odynophagia, and difficulty breathing through nose and weight loss of 20 pounds in the preceding 2 months. A nasopharyngoscopy revealed a fleshy nasopharyngeal mass compressing the soft and hard palate. Head and neck MRI revealed a large mass in the nasopharynx extending into the bilateral choana and oropharynx. Biopsy of the mass was taken under general anesthesia with endotracheal intubation. Immediately after extubation he developed oxygen desaturation, which did not improve with bag mask ventilation with 100% of oxygen, but improved after a dose of succinylcholine. He was re-intubated and pink, frothy fluid was suctioned from the endotracheal tube. Chest radiograph (CXR) was suggestive of an acute pulmonary edema. He improved with mechanical ventilation and intravenous furosemide. His pulmonary edema resolved over the next 24 h. POPE is a rare but serious complication associated with upper airway obstruction. The pathophysiology of POPE involves hemodynamic changes occurring in the lung and the heart during forceful inspiration against a closed airway due to an acute or chronic airway obstruction. This case illustrates the importance of considering the development of POPE with general anesthesia, laryngospasm and removal of endotracheal tube to make prompt diagnosis and to initiate appropriate management. PMID:26744691

  10. 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

  11. High-altitude pulmonary edema: diagnosis, prevention, and treatment.

    PubMed

    Pennardt, Andre

    2013-01-01

    High-altitude pulmonary edema (HAPE) is a lethal, noncardiogenic form of pulmonary edema that afflicts susceptible individuals after rapid ascent to high altitude above 2,500 m. Prevention of HAPE is achieved most effectively by gradual ascent allowing time for proper acclimatization. Certain prophylactic medications may further reduce the risk of ascending to high altitude in individuals with a prior history of HAPE. The most effective and reliable treatment of HAPE is immediate descent and administration of supplemental oxygen. PMID:23478563

  12. Acute Pulmonary Edema Associated With Propofol: An Unusual Complication

    PubMed Central

    Waheed, Mian Adnan; Oud, Lavi

    2014-01-01

    Propofol is frequently used in the emergency department to provide procedural sedation for patients undergoing various procedures and is considered to be safe when administered by trained personnel. Pulmonary edema after administration of propofol has rarely been reported. We report a case of a 23-year-old healthy male who developed acute cough, hemoptysis and hypoxia following administration of propofol for splinting of a foot fracture. Chest radiography showed bilateral patchy infiltrates. The patient was treated successfully with supportive care. This report emphasizes the importance of this potentially fatal propofol-associated complication and discusses possible underlying mechanisms and related literature. PMID:25493132

  13. High-permeability pulmonary edema: nursing assessment, diagnosis, and interventions.

    PubMed

    Roberts, S L

    1990-05-01

    High-permeability pulmonary edema (HPPE) is a problem affecting 150,000 to 200,000 critically ill patients yearly. In HPPE the alveolar-capillary membrane is injured. The resulting increased permeability of the alveolar-capillary membrane allows shifts of fluid and protein into the interstitial fluid space and alveolus. As hypoxemia develops, the nurse assesses cardinal signs and symptoms derived from the physical examination and observations. Clinical data consisting of results from various laboratory and diagnostic studies confirm the diagnosis of HPPE. Finally, nursing diagnoses can be delineated as the basis on which expert nursing care is planned and implemented. PMID:2187834

  14. 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

  15. Bronchial artery ligation modifies pulmonary edema after exposure to smoke with acrolein.

    PubMed

    Hales, C A; Barkin, P; Jung, W; Quinn, D; Lamborghini, D; Burke, J

    1989-09-01

    Pulmonary edema can follow smoke inhalation and is believed to be due to the multiple chemical toxins in smoke, not the heat. We have developed a synthetic smoke composed of aerosolized charcoal particles to which one toxin at a time can be added to determine whether it produces pulmonary edema. Acrolein, a common component of smoke, when added to the synthetic smoke, produced a delayed-onset pulmonary edema in dogs in which the extravascular lung water (EVLW) as detected by a double-indicator technique began to rise after 42 +/- 2 (SE) min from 148 +/- 16 to 376 +/- 60 ml at 165 min after smoke exposure. The resulting pulmonary edema was widespread macroscopically but appeared focal microscopically with fibrin deposits in alveoli adjacent to small bronchi and bronchioles. Bronchial vessels were markedly dilated and congested. Monastral blue B when injected intravenously leaked into the walls of the bronchial vessels down to the region of the small bronchioles (less than or equal to 0.5 mm ID) of acrolein-smoke-exposed dogs but not into the pulmonary vessels. Furthermore, ligation of the bronchial arteries delayed the onset of pulmonary edema (87 +/- 3 min, P less than 0.05) and lessened the magnitude (232 +/- 30 ml, P less than 0.05) at 166 +/- 3 min after acrolein-smoke exposure.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:2793693

  16. 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

  17. [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. PMID:24930078

  18. 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

  19. High-altitude pulmonary edema at a ski resort.

    PubMed Central

    Hultgren, H N; Honigman, B; Theis, K; Nicholas, D

    1996-01-01

    Medical records of 150 patients with high-altitude pulmonary edema seen over a 39-month period in a Colorado Rocky Mountain ski area at 2,928 m (9,600 ft) (mean age 34.4 years; 84% male) were reviewed. The mean time to the onset of symptoms was 3 +/- 1.3 days after arrival. Common symptoms were dyspnea, cough, headache, chest congestion, nausea, fever, and weakness. Orthopnea, hemoptysis, and vomiting were rare, occurring in 7%, 6%, and 16%, respectively. Symptoms of cerebral edema occurred in 14%. A temperature exceeding 100 degrees F occurred in 20%, and 17% had a systolic blood pressure of 150 mm of mercury or higher. Blood pressures were higher in patients older than 50 years (142 mm of mercury). Rales were present in 85%, and a pulmonary infiltrate was present in 88%; both were most commonly bilateral or on the right side. The amount of infiltrate was mild. Men appeared to be more susceptible than women to high-altitude pulmonary edema. Pulse oximetry in 45 patients showed a mean oxygen saturation of 74% (38% to 93%). Treatment methods depended on severity and included a return to quarters for portable nasal oxygen, an overnight stay in the clinic for continuing oxygen, or a descent to Denver for recovery or admission to a hospital. All patients received oxygen for 2 to 4 hours in the clinic. There were no deaths or complications. Images Figure 2. Figure 3. PMID:8775933

  20. [Non-cardiogenic pulmonary edema, acute respiratory distress syndrome].

    PubMed

    Skalická, Hana; Bělohlávek, Jan

    2015-01-01

    Non-cardiogenic pulmonary edema is a clinical syndrome manifested by rapidly progressive respiratory distress leading, without therapy, to severe respiratory insufficiency and subsequent multiorgan failure. The pathophysiological causes are: the change in the pressure gradients in the pulmonary capillaries, the impaired membrane permeability of the alveolocapillary in the lungs, and impaired lymphatic drainage. Unlike in cardiogenic pulmonary edema, cardiac disease is not a cause, and there is no increase in wedge pressure (< 18 mm Hg). The aetiological base is diverse and includes more clinical pathological factors. The diagnosis and evaluation are usually very difficult due to the rapidly deteriorating clinical condition of the patients. A decisive, quick and comprehensive approach, using all available invasive and non-invasive methods is necessary. The basic steps of treatment are: the use of different types of ventilatory support in order to achieve adequate oxygenation, dealing with possible hemodynamic instability, and, when needed, other specific procedures. It is always important to keep in mind that this is a very serious condition with a high mortality rate. And there is a need for fast and efficient access to the best specialized clinic. PMID:26750623

  1. Rhodiola crenulata Extract Alleviates Hypoxic Pulmonary Edema in Rats

    PubMed Central

    Li, Min-Hui; Shi, Li-Shian; Ho, Cheng-Wen

    2013-01-01

    Sudden exposure of nonacclimatized individuals to high altitude can easily lead to high altitude illnesses. High altitude pulmonary edema (HAPE) is the most lethal form of high altitude illness. The present study was designed to investigate the ability of Rhodiola crenulata extract (RCE), an herbal medicine traditionally used as an antiacute mountain sickness remedy, to attenuate hypoxia-induced pulmonary injury. Exposure of animals to hypobaric hypoxia led to a significant increase in pathological indicators for pulmonary edema, including the lung water content, disruption of the alveolar-capillary barrier, and protein-rich fluid in the lungs. In addition, hypobaric hypoxia also increased oxidative stress markers, including (ROS) production, (MDA) level, and (MPO) activity. Furthermore, overexpression of plasma (ET-1), (VEGF) in (BALF), and (HIF-1α) in lung tissue was also found. However, pretreatment with RCE relieved the HAPE findings by curtailing all of the hypoxia-induced lung injury parameters. These findings suggest that RCE confers effective protection for maintaining the integrity of the alveolar-capillary barrier by alleviating the elevated ET-1 and VEGF levels; it does so by reducing hypoxia-induced oxidative stress. Our results offer substantial evidence to support arguments in favor of traditional applications of Rhodiola crenulata for antihigh altitude illness. PMID:23710233

  2. Pulmonary edema following scorpion envenomation: mechanisms, clinical manifestations, diagnosis and treatment.

    PubMed

    Bahloul, Mabrouk; Chaari, Anis; Dammak, Hassen; Samet, Mohamed; Chtara, Kamilia; Chelly, Hedi; Ben Hamida, Chokri; Kallel, Hatem; Bouaziz, Mounir

    2013-01-10

    Scorpion envenomation is common in tropical and subtropical regions. Cardio-respiratory manifestations, mainly cardiogenic shock and pulmonary edema, are the leading causes of death after scorpion envenomation. The mechanism of pulmonary edema remains unclear and contradictory conclusions were published. However, most publications confirm that pulmonary edema has been attributed to acute left ventricular failure. Cardiac failure can result from massive release of catecholamines, myocardial damage induced by the venom or myocardial ischemia. Factors usually associated with the diagnosis of pulmonary edema were young age, tachypnea, agitation, sweating, or the presence of high plasma protein concentrations. Treatment of scorpion envenomation has two components: antivenom administration and supportive care. The latter mainly targets hemodynamic impairment and cardiogenic pulmonary edema. In Latin America, and India, the use of Prazosin is recommended for treatment of pulmonary edema because pulmonary edema is associated with arterial hypertension. However, in North Africa, scorpion leads to cardiac failure with systolic dysfunction with normal vascular resistance and dobutamine was recommended. Dobutamine infusion should be used as soon as we have enough evidence suggesting the presence of pulmonary edema, since it has been demonstrated that scorpion envenomation can result in pulmonary edema secondary to acute left ventricular failure. In severe cases, mechanical ventilation can be required. PMID:22075406

  3. 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

  4. Acute pulmonary edema secondary to hyperbaric oxygen therapy.

    PubMed

    Obiagwu, Chukwudi; Paul, Vishesh; Chadha, Sameer; Hollander, Gerald; Shani, Jacob

    2015-02-01

    Hyperbaric oxygen therapy (HBOT) has been shown to be effective in the treatment of diabetic ulcers, air embolism, carbon monoxide poisoning and gas gangrene with minimal adverse effects. Very few cases of HBOT causing acute pulmonary edema (PE) has been described; with a study on dogs suggesting that a complication of this therapy could be PE. We describe the case of an 80-year-old man with a history of stable systolic heart failure and diabetes mellitus presenting with acute PE following treatment with HBOT for diabetic foot. PMID:25988073

  5. Acute pulmonary edema secondary to hyperbaric oxygen therapy

    PubMed Central

    Obiagwu, Chukwudi; Paul, Vishesh; Chadha, Sameer; Hollander, Gerald; Shani, Jacob

    2015-01-01

    Hyperbaric oxygen therapy (HBOT) has been shown to be effective in the treatment of diabetic ulcers, air embolism, carbon monoxide poisoning and gas gangrene with minimal adverse effects. Very few cases of HBOT causing acute pulmonary edema (PE) has been described; with a study on dogs suggesting that a complication of this therapy could be PE. We describe the case of an 80-year-old man with a history of stable systolic heart failure and diabetes mellitus presenting with acute PE following treatment with HBOT for diabetic foot. PMID:25988073

  6. 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.

  7. Radiographically Severe but Clinically Mild Reexpansion Pulmonary Edema following Decompression of a Spontaneous Pneumothorax.

    PubMed

    Harner, William E; Crawley, Eric A

    2014-01-01

    The case is a 48-year-old female who presented with mild dyspnea on exertion and cough with unremarkable vital signs and was found to have a large right sided pneumothorax. She underwent small bore chest tube decompression with immediate reexpansion of the collapsed lung. However, she rapidly developed moderate hypoxemia and radiographic evidence of reexpansion pulmonary edema (REPE) on both the treated and contralateral sides. Within a week, she had a normal chest X-ray and was asymptomatic. This case describes a rare complication of spontaneous pneumothorax and highlights the lack of correlation between symptoms, sequelae, and radiographic severity of pneumothorax and reexpansion pulmonary edema. Proposed pathophysiologic mechanisms include increased production of reactive oxygen species with subsequent loss of surfactant and increased vascular permeability, and loss of vasoregulatory tone. PMID:25165607

  8. A multicenter prospective cohort study of volume management after subarachnoid hemorrhage: circulatory characteristics of pulmonary edema after subarachnoid hemorrhage.

    PubMed

    Obata, Yoshiki; Takeda, Junichi; Sato, Yohei; Ishikura, Hiroyasu; Matsui, Toru; Isotani, Eiji

    2016-08-01

    OBJECT Subarachnoid hemorrhage (SAH) is often accompanied by pulmonary complications, which may lead to poor outcomes and death. This study investigated the incidence and cause of pulmonary edema in patients with SAH by using hemodynamic monitoring with PiCCO-plus pulse contour analysis. METHODS A total of 204 patients with SAH were included in a multicenter prospective cohort study to investigate hemodynamic changes after surgical clipping or coil embolization of ruptured cerebral aneurysms by using a PiCCO-plus device. Changes in various hemodynamic parameters after SAH were analyzed statistically. RESULTS Fifty-two patients (25.5%) developed pulmonary edema. Patients with pulmonary edema (PE group) were significantly older than those without pulmonary edema (non-PE group) (p = 0.017). The mean extravascular lung water index was significantly higher in the PE group than in the non-PE group throughout the study period. The pulmonary vascular permeability index (PVPI) was significantly higher in the PE group than in the non-PE group on Day 6 (p = 0.029) and Day 10 (p = 0.011). The cardiac index of the PE group was significantly decreased biphasically on Days 2 and 10 compared with that of the non-PE group. In the early phase (Days 1-5 after SAH), the daily water balance of the PE group was slightly positive. In the delayed phase (Days 6-14 after SAH), the serum C-reactive protein level and the global end-diastolic volume index were significantly higher in the PE group than in the non-PE group, whereas the PVPI tended to be higher in the PE group. CONCLUSIONS Pulmonary edema that occurs in the early and delayed phases after SAH is caused by cardiac failure and inflammatory (i.e., noncardiogenic) conditions, respectively. Measurement of the extravascular lung water index, cardiac index, and PVPI by PiCCO-plus monitoring is useful for identifying pulmonary edema in patients with SAH. PMID:26613172

  9. Edema

    MedlinePlus

    Edema means swelling caused by fluid in your body's tissues. It usually occurs in the feet, ankles ... it can involve your entire body. Causes of edema include Eating too much salt Sunburn Heart failure ...

  10. The Effect of TIP on Pneumovirus-Induced Pulmonary Edema in Mice

    PubMed Central

    van den Berg, Elske; Bem, Reinout A.; Bos, Albert P.; Lutter, Rene; van Woensel, Job B. M.

    2014-01-01

    Background Pulmonary edema plays a pivotal role in the pathophysiology of respiratory syncytial virus (RSV)-induced respiratory failure. In this study we determined whether treatment with TIP (AP301), a synthetic cyclic peptide that mimics the lectin-like domain of human TNF, decreases pulmonary edema in a mouse model of severe human RSV infection. TIP is currently undergoing clinical trials as a therapy for pulmonary permeability edema and has been shown to decrease pulmonary edema in different lung injury models. Methods C57BL/6 mice were infected with pneumonia virus of mice (PVM) and received TIP or saline (control group) by intratracheal instillation on day five (early administration) or day seven (late administration) after infection. In a separate set of experiments the effect of multiple dose administration of TIP versus saline was tested. Pulmonary edema was determined by the lung wet-to-dry (W/D) weight ratio and was assessed at different time-points after the administration of TIP. Secondary outcomes included clinical scores and lung cellular response. Results TIP did not have an effect on pulmonary edema in different dose regimens at different time points during PVM infection. In addition, TIP administration did not affect clinical severity scores or lung cellular response. Conclusion In this murine model of severe RSV infection TIP did not affect pulmonary edema nor course of disease. PMID:25047452

  11. 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. PMID:26522587

  12. 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.

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

    PubMed Central

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

    2015-01-01

    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. PMID:26459926

  14. 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. PMID:27549541

  15. 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

  16. 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.

  17. 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. PMID:23158869

  18. 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.

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

    PubMed

    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

  20. 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

  1. 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

  2. A human disease model of drug toxicity-induced pulmonary edema in a lung-on-a-chip microdevice.

    PubMed

    Huh, Dongeun; Leslie, Daniel C; Matthews, Benjamin D; Fraser, Jacob P; Jurek, Samuel; Hamilton, Geraldine A; Thorneloe, Kevin S; McAlexander, Michael Allen; Ingber, Donald E

    2012-11-01

    Preclinical drug development studies currently rely on costly and time-consuming animal testing because existing cell culture models fail to recapitulate complex, organ-level disease processes in humans. We provide the proof of principle for using a biomimetic microdevice that reconstitutes organ-level lung functions to create a human disease model-on-a-chip that mimics pulmonary edema. The microfluidic device, which reconstitutes the alveolar-capillary interface of the human lung, consists of channels lined by closely apposed layers of human pulmonary epithelial and endothelial cells that experience air and fluid flow, as well as cyclic mechanical strain to mimic normal breathing motions. This device was used to reproduce drug toxicity-induced pulmonary edema observed in human cancer patients treated with interleukin-2 (IL-2) at similar doses and over the same time frame. Studies using this on-chip disease model revealed that mechanical forces associated with physiological breathing motions play a crucial role in the development of increased vascular leakage that leads to pulmonary edema, and that circulating immune cells are not required for the development of this disease. These studies also led to identification of potential new therapeutics, including angiopoietin-1 (Ang-1) and a new transient receptor potential vanilloid 4 (TRPV4) ion channel inhibitor (GSK2193874), which might prevent this life-threatening toxicity of IL-2 in the future. PMID:23136042

  3. 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. PMID:19739476

  4. 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

  5. [Case of fluminant myocarditis with fatal pulmonary edema even after introduction of bi-ventricular assist devices].

    PubMed

    Sawada, Masahiro; Hashiba, Eiji; Kudo, Tomoyuki; Okawa, Hirobumi; Tsubo, Toshihito; Ishihara, Hironori; Hirota, Kazuyoshi

    2012-07-01

    A 15-year-old man developed cardiopulmonary dysfunction 4 days after flu-like symptom, and was transfered to our hospital and diagnosed as a fulminant myocarditis (FM). Intraaortic ballon pumping (IABP) and percutaneous cardiopulmonary support (PCPS) were immediately initiated. However, cardiac function did not recover until 7 days after admission to the ICU, and bilateral ventricular assist devices (BiVAD) were introduced with extracorporeal membrane oxygenation (ECMO). Right ventricular assist device (RVAD) with ECMO was established by right atrial blood withdrawal and pulmonary arterial blood supply using centrifugal pump. After operation of BiVAD, to main LVAD flow, frequent blood-and-fluids volume loading and increase in RVAD flow were necessary due to postoperative bleeding and massive foamy sputum. However, even after hemostasis had been established, the pulmonary edema continued and it was difficult to maintain LVAD flow because of endless transudation from the lungs. Eventually, he developed MOF and passed away 9 days after the admission to ICU. As in cases of end-stage dilated cardiomyopathy, outflow of RVAD into the left atrium instead of the pulmonary artery was demonstrated effective in avoiding trans-pulmonary leakage, and outflow of RVAD into the left atrium may be beneficial to patients with FM who need BiVAD but suffered severe pulmonary edema. PMID:22860309

  6. 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

  7. 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. PMID:26517502

  8. 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. PMID:17679517

  9. Acute pulmonary edema due to stress cardiomyopathy in a patient with aortic stenosis: a case report

    PubMed Central

    2009-01-01

    Introduction Stress cardiomyopathy is a condition of chest pain, breathlessness, abnormal heart rhythms and sometimes congestive heart failure or shock precipitated by intense mental or physical stress. Case presentation A 64-year-old male with a known diagnosis of moderate-to-severe aortic stenosis and advised that valve replacement was not urgent, presented with acute pulmonary edema following extraordinary mental distress. The patient was misdiagnosed as having a "massive heart attack" and died when managed by a traditional protocol for acute myocardial infarction/coronary artery disease, irrespective of his known aortic stenosis. Conclusion Intense mental stress poses a considerable risk, particularly to patients with significant aortic stenosis. As described here, it can precipitate acute pulmonary edema. Importantly, effective management of acute pulmonary edema due to stress cardiomyopathy in patients with known aortic stenosis requires its distinction from acute pulmonary edema caused by an acute myocardial infarction. Treatment options include primarily urgent rhythm and/or rate control, as well as cautious vasodilation. PMID:20062645

  10. [Successful perioperative use of noninvasive positive pressure ventilation in a pregnant woman with acute pulmonary edema].

    PubMed

    Fujita, Naoko; Tachibana, Kazuya; Takeuchi, Muneyuki; Kinouchi, Keiko

    2014-05-01

    A 32-year-old woman (148 cm, 59 kg, gravida 2, para 2) with quadruplet pregnancy was admitted to our hospital for the threatened preterm labor at 23 weeks and 2 days of gestation. She was treated with ritodrine, magnesium sulfate and nifedipine to maintain tocolysis. Betamethasone was administered to accelerate fetal lung maturity. After ritodrine dose was increased at 23 weeks and 5 days of gestation, she developed dyspnea with desaturation. Acute pulmonary edema was revealed on chest X-ray. The decision was made to proceed with emergency cesarean delivery. On arrival at the operating room, the blood pressure was 123/53 mmHg, heart rate 111 beats x min(-1), and oxygen saturation (SpO2) 84% with supplemental oxygen 15 l x min(-1) via a reserved face mask. Noninvasive positive pressure ventilation (NPPV) was initiated with S/T mode (FIO2 1.0, inspiratory positive airway pressure 10 cmH2O, expiratory positive airway pressure 6 cmH2O). The dyspnea was improved with her SpO2 100%. Spinal anesthesia was performed at L 34 using 2.5 ml of 0.5% bupivacaine and 100 microg morphine. Throughout the operation (operation time 44 minutes), she did not develop dyspnea under NPPV. NPPV was discontinued after the operation. Her SpO2 declined, and pulmonary edema on chest X-ray was exacerbated. She was transferred to the intensive care unit and NPPV was continued for 22 hours after the operation. She was discharged from the intensive care unit on the next day and was discharged from the hospital on the 6th postoperative day. PMID:24864580

  11. Pulmonary edema following post-operative laryngospasm: a case report and review of the literature.

    PubMed

    Halow, K D; Ford, E G

    1993-07-01

    The pathophysiology of acute, negative-pressure pulmonary edema following post-anesthetic laryngospasm (PLPE) is unclear. We present a patient and review the literature to propose etiology and management. Nineteen reported patients (3 female, 16 male, aged 3 months to 60 years) with PLPE had undergone 10 otolaryngologic, three orthopedic, four skin/soft tissue, one intraabdominal, and one ophthalmologic procedures. Twelve patients (63%) had significant medical history. Initial intubation was performed without difficulty in 17 patients, there were no predisposing trends in anesthetic management, and post-anesthetic extubation was performed without difficulty in 18 patients. Thirteen patients developed laryngospasm in less than 2 minutes. Eight were ventilated with bag/mask, 15 required reintubation, and nine required paralysis. Onset of PLPE was less than 3 minutes in 12 patients; chest roentgenograms showed edema in 17 patients. Mechanical ventilation was required for less than 24 hours in all patients. PLPE cleared in less than 24 hours in most patients. Furosemide was administered in nine patients, digoxin in one, theophylline in two, and steroids in four patients. The precise pathophysiologic mechanism of PLPE is unclear despite numerous proposed mechanisms. PLPE resolves rapidly with short-term ventilatory support. Use of diuretics/airway dilators is variable, and their contribution to management is unclear. PMID:8323077

  12. Baroreflex failure increases the risk of pulmonary edema in conscious rats with normal left ventricular function.

    PubMed

    Sakamoto, Kazuo; Hosokawa, Kazuya; Saku, Keita; Sakamoto, Takafumi; Tobushi, Tomoyuki; Oga, Yasuhiro; Kishi, Takuya; Ide, Tomomi; Sunagawa, Kenji

    2016-01-15

    In heart failure with preserved ejection fraction (HFpEF), the complex pathogenesis hinders development of effective therapies. Since HFpEF and arteriosclerosis share common risk factors, it is conceivable that stiffened arterial wall in HFpEF impairs baroreflex function. Previous investigations have indicated that the baroreflex regulates intravascular stressed volume and arterial resistance in addition to cardiac contractility and heart rate. We hypothesized that baroreflex dysfunction impairs regulation of left atrial pressure (LAP) and increases the risk of pulmonary edema in freely moving rats. In 15-wk Sprague-Dawley male rats, we conducted sinoaortic denervation (SAD, n = 6) or sham surgery (Sham, n = 9), and telemetrically monitored ambulatory arterial pressure (AP) and LAP. We compared the mean and SD (lability) of AP and LAP between SAD and Sham under normal-salt diet (NS) or high-salt diet (HS). SAD did not increase mean AP but significantly increased AP lability under both NS (P = 0.001) and HS (P = 0.001). SAD did not change mean LAP but significantly increased LAP lability under both NS (SAD: 2.57 ± 0.43 vs. Sham: 1.73 ± 0.30 mmHg, P = 0.01) and HS (4.13 ± 1.18 vs. 2.45 ± 0.33 mmHg, P = 0.02). SAD markedly increased the frequency of high LAP, and SAD with HS prolonged the duration of LAP > 18 mmHg by nearly 20-fold compared with Sham (SAD + HS: 2,831 ± 2,366 vs. Sham + HS: 148 ± 248 s, P = 0.01). We conclude that baroreflex failure impairs volume tolerance and together with salt loading increases the risk of pulmonary edema even in the absence of left ventricular dysfunction. Baroreflex failure may contribute in part to the pathogenesis of HFpEF. PMID:26589328

  13. Adenosine protected against pulmonary edema through transporter- and receptor A2-mediated endothelial barrier enhancement

    PubMed Central

    Lu, Qing; Harrington, Elizabeth O.; Newton, Julie; Casserly, Brian; Radin, Gregory; Warburton, Rod; Zhou, Yang; Blackburn, Michael R.

    2010-01-01

    development of edema before ALI but also partially reversed edema after ALI. The data suggest that adenosine deaminase inhibition may be useful in treatment of pulmonary edema in settings of ALI. PMID:20228181

  14. Successful lung salvage by ex vivo reconditioning of neurogenic pulmonary edema: case report.

    PubMed

    Sanchez, P G; Iacono, A T; Rajagopal, K; Griffith, B P

    2014-09-01

    Liberalization in donor selection criteria allowed centers to increase the number of lung transplants, yet less than 25% of all donors had lungs utilized for transplantation in the United States in 2013. Less than 5% of all transplanted donors deviate 3 or more criteria from the ideal donor. Ex vivo lung perfusion (EVLP) provides the opportunity to increase the percentage of used donors by acting on modifiable selection criteria such as oxygenation, contusion and pulmonary infiltrates. We report the pre-transplant use of EVLP in the salvage of lungs from a donor that developed neurogenic pulmonary edema -PaO2 188 mmHg-. The recipient had a lung allocation score of 69.3. The post-operative course was excellent and was discharged home after 15 days. He is alive and doing well 780 days after transplant. In this report the pre-transplant use of EVLP led not only to transplanting lungs that otherwise would not have been used by many centers, but also to a very short and typical period of post-operative mechanical ventilation and hospital stay. PMID:25242800

  15. 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

  16. Morphine blocks the Mesobuthus tamulus venom-induced augmentation of phenyldiguanide reflex and pulmonary edema in anesthetized rats

    PubMed Central

    Akella, Aparna; Tiwari, Anil K.; Rai, Om P.; Deshpande, Shripad B.

    2016-01-01

    Objective: Pulmonary edema, a manifestation of scorpion envenomation syndrome, is attributed to cardiogenic or noncardiogenic factors. Morphine is a drug used for cardiogenic pulmonary edema and its effect on Mesobuthus tamulus (MBT) venom-induced changes is not known. Therefore, we hypothesized that morphine blocks the MBT venom-induced augmentation of phenyldiguanide (PDG) reflex and pulmonary edema. Materials and Methods: Experiments were performed on anesthetized adult female rats. Trachea and jugular vein were cannulated, and the electrocardiographic potentials were recorded by connecting needle electrodes in limb lead II configuration. PDG (10 ΅g/kg, IV, bolus injection) responses were elicited by bolus injection initially, after saline/morphine (1 mg/kg) and after injecting MBT venom (100 μg/kg). The time-response area of the PDG-induced bradycardiac response after treatment was calculated as % of the initial PDG response area. At the end of experiments, lungs were excised for determination of pulmonary water content. Results: PDG produced bradycardiac response that lasted for >60 s. MBT venom augmented the PDG reflex response by 2.5 times. In morphine pretreated group, augmentation of bradycardiac response induced by MBT venom was absent. MBT venom increased the pulmonary water content, and the increase was absent in morphine pretreated animals. Conclusion: The results reveal that morphine prevents the MBT venom-induced augmentation of PDG reflex response and pulmonary edema. Thus, morphine can be useful in scorpion envenomation syndrome associated with pulmonary edema. PMID:26997727

  17. Hypoxic preconditioning with cobalt ameliorates hypobaric hypoxia induced pulmonary edema in rat.

    PubMed

    Shukla, Dhananjay; Saxena, Saurabh; Purushothaman, Jayamurthy; Shrivastava, Kalpana; Singh, Mrinalini; Shukla, Shirish; Malhotra, Vineet Kumar; Mustoori, Sairam; Bansal, Anju

    2011-04-10

    Exposure to high altitude results in hypobaric hypoxia which is considered as an acute physiological stress and often leads to high altitude maladies such as high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). The best way to prevent high altitude injuries is hypoxic preconditioning which has potential clinical usefulness and can be mimicked by cobalt chloride. Preconditioning with cobalt has been reported to provide protection in various tissues against ischemic injury. However, the effect of preconditioning with cobalt against high altitude induced pulmonary edema has not been investigated in vivo. Therefore, in the present study, rats pretreated with saline or cobalt (12.5mg/kg body weight) for 7days were exposed to hypobaric hypoxia of 9142m for 5h at 24°C. Formation of pulmonary edema was assessed by measuring transvascular leakage of sodium fluorescein dye and lung water content. Total protein content, albumin content, vascular endothelial growth factor (VEGF) and cytokine levels were measured in bronchoalveolar lavage fluid. Expression of HO-1, MT, NF-κB DNA binding activity and lung tissue pathology were evaluated to determine the effect of preconditioning on HAPE. Hypobaric hypoxia induced increase in transvascular leakage of sodium fluorescein dye, lung water content, lavage total protein, albumin, VEGF levels, pro-inflammatory cytokine levels, tissue expression of cell adhesion molecules and NF-κB DNA binding activity were reduced significantly after hypoxic preconditioning with cobalt. Expression of anti-inflammatory protein HO-1, MT, TGF-β and IL-6 were increased after hypoxic preconditioning. These data suggest that hypoxic preconditioning with cobalt has protective effect against HAPE. PMID:21296072

  18. Inositol-trisphosphate reduces alveolar apoptosis and pulmonary edema in neonatal lung injury.

    PubMed

    Preuss, Stefanie; Stadelmann, Sabrina; Omam, Friede D; Scheiermann, Julia; Winoto-Morbach, Supandi; von Bismarck, Philipp; Knerlich-Lukoschus, Friederike; Lex, Dennis; Adam-Klages, Sabine; Wesch, Daniela; Held-Feindt, Janka; Uhlig, Stefan; Schütze, Stefan; Krause, Martin F

    2012-08-01

    D-myo-inositol-1,2,6-trisphosphate (IP3) is an isomer of the naturally occurring second messenger D-myo-inositol-1,4,5-trisphosphate, and exerts anti-inflammatory and antiedematous effects in the lung. Myo-inositol (Inos) is a component of IP3, and is thought to play an important role in the prevention of neonatal pulmonary diseases such as bronchopulmonary dysplasia and neonatal acute lung injury (nALI). Inflammatory lung diseases are characterized by augmented acid sphingomyelinase (aSMase) activity leading to ceramide production, a pathway that promotes increased vascular permeability, apoptosis, and surfactant alterations. A novel, clinically relevant triple-hit model of nALI was developed, consisting of repeated airway lavage, injurious ventilation, and lipopolysaccharide instillation into the airways, every 24 hours. Thirty-five piglets were randomized to one of four treatment protocols: control (no intervention), surfactant alone, surfactant + Inos, and surfactant + IP3. After 72 hours of mechanical ventilation, lungs were excised from the thorax for subsequent analyses. Clinically, oxygenation and ventilation improved, and extravascular lung water decreased significantly with the S + IP3 intervention. In pulmonary tissue, we observed decreased aSMase activity and ceramide concentrations, decreased caspase-8 concentrations, reduced alveolar epithelial apoptosis, the reduced expression of interleukin-6, transforming growth factor-β1, and amphiregulin (an epithelial growth factor), reduced migration of blood-borne cells and particularly of CD14(+)/18(+) cells (macrophages) into the airspaces, and lower surfactant surface tensions in S + IP3-treated but not in S + Inos-treated piglets. We conclude that the admixture of IP3 to surfactant, but not of Inos, improves gas exchange and edema in our nALI model by the suppression of the governing enzyme aSMase, and that this treatment deserves clinical evaluation. PMID:22403805

  19. 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

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

    PubMed

    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

  1. Molecular pathology of pulmonary edema after injury in forensic autopsy cases.

    PubMed

    Wang, Qi; Ishikawa, Takaki; Michiue, Tomomi; Zhu, Bao-Li; Guan, Da-Wei; Maeda, Hitoshi

    2012-11-01

    The lung is vulnerable to trauma; pulmonary edema starts quickly as part of the systemic responses involved in shock. The present study investigated the molecular pathology of posttraumatic alveolar damage and responses involving pulmonary edema in forensic autopsy cases of injury (n = 66) compared with acute cardiac death cases (n = 13). Intrapulmonary mRNA and immunohistochemical expressions of matrix metalloproteinases (MMPs; MMP-2 and MMP-9), intercellular adhesion molecule-1, claudin-5, and aquaporins (AQPs, AQP-1 and AQP-5) were examined. Subacute injury deaths showed an increase in lung weight similar to that in acute cardiac death, but relative mRNA quantification using the Taqman real-time PCR assay demonstrated different findings among the causes of death; higher expressions were detected for all markers, except for AQP-5 in sharp instrument injury, for MMP-2 in blunt brain injury, and for MMP-9 in non-brain blunt injury, but these expression levels were lower in acute cardiac death. In immunostaining, only MMPs showed differences among the causes of death: MMP-2 expression was evident in most subacute deaths due to blunt brain injury and sharp instrument injury, whereas MMP-9 was intensely positive in those of non-brain blunt injury and sharp instrument injury. These findings suggest significant differences in the mechanism of pulmonary edema among fatal injuries and acute cardiac death, especially between blunt and sharp instrument injury. Systematic analysis of gene expressions using real-time PCR in combination with immunohistochemistry may be useful in evaluating pulmonary damage and responses after injury in death investigations, especially in connection with posttraumatic shock. PMID:22885909

  2. A 45-Year-Old Man With Recurrent Dyspnea and Hemoptysis during Exercise: Exercise-Induced Pulmonary Hemorrhage/Edema

    PubMed Central

    Kim, Dae Sung; Lee, Minhyeok; Kwon, Oh Jung; Jeong, Inbeom; Son, Ji Woong; Na, Moon Jun

    2015-01-01

    A 45-year-old man presented with dyspnea and hemoptysis during exercise. A chest computed tomography (CT) revealed multifocal diffuse patchy ground glass opacity and interlobular septal thickening in both the lungs. Permeability pulmonary edema or pulmonary hemorrhage was suspected. Serologic studies for autoimmune disorders and vasculitis were negative. There was no laboratory evidence of coagulopathy, other hematopoietic disease or infectious disease. Considering correlation with exercise, we diagnosed exercise-induced pulmonary hemorrhage (EIPH) or exercise-induced pulmonary edema (EIPE). The patient was managed with antifibrinolytics, antibiotics, and antitussive agent. After a week, follow-up chest CT revealed completely resolved pulmonary hemorrhage. About 2 months after the first event, he visited again with dyspnea and hemoptysis during running. In the present study, we report a case of recurrent pulmonary hemorrhage after exercise. PMID:26508928

  3. Reexpansion pulmonary edema after surgery for spontaneous pneumothorax in a patient with anorexia nervosa

    PubMed Central

    Ozawa, Yuichiro; Ichimura, Hideo; Sakai, Mitsuaki

    2016-01-01

    Introduction Several adverse effects on the pulmonary system in patients with anorexia nervosa (AN) have been reported. We present a case of AN who presented with a complicated reexpansion pulmonary edema (RPE) after video-assisted thoracic surgery (VATS) for spontaneous pneumothorax. Presentation of case A 23-year-old woman with severe anorexia nervosa (weight: 25 kg, body mass index: 8.96 kg/m2) underwent VATS for spontaneous pneumothorax. Five hours after the surgery, she immediately presented acute cardiorespiratory insufficiency. Chest radiography showed an infiltrating shadow in the entire right lung. She was diagnosed with reexpansion pulmonary edema that was treated with methylprednisolone pulse therapy and mechanical ventilation. She recovered and was extubated on postoperative day 4. The chest drain tube was removed on postoperative day 5. Discussion Bullectomy or ligation of bullae for spontaneous pneumothorax in a patient with AN has never been reported. In our case, bullae were identified in preoperative CT and we chose ligation of the bullae instead of the bullectomy using automatic suture device because of poor wound healing concerned. Conclusion We present a case of RPE after VATS for spontaneous pneumothorax in a patient with AN. Malnutrition owing to AN results in critical complications such as RPE. PMID:27158490

  4. Exercise-induced interstitial pulmonary edema at sea-level in young and old healthy humans

    PubMed Central

    Taylor, Bryan J.; Carlson, Alex R.; Miller, Andrew D.; Johnson, Bruce D.

    2014-01-01

    We asked whether aged adults are more susceptible to exercise-induced pulmonary edema relative to younger individuals. Lung diffusing capacity for carbon monoxide (DLCO), alveolar-capillary membrane conductance (Dm) and pulmonary-capillary blood volume (Vc) were measured before and after exhaustive discontinuous incremental exercise in 10 young (YNG; 27±3 yr) and 10 old (OLD; 69±5 yr) males. In YNG subjects, Dm increased (11±7%, P=0.031), Vc decreased (−10±9%, P=0.01) and DLCO was unchanged (30.5±4.1 vs. 29.7±2.9 ml/min/mmHg, P=0.44) pre- to post-exercise. In OLD subjects, DLCO and Dm increased (11±14%, P=0.042; 16±14%, P=0.025) but Vc was unchanged (58±23 vs. 56±23 ml, P=0.570) pre- to post-exercise. Group-mean Dm/Vc was greater after vs. before exercise in the YNG and OLD subjects. However, Dm/Vc was lower post-exercise in 2 of the 10 YNG (−7±4%) and 2 of the 10 OLD subjects (−10±5%). These data suggest that exercise decreases interstitial lung fluid in most YNG and OLD subjects, with a small number exhibiting evidence for exercise-induced pulmonary edema. PMID:24200644

  5. Caspase-1 inhibitor Prevents Neurogenic Pulmonary Edema after Subarachnoid Hemorrhage in Mice

    PubMed Central

    Suzuki, Hidenori; Sozen, Takumi; Hasegawa, Yu; Chen, Wanqiu; Zhang, John H.

    2009-01-01

    Background and Purpose We examined the effects of a caspase-1 inhibitor, N-Ac-Tyr-Val-Ala-Asp-chloromethyl ketone (Ac-YVAD-CMK), on neurogenic pulmonary edema (NPE) in the endovascular perforation model of subarachnoid hemorrhage (SAH) in mice. Methods Ninety-seven mice were assigned to sham, SAH+vehicle, SAH+Ac-YVAD-CMK (6 or 10mg/kg) and SAH+Z-Val-Ala-Asp-fluoromethylketone (Z-VAD-FMK, 6mg/kg) groups. Drugs were intraperitoneally injected 1 hour post-SAH. Pulmonary edema measurements, Western blot for interleukin-1β, interleukin-18, myeloperoxidase, matrix metalloproteinase (MMP)-2, MMP-9, cleaved caspase-3 and zona occludens (ZO)-1, MMP zymography, TUNEL staining and immunostaining were performed on the lung at 24 hours post-SAH. Results Ten- but not 6-mg/kg of Ac-YVAD-CMK significantly inhibited a post-SAH increase in the activation of interleukin-1β and caspase-3 and the number of TUNEL-positive pulmonary endothelial cells, preventing NPE. Another antiapoptotic drug Z-VAD-FMK also reduced NPE. SAH did not change interleukin-18, myeloperoxidase, MMP-2, MMP-9, ZO-1 levels and MMP activity. Conclusions We report for the first time that Ac-YVAD-CMK prevents lung cell apoptosis and NPE after SAH in mice. PMID:19875734

  6. Agonist of growth hormone-releasing hormone reduces pneumolysin-induced pulmonary permeability edema

    PubMed Central

    Lucas, Rudolf; Sridhar, Supriya; Rick, Ferenc G.; Gorshkov, Boris; Umapathy, Nagavedi S.; Yang, Guang; Oseghale, Aluya; Verin, Alexander D.; Chakraborty, Trinad; Matthay, Michael A.; Zemskov, Evgeny A.; White, Richard; Block, Norman L.; Schally, Andrew V.

    2012-01-01

    Aggressive treatment with antibiotics in patients infected with Streptococcus pneumoniae induces release of the bacterial virulence factor pneumolysin (PLY). Days after lungs are sterile, this pore-forming toxin can still induce pulmonary permeability edema in patients, characterized by alveolar/capillary barrier dysfunction and impaired alveolar liquid clearance (ALC). ALC is mainly regulated through Na+ transport by the apically expressed epithelial sodium channel (ENaC) and the basolaterally expressed Na+/K+-ATPase in type II alveolar epithelial cells. Because no standard treatment is currently available to treat permeability edema, the search for novel therapeutic candidates is of high priority. We detected mRNA expression for the active receptor splice variant SV1 of the hypothalamic polypeptide growth hormone-releasing hormone (GHRH), as well as for GHRH itself, in human lung microvascular endothelial cells (HL-MVEC). Therefore, we have evaluated the effect of the GHRH agonist JI-34 on PLY-induced barrier and ALC dysfunction. JI-34 blunts PLY-mediated endothelial hyperpermeability in monolayers of HL-MVEC, in a cAMP-dependent manner, by means of reducing the phosphorylation of myosin light chain and vascular endothelial (VE)-cadherin. In human airway epithelial H441 cells, PLY significantly impairs Na+ uptake, but JI-34 restores it to basal levels by means of increasing cAMP levels. Intratracheal instillation of PLY into C57BL6 mice causes pulmonary alveolar epithelial and endothelial hyperpermeability as well as edema formation, all of which are blunted by JI-34. These findings point toward a protective role of the GHRH signaling pathway in PLY-induced permeability edema. PMID:22308467

  7. Inherent variations in CO-H2S-mediated carotid body O2 sensing mediate hypertension and pulmonary edema.

    PubMed

    Peng, Ying-Jie; Makarenko, Vladislav V; Nanduri, Jayasri; Vasavda, Chirag; Raghuraman, Gayatri; Yuan, Guoxiang; Gadalla, Moataz M; Kumar, Ganesh K; Snyder, Solomon H; Prabhakar, Nanduri R

    2014-01-21

    Oxygen (O2) sensing by the carotid body and its chemosensory reflex is critical for homeostatic regulation of breathing and blood pressure. Humans and animals exhibit substantial interindividual variation in this chemosensory reflex response, with profound effects on cardiorespiratory functions. However, the underlying mechanisms are not known. Here, we report that inherent variations in carotid body O2 sensing by carbon monoxide (CO)-sensitive hydrogen sulfide (H2S) signaling contribute to reflex variation in three genetically distinct rat strains. Compared with Sprague-Dawley (SD) rats, Brown-Norway (BN) rats exhibit impaired carotid body O2 sensing and develop pulmonary edema as a consequence of poor ventilatory adaptation to hypobaric hypoxia. Spontaneous Hypertensive (SH) rat carotid bodies display inherent hypersensitivity to hypoxia and develop hypertension. BN rat carotid bodies have naturally higher CO and lower H2S levels than SD rat, whereas SH carotid bodies have reduced CO and greater H2S generation. Higher CO levels in BN rats were associated with higher substrate affinity of the enzyme heme oxygenase 2, whereas SH rats present lower substrate affinity and, thus, reduced CO generation. Reducing CO levels in BN rat carotid bodies increased H2S generation, restoring O2 sensing and preventing hypoxia-induced pulmonary edema. Increasing CO levels in SH carotid bodies reduced H2S generation, preventing hypersensitivity to hypoxia and controlling hypertension in SH rats. PMID:24395806

  8. 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. PMID:23497776

  9. Elevated plasma atrial natriuretic factor and vasopressin in high-altitude pulmonary edema.

    PubMed

    Cosby, R L; Sophocles, A M; Durr, J A; Perrinjaquet, C L; Yee, B; Schrier, R W

    1988-11-15

    A diagnosis of acute high-altitude pulmonary edema was made in five male skiers (age, 35.0 +/- 1.8 years) by history and physical examination and was confirmed by a characteristic chest radiogram showing alveolar infiltrates associated with a normal cardiac silhouette. Five healthy age- and sex-matched subjects with similar physical activity at the same altitude served as controls. Plasma sodium was 135.0 +/- 1.5 mmol/L in the acutely ill patients compared with 144.0 +/- 3.3 mmol/L in the controls (P less than 0.025). Mean plasma atrial natriuretic factor immunoreactivity averaged 17.6 +/- 5.6 pmol/L in patients with high-altitude pulmonary edema compared with 6.8 +/- 0.7 pmol/L in the controls at the same altitude (P less than 0.05). Elevated atrial natriuretic factor levels normalized to 7.5 +/- 1.9 pmol/L (P less than 0.05) during recovery in Denver (altitude, 1600 meters) 24 hours later. Plasma arginine vasopressin levels were 1.8 +/- 0.37 pmol/L in patients with high-altitude pulmonary edema at diagnosis compared with 0.92 +/- 0.28 pmol/L in controls (P = 0.07). The inappropriately elevated arginine vasopressin levels decreased to 1.29 +/- 0.37 pmol/L during recovery (P less than 0.025), but the lowered plasma sodium concentration had not normalized by discharge within 24-hours of transfer to Denver and averaged 135.8 +/- 1.2 mmol/L. The pathophysiologic implications of these findings are discussed. PMID:2973274

  10. Pulmonary edema

    MedlinePlus

    ... failure: pathophysiology and diagnosis. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine . 24th ed. Philadelphia, PA: ... failure: management and prognosis. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine . 24th ed. Philadelphia, PA: ...

  11. Nicardipine-Induced Acute Pulmonary Edema: A Rare but Severe Complication of Tocolysis

    PubMed Central

    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

  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. [Effectiveness of artificial ventilation in oil microembolism followed by pulmonary edema].

    PubMed

    Tarakanov, I A; Kuz'michev, S A; Semkina, G A

    1992-07-01

    In experiments on sodium pentobarbital (40 mg/kg, i.p.) anesthetized mongrel cats of either sex weighting from 2.0 to 4.0 kg, it was found, that in conditions of oil pulmonary microembolization, followed by pulmonary edema, the most suitable is rapid and shallow pattern of ventilation, ensuring optimal ventilation/perfusion interrelation. The oil microembolization was introduced with intravenous administration (1 mg per kg of body weight during 2 min) of olive oil. It is necessary to provide flexible regimens of artificial ventilation and conformity of respiratory pattern and body's demands can be controlled according to pHa and PaO2. It is desirable that pH and pO2 can be evaluated continuously. PMID:1421295

  14. Pulmonary Edema Due to Oral Gavage in a Toxicological Study Related to Aquaporin-1, -4 and -5 Expression

    PubMed Central

    Singha, Ornuma; Kengkoom, Kanchana; Chaimongkolnukul, Khuanjit; Cherdyu, Sompong; Pongponratn, Emsri; Ketjareon, Taweesak; Panavechkijkul, Yaowaluk; Ampawong, Sumate

    2013-01-01

    A one-time oral gavage can be enough to cause of alveologenic edema with higher expression of AQP-1 and -4 than that with repeated-dose oral gavage, which caused both profound perivascular edema and hydrostatic pressure edema, while AQP-5 was similarly expressed. The alteration of AQPs expression was probably related to alveolar fluid clearance across the alveolar and bronchiolar epithelium in different stages of lung injury. The results clarified the type of lung edema in acute and sub-chronic toxicity studies without treatment related effect of tested material. The pathogenesis of pulmonary edema due to oral gavage toxicological study is associated with the cellular immune response to the reflux materials. Mast cell and leukocyte accumulation may contribute to increase vascular permeability leading to permeability edema. The increase in alveolar septum epithelium, perivascular and peribronchial cuffing, accumulation alveolar lipid containing macrophage and medial hyperplasia of the pulmonary artery might have been caused to increase airway resistance, which resulted in hydrostatic pressure edema. PMID:24155561

  15. An uncommon complication of a common clinical scenario: exploring reexpansion pulmonary edema with a case report and literature review

    PubMed Central

    Meeker, Jared W.; Jaeger, Amy L.; Tillis, William P.

    2016-01-01

    Reexpansion pulmonary edema (RPE) is a rare complication that can occur after rapid reinflation of the lung following thoracentesis of a pleural effusion or chest tube drainage of pneumothorax. The severity in clinical presentation can be widely varied from radiographic changes only to rapidly progressive respiratory failure requiring mechanical ventilation. The quick nature of onset and potential for serious decline in a previously stable patient makes it important to prepare, recognize, diagnose, and appropriately manage patients who develop RPE. The standard treatment for RPE consists of supportive care, and there are certain measures that may be taken to reduce the risk, including limiting the amount drained and avoiding excessive negative pleural pressure. Exactly how to prevent RPE remains unclear, however, and varying recommendations exist. This is a case report of RPE after thoracentesis for a pleural effusion and a brief review of literature to date, including potential preventative strategies. PMID:27406463

  16. [Reexpansion Pulmonary Edema during Emergency Surgery in a Patient with Spontaneous Hemopneumothorax].

    PubMed

    Yamaguchi, Satoshi; Hirakawa, Kei

    2015-06-01

    A 43-year-old male patient with spontaneous hemopneumothorax of the right lung underwent emergency video-assisted thoracoscopic surgery for drainage, hemostasis and bullae resection. Fifteen minutes after reexpansion of the right lung, we found bubbly sputum coming out from the right tracheal tube and cloudy shadow in the right field of his chest X-ray. The occurrence of reexpansion pulmonary edema (RPE) was considered. Subsequent mechanical ventilation with PEEP and administration of steroid and diuretic was done as his treatment. His respiratory state was stabiized in the next two days. As the lung collapse following spontaneous hemopneumothorax often becomes more severe, we should pay attention to the occurrence of RPE after expansion of affected side lung. And, if it occurred, appropriate and prompt treatment as above should be done because of its high mortality. PMID:26437555

  17. High-altitude pulmonary edema among visitors to Summit County, Colorado.

    PubMed

    Sophocles, A M; Bachman, J

    1983-12-01

    Twenty-nine cases of high-altitude pulmonary edema (HAPE) affecting visitors to Summit County, Colorado, were analyzed. The mean age of the group was 37.8 years, and all the patients were male. These results differ from previous studies and suggest that there are two varieties of HAPE. The first type (type 1, or nonresident-ascent HAPE) affects visitors to altitudes above 8,000 ft (2,439 m). At altitudes up to 11,000 ft (3,354 m), it is a disease that affects primarily adult men. The second variety (type 2, or resident-reascent HAPE) affects residents of high altitudes when they descend to an elevation below 8,000 ft (2,430 m) and then return to high altitude. This type of HAPE affects male and female residents almost equally and is a disease of childhood and adolescence. PMID:6644250

  18. High-altitude pulmonary edema in Vail, Colorado, 1975-1982.

    PubMed

    Sophocles, A M

    1986-05-01

    Between 1975 and 1982 a total of 47 cases of high-altitude pulmonary edema occurred in Vail, Colorado, elevation 2,500 m (8,200 ft). All occurred in visitors from lower altitudes. The mean age of the patients was 35.6 years, and 93% were men. Most patients had tachycardia, tachypnea and fever. The mean time of onset of cough and shortness of breath was 2.5 days after arrival. The average total ascent of the patients was 2,330 m (7,644 ft) in less than one day from a mean residential elevation of 170 m (556 ft). Also, 91% of the cases occurred between December and April, when the average daily temperature was -4.3 degrees C (24.3 degrees F) and the ambient barometric pressure was 22.37 in of mercury. PMID:3716417

  19. Rural treatment of acute cardiogenic pulmonary edema: applying the evidence to achieve success with failure.

    PubMed

    Bosomworth, John

    2008-01-01

    Rural management of acute cardiogenic pulmonary edema should be based on avoidance of adverse outcomes such as in-hospital mortality, the need for intensive care unit care, and the need for intubation and mechanical ventilation. Current evidence suggests that early noninvasive continuous positive airway pressure and early aggressive preload reduction with intravenous nitroglycerin are first-line interventions. Afterload reduction with sublingual captopril, with or without nitroglycerin, improves outcomes and is a second-line intervention. Furosemide is associated with adverse outcomes when used alone and should be given only after vasodilator therapy as a third-line intervention. Inotropes should be used only with demonstrably poor perfusion as they do not improve outcomes and may indeed be associated with increased mortality. Concurrent vasodilator therapy should be considered as soon as possible. Morphine should not be used as it is associated with adverse outcomes. If sedation is desirable, benzodiazepines should be considered. PMID:18796257

  20. N-acetylcysteine prevents pulmonary edema and acute kidney injury in rats with sepsis submitted to mechanical ventilation.

    PubMed

    Campos, Renata; Shimizu, Maria Heloísa Massola; Volpini, Rildo Aparecido; de Bragança, Ana Carolina; Andrade, Lucia; Lopes, Fernanda Degobbi Tenório Quirino Dos Santos; Olivo, Clarice; Canale, Daniele; Seguro, Antonio Carlos

    2012-04-01

    Sepsis is a common cause of acute kidney injury (AKI) and acute lung injury. Oxidative stress plays as important role in such injury. The aim of this study was to evaluate the effects that the potent antioxidant N-acetylcysteine (NAC) has on renal and pulmonary function in rats with sepsis. Rats, treated or not with NAC (4.8 g/l in drinking water), underwent cecal ligation and puncture (CLP) 2 days after the initiation of NAC treatment, which was maintained throughout the study. At 24 h post-CLP, renal and pulmonary function were studied in four groups: control, control + NAC, CLP, and CLP + NAC. All animals were submitted to low-tidal-volume mechanical ventilation. We evaluated respiratory mechanics, the sodium cotransporters Na-K-2Cl (NKCC1) and the α-subunit of the epithelial sodium channel (α-ENaC), polymorphonuclear neutrophils, the edema index, oxidative stress (plasma thiobarbituric acid reactive substances and lung tissue 8-isoprostane), and glomerular filtration rate. The CLP rats developed AKI, which was ameliorated in the CLP + NAC rats. Sepsis-induced alterations in respiratory mechanics were also ameliorated by NAC. Edema indexes were lower in the CLP + NAC group, as was the wet-to-dry lung weight ratio. In CLP + NAC rats, α-ENaC expression was upregulated, whereas that of NKCC1 was downregulated, although the difference was not significant. In the CLP + NAC group, oxidative stress was significantly lower and survival rates were significantly higher than in the CLP group. The protective effects of NAC (against kidney and lung injury) are likely attributable to the decrease in oxidative stress, suggesting that NAC can be useful in the treatment of sepsis. PMID:22268121

  1. Elevated pulmonary artery pressure and brain natriuretic peptide in high altitude pulmonary edema susceptible non-mountaineers

    PubMed Central

    Gupta, Rajinder K.; Himashree, G.; Singh, Krishan; Soree, Poonam; Desiraju, Koundinya; Agrawal, Anurag; Ghosh, Dishari; Dass, Deepak; Reddy, Prassana K.; Panjwani, Usha; Singh, Shashi Bala

    2016-01-01

    Exaggerated pulmonary pressor response to hypoxia is a pathgonomic feature observed in high altitude pulmonary edema (HAPE) susceptible mountaineers. It was investigated whether measurement of basal pulmonary artery pressure (Ppa) and brain natriuretic peptide (BNP) could improve identification of HAPE susceptible subjects in a non-mountaineer population. We studied BNP levels, baseline hemodynamics and the response to hypoxia (FIo2 = 0.12 for 30 min duration at sea level) in 11 HAPE resistant (no past history of HAPE, Control) and 11 HAPE susceptible (past history of HAPE, HAPE-S) subjects. Baseline Ppa (19.31 ± 3.63 vs 15.68 ± 2.79 mm Hg, p < 0.05) and plasma BNP levels (52.39 ± 32.9 vs 15.05 ± 9.6 pg/ml, p < 0.05) were high and stroke volume was less (p < 0.05) in HAPE-S subjects compared to control. Acute hypoxia produced an exaggerated increase in heart rate (p < 0.05), mean arterial pressure (p < 0.05) and Ppa (28.2 ± 5.8 vs 19.33 ± 3.74 mm Hg, p < 0.05) and fall in peripheral oxygen saturation (p < 0.05) in HAPE-S compared to control. Receiver operating characteristic (ROC) curves showed that Ppa response to acute hypoxia was the best variable to identify HAPE susceptibility (AUC 0.92) but BNP levels provided comparable information (AUC 0.85). BNP levels are easy to determine and may represent an important marker for the determination of HAPE susceptibility. PMID:26892302

  2. Elevated pulmonary artery pressure and brain natriuretic peptide in high altitude pulmonary edema susceptible non-mountaineers.

    PubMed

    Gupta, Rajinder K; Himashree, G; Singh, Krishan; Soree, Poonam; Desiraju, Koundinya; Agrawal, Anurag; Ghosh, Dishari; Dass, Deepak; Reddy, Prassana K; Panjwani, Usha; Singh, Shashi Bala

    2016-01-01

    Exaggerated pulmonary pressor response to hypoxia is a pathgonomic feature observed in high altitude pulmonary edema (HAPE) susceptible mountaineers. It was investigated whether measurement of basal pulmonary artery pressure (Ppa) and brain natriuretic peptide (BNP) could improve identification of HAPE susceptible subjects in a non-mountaineer population. We studied BNP levels, baseline hemodynamics and the response to hypoxia (FIo2 = 0.12 for 30 min duration at sea level) in 11 HAPE resistant (no past history of HAPE, Control) and 11 HAPE susceptible (past history of HAPE, HAPE-S) subjects. Baseline Ppa (19.31 ± 3.63 vs 15.68 ± 2.79 mm Hg, p < 0.05) and plasma BNP levels (52.39 ± 32.9 vs 15.05 ± 9.6 pg/ml, p < 0.05) were high and stroke volume was less (p < 0.05) in HAPE-S subjects compared to control. Acute hypoxia produced an exaggerated increase in heart rate (p < 0.05), mean arterial pressure (p < 0.05) and Ppa (28.2 ± 5.8 vs 19.33 ± 3.74 mm Hg, p < 0.05) and fall in peripheral oxygen saturation (p < 0.05) in HAPE-S compared to control. Receiver operating characteristic (ROC) curves showed that Ppa response to acute hypoxia was the best variable to identify HAPE susceptibility (AUC 0.92) but BNP levels provided comparable information (AUC 0.85). BNP levels are easy to determine and may represent an important marker for the determination of HAPE susceptibility. PMID:26892302

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

    PubMed

    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

  4. 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

  5. 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

  6. Platelet-activating factor-induced pulmonary edema is partly mediated by prostaglandin E(2), E-prostanoid 3-receptors, and potassium channels.

    PubMed

    Göggel, Rolf; Hoffman, Sven; Nüsing, Rolf; Narumiya, Suh; Uhlig, Stefan

    2002-09-01

    Platelet-activating factor (PAF) is an important endogenous mediator of pulmonary edema in many models of acute lung injury. PAF triggers edema formation by simultaneous activation of two independent pathways; one is mediated by a cyclooxygenase metabolite, and the other is blocked by quinine. We examined the hypothesis that the cyclooxygenase-dependent part of PAF-induced edema is mediated by prostaglandin E(2) (PGE(2)). In isolated rat lungs, PAF administration stimulated release of PGE(2) into the venous effluate and increased lung weight as a measure of edema formation. Perfusion with a neutralizing PGE(2) antibody attenuated the PAF-induced edema formation. In vivo, E-prostanoid 3-receptor-deficient mice showed less pulmonary Evans blue extravasation in response to PAF injection than did mice deficient in EP1, EP2, or EP4 receptors. Perfusion of rat lungs with PGE(2) caused pulmonary edema, which was largely prevented by inhibition of voltage-gated potassium channels (25 nM beta-dendrotoxin), but not by blocking calcium-dependent potassium currents (100 micro M paxilline). In line with its effects on PGE(2)-induced edema formation, beta-dendrotoxin attenuated PAF-induced edema partly if given alone, and completely in combination with quinine. Our findings suggest that PAF-triggered edema is partly mediated by the release of PGE(2), activation of EP3 receptors, and activation of voltage-gated potassium channels. PMID:12204861

  7. 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

  8. Novel Peptide for Attenuation of Hyperoxia-induced Disruption of Lung Endothelial Barrier and Pulmonary Edema via Modulating Peroxynitrite Formation*

    PubMed Central

    Kondrikov, Dmitry; Gross, Christine; Black, Stephen M.; Su, Yunchao

    2014-01-01

    Pulmonary damages of oxygen toxicity include vascular leakage and pulmonary edema. We have previously reported that hyperoxia increases the formation of NO and peroxynitrite in lung endothelial cells via increased interaction of endothelial nitric oxide (eNOS) with β-actin. A peptide (P326TAT) with amino acid sequence corresponding to the actin binding region of eNOS residues 326–333 has been shown to reduce the hyperoxia-induced formation of NO and peroxynitrite in lung endothelial cells. In the present study, we found that exposure of pulmonary artery endothelial cells to hyperoxia (95% oxygen and 5% CO2) for 48 h resulted in disruption of monolayer barrier integrity in two phases, and apoptosis occurred in the second phase. NOS inhibitor NG-nitro-l-arginine methyl ester attenuated the endothelial barrier disruption in both phases. Peroxynitrite scavenger uric acid did not affect the first phase but ameliorated the second phase of endothelial barrier disruption and apoptosis. P326TAT inhibited hyperoxia-induced disruption of monolayer barrier integrity in two phases and apoptosis in the second phase. More importantly, injection of P326TAT attenuated vascular leakage, pulmonary edema, and endothelial apoptosis in the lungs of mice exposed to hyperoxia. P326TAT also significantly reduced the increase in eNOS-β-actin association and protein tyrosine nitration. Together, these results indicate that peptide P326TAT ameliorates barrier dysfunction of hyperoxic lung endothelial monolayer and attenuates eNOS-β-actin association, peroxynitrite formation, endothelial apoptosis, and pulmonary edema in lungs of hyperoxic mice. P326TAT can be a novel therapeutic agent to treat or prevent acute lung injury in oxygen toxicity. PMID:25315770

  9. 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. PMID:26228998

  10. Evaluation of a thoracic ultrasound training module for the detection of pneumothorax and pulmonary edema by prehospital physician care providers

    PubMed Central

    Noble, Vicki E; Lamhaut, Lionel; Capp, Roberta; Bosson, Nichole; Liteplo, Andrew; Marx, Jean-Sebastian; Carli, Pierre

    2009-01-01

    Background While ultrasound (US) has continued to expedite diagnosis and therapy for critical care physicians inside the hospital system, the technology has been slow to diffuse into the pre-hospital system. Given the diagnostic benefits of thoracic ultrasound (TUS), we sought to evaluate image recognition skills for two important TUS applications; the identification of B-lines (used in the US diagnosis of pulmonary edema) and the identification of lung sliding and comet tails (used in the US diagnosis of pneumothorax). In particular we evaluated the impact of a focused training module in a pre-hospital system that utilizes physicians as pre-hospital providers. Methods 27 Paris Service D'Aide Médicale Urgente (SAMU) physicians at the Hôpital Necker with varying levels of US experience were given two twenty-five image recognition pre-tests; the first test had examples of both normal and pneumothorax lung US and the second had examples of both normal and pulmonary edema lung US. All 27 physicians then underwent the same didactic training modules. A post-test was administered upon completing the training module and results were recorded. Results Pre and post-test scores were compared for both the pneumothorax and the pulmonary edema modules. For the pneumothorax module, mean test scores increased from 10.3 +/- 4.1 before the training to 20.1 +/- 3.5 after (p < 0.0001), out of 25 possible points. The standard deviation decreased as well, indicating a collective improvement. For the pulmonary edema module, mean test scores increased from 14.1 +/- 5.2 before the training to 20.9 +/- 2.4 after (p < 0.0001), out of 25 possible points. The standard deviation decreased again by more than half, indicating a collective improvement. Conclusion This brief training module resulted in significant improvement of image recognition skills for physicians both with and without previous ultrasound experience. Given that rapid diagnosis of these conditions in the pre-hospital system

  11. 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

  12. Molecular pathology of pulmonary edema in forensic autopsy cases with special regard to fatal hyperthermia and hypothermia.

    PubMed

    Wang, Qi; Ishikawa, Takaki; Michiue, Tomomi; Zhu, Bao-Li; Guan, Da-Wei; Maeda, Hitoshi

    2013-05-10

    Fatalities due to an extreme ambient temperature might present with poor or nonspecific pathologies; thus, the diagnosis of the cause of death in such cases is one of the most difficult tasks in forensic pathology. The present study investigated the molecular pathology of alveolar damage involving pulmonary edema with special regard to hyperthermia (heatstroke) and hypothermia (cold exposure) in forensic autopsy cases (total, n=122; within 48 h postmortem). Intrapulmonary mRNA and immunohistochemical expressions of matrix metalloproteinases (MMPs), intercellular adhesion molecule-1 (ICAM-1), claudin-5 (CLDN-5) and aquaporins (AQPs) were examined. Relative mRNA quantification using Taqman real-time PCR assay demonstrated higher expressions of all markers except for AQP-5 in fatal hyperthermia, and higher expression of MMP-9 in fatal hypothermia. Acute cardiac death, mechanical asphyxiation, fire fatality and intoxication did not present any characteristic findings. In immunostaining, only MMPs showed evident differences among the causes of death: MMP-9 was intensely positive in most cases of hyperthermia and hypothermia, but MMP-2 expression was evident only in hyperthermia. These findings suggest alveolar damage involving pulmonary edema, characteristic of fatal hyperthermia and hypothermia. Systematic analysis of gene expressions using real-time PCR might be a useful procedure in forensic death investigation. PMID:23597750

  13. 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. PMID:27001080

  14. Levels of interleukin-6, superoxide dismutase and malondialdehyde in the lung tissue of a rat model of hypoxia-induced acute pulmonary edema

    PubMed Central

    GAO, HENGBO; TIAN, YINGPING; WANG, WEI; YAO, DONGQI; ZHENG, TUOKANG; MENG, QINGBING

    2016-01-01

    The present study aimed to investigate the levels of malondialdehyde (MDA), superoxide dismutase (SOD) and interleukin (IL)-6 in the lung tissue of a rat model of acute pulmonary edema induced by acute hypoxia, and its pathophysiological significance. A total of 48 adult Wistar rats were randomly divided into group A, a normal group; group B, a model of acute pulmonary edema induced by hypoxia for 24 h; group C, a model of acute pulmonary edema induced by hypoxia for 48 h; and group D, a model of acute pulmonary edema induced by hypoxia for 72 h. The rats in groups B-D were intraperitoneally injected with 6% ammonium chloride to establish the model of acute pulmonary edema, and were subsequently sacrificed following successful modeling for 24, 48 and 72 h. The plasma of rats was isolated and the lungs of the rats were removed. Subsequently, a 10% lung homogenate was prepared and the contents and the activities of MDA, SOD and IL-6 in the lung tissue and IL-6 in the plasma were detected by enzyme-linked immunosorbent assay. MDA and IL-6 expression levels increased and SOD activity decreased in the lung tissue in group B as compared with group A; however the difference did not reach significance (P>0.05). MDA, IL-6 and SOD levels in the lung tissue of rats were significantly altered following the increased duration of pulmonary edema in groups C and D, as compared group A (P<0.05). The plasma IL-6 levels of the rats in groups B-D significantly increased, as compared with those in group A (P<0.05). In conclusion, the results of the present study demonstrated that the incidence of acute pulmonary edema may be associated with oxidative stress. Furthermore, decreased antioxidant capacity and increased free radical levels may be associated with pulmonary edema, as in the present study the levels of IL-6, SOD and MDA in the lung tissue were observed to be associated with the pathological changes of the disease. PMID:26998026

  15. 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

  16. 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.

  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. 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

  19. Involvement of COX2-Thromboxane Pathway in TCDD-Induced Precardiac Edema in Developing Zebrafish

    PubMed Central

    Teraoka, Hiroki; Okuno, Yuki; Nijoukubo, Daisuke; Yamakoshi, Ayumi; Peterson, Richard E.; Stegeman, John J.; Kitazawa, Takio; Hiraga, Takeo; Kubota, Akira

    2015-01-01

    The cardiovascular system is one of the most characteristic and important targets for developmental toxicity by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in fish larvae. However, knowledge of the mechanism of TCDD-induced edema after heterodimerization of aryl hydrocarbon receptor type 2 (AHR2) and AHR nuclear translocator type 1 (ARNT1) is still limited. In the present study, microscopic analysis with a high-speed camera revealed that TCDD increased the size of a small cavity between the heart and body wall in early eleutheroembryos, a toxic effect that we designate as precardiac edema. A concentration-response curve for precardiac edema at 2 days post fertilization (dpf) showed close similarity to that for conventional pericardial edema at 3 dpf. Precardiac edema caused by TCDD was reduced by morpholino knockdown of AHR2 and ARNT1, as well as by an antioxidant (ascorbic acid). A selective inhibitor of cyclooxygenase type 2 (COX2), NS398, also markedly inhibited TCDD-induced precardiac edema. A thromboxane receptor (TP) antagonist, ICI-192,605 almost abolished TCDD-induced precardiac edema and this effect was cancelled by U46619, a TP agonist, which was not influential in the action of TCDD by itself. Knockdown of COX2b and thromboxane A synthase 1 (TBXS), but not COX2a, strongly reduced TCDD-induced precardiac edema. Knockdown of COX2b was without effect on mesencephalic circulation failure caused by TCDD. The edema by TCDD was also inhibited by knockdown of c-mpl, a thrombopoietin receptor necessary for thromobocyte production. Finally, induction of COX2b, but not COX2a, by TCDD was seen in eleutheroembryos at 3 dpf. These results suggest a role of the COX2b-thromboxane pathway in precardiac edema formation following TCDD exposure in developing zebrafish. PMID:24858302

  20. Involvement of COX2-thromboxane pathway in TCDD-induced precardiac edema in developing zebrafish.

    PubMed

    Teraoka, Hiroki; Okuno, Yuki; Nijoukubo, Daisuke; Yamakoshi, Ayumi; Peterson, Richard E; Stegeman, John J; Kitazawa, Takio; Hiraga, Takeo; Kubota, Akira

    2014-09-01

    The cardiovascular system is one of the most characteristic and important targets for developmental toxicity by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in fish larvae. However, knowledge of the mechanism of TCDD-induced edema after heterodimerization of aryl hydrocarbon receptor type 2 (AHR2) and AHR nuclear translocator type 1 (ARNT1) is still limited. In the present study, microscopic analysis with a high-speed camera revealed that TCDD increased the size of a small cavity between the heart and body wall in early eleutheroembryos, a toxic effect that we designate as precardiac edema. A concentration-response curve for precardiac edema at 2 days post fertilization (dpf) showed close similarity to that for conventional pericardial edema at 3 dpf. Precardiac edema caused by TCDD was reduced by morpholino knockdown of AHR2 and ARNT1, as well as by an antioxidant (ascorbic acid). A selective inhibitor of cyclooxygenase type 2 (COX2), NS398, also markedly inhibited TCDD-induced precardiac edema. A thromboxane receptor (TP) antagonist, ICI-192,605 almost abolished TCDD-induced precardiac edema and this effect was canceled by U46619, a TP agonist, which was not influential in the action of TCDD by itself. Knockdown of COX2b and thromboxane A synthase 1 (TBXS), but not COX2a, strongly reduced TCDD-induced precardiac edema. Knockdown of COX2b was without effect on mesencephalic circulation failure caused by TCDD. The edema by TCDD was also inhibited by knockdown of c-mpl, a thrombopoietin receptor necessary for thromobocyte production. Finally, induction of COX2b, but not COX2a, by TCDD was seen in eleutheroembryos at 3 dpf. These results suggest a role of the COX2b-thromboxane pathway in precardiac edema formation following TCDD exposure in developing zebrafish. PMID:24858302

  1. Metabolomic analysis of the plasma of patients with high-altitude pulmonary edema (HAPE) using 1H NMR.

    PubMed

    Luo, Yongjun; Zhu, Junyu; Gao, Yuqi

    2012-06-01

    Upon rapid ascent to a high altitude, non-acclimatized individuals, although healthy, are highly prone to contracting high-altitude pulmonary edema (HAPE). Early diagnosis is difficult and there is no reliable biomarker available. We used proton ((1)H) NMR metabolomics to profile the altered metabolic patterns of blood plasma from HAPE patients. The plasmas of ten patients with HAPE and ten individuals without HAPE were collected and compared using (1)H NMR spectroscopy. Data were evaluated with several multivariate statistical analyses, including the principal components, the orthogonal partial least-squares discriminant, and the orthogonal signal correction partial least-squares discriminant. Multivariate statistical analyses revealed a significant disparity between subjects with HAPE and those in the control group. Compared to the plasma of the controls, the HAPE patients had significant increases in valine, lysine, leucine, isoleucine, glycerol phosphoryl choline, glycine, glutamine, glutamic acid, creatinine, citrate, and methyl histidine. These were accompanied by decreases in α- and β-glucose, trimethylamine, and the metabolic products of lipids. The data demonstrate that metabolomics may be effective for the diagnosis of HAPE in the future, and can be used for further understanding HAPE pathogenesis. PMID:22498880

  2. 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; Grant Rowe, R

    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

  3. 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 Central

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

    2015-01-01

    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 [3H]-ouabain binding. However, amiloride-sensitive uptake of 22Na+ 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. PMID:26333829

  4. 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

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

    PubMed

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

    2013-02-01

    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

  6. 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

  7. 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

  8. Micromechanics of alveolar edema.

    PubMed

    Perlman, Carrie E; Lederer, David J; Bhattacharya, Jahar

    2011-01-01

    The decrease of lung compliance in pulmonary edema underlies ventilator-induced lung injury. However, the cause of the decrease in compliance is unknown. We tested the hypothesis that in pulmonary edema, the mechanical effects of liquid-filled alveoli increase tissue stress in adjacent air-filled alveoli. By micropuncture of isolated, perfused rat lungs, we established a single-alveolus model of pulmonary edema that we imaged using confocal microscopy. In this model, we viewed a liquid-filled alveolus together with its air-filled neighbor at different transpulmonary pressures, both before and after liquid-filling. Instilling liquid in an alveolus caused alveolar shrinkage. As a result, the interalveolar septum was stretched, causing the neighboring air-filled alveolus to bulge. Thus, the air-filled alveolus was overexpanded by virtue of its adjacency to a liquid-filled alveolus. Confocal microscopy at different depths of the liquid-filled alveolus revealed a meniscus. Lung inflation to near-total lung capacity (TLC) demonstrated decreased compliance of the air-filled but not liquid-filled alveolus. However, at near TLC, the air-filled alveolus was larger than it was in the pre-edematous control tissue. In pulmonary edema, liquid-filled alveoli induce mechanical stress on air-filled alveoli, reducing the compliance of air-filled alveoli, and hence overall lung compliance. Because of increased mechanical stress, air-filled alveoli may be susceptible to overdistension injury during mechanical ventilation of the edematous lung. PMID:20118224

  9. 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

  10. Lipopolysaccharide-induced pulmonary endothelial barrier disruption and lung edema: critical role for bicarbonate stimulation of AC10.

    PubMed

    Nickols, Jordan; Obiako, Boniface; Ramila, K C; Putinta, Kevin; Schilling, Sarah; Sayner, Sarah L

    2015-12-15

    Bacteria-induced sepsis is a common cause of pulmonary endothelial barrier dysfunction and can progress toward acute respiratory distress syndrome. Elevations in intracellular cAMP tightly regulate pulmonary endothelial barrier integrity; however, cAMP signals are highly compartmentalized: whether cAMP is barrier-protective or -disruptive depends on the compartment (plasma membrane or cytosol, respectively) in which the signal is generated. The mammalian soluble adenylyl cyclase isoform 10 (AC10) is uniquely stimulated by bicarbonate and is expressed in pulmonary microvascular endothelial cells (PMVECs). Elevated extracellular bicarbonate increases cAMP in PMVECs to disrupt the endothelial barrier and increase the filtration coefficient (Kf) in the isolated lung. We tested the hypothesis that sepsis-induced endothelial barrier disruption and increased permeability are dependent on extracellular bicarbonate and activation of AC10. Our findings reveal that LPS-induced endothelial barrier disruption is dependent on extracellular bicarbonate: LPS-induced barrier failure and increased permeability are exacerbated in elevated bicarbonate compared with low extracellular bicarbonate. The AC10 inhibitor KH7 attenuated the bicarbonate-dependent LPS-induced barrier disruption. In the isolated lung, LPS failed to increase Kf in the presence of minimal perfusate bicarbonate. An increase in perfusate bicarbonate to the physiological range (24 mM) revealed the LPS-induced increase in Kf, which was attenuated by KH7. Furthermore, in PMVECs treated with LPS for 6 h, there was a dose-dependent increase in AC10 expression. Thus these findings reveal that LPS-induced pulmonary endothelial barrier failure requires bicarbonate activation of AC10. PMID:26475732

  11. 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

  12. 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

  13. An insilico approach to high altitude pulmonary edema - Molecular modeling of human beta2 adrenergic receptor and its interaction with Salmeterol & Nifedipine.

    PubMed

    Chandramoorthi, Gayathri Devi; Piramanayagam, Shanmughavel; Marimuthu, Parthiban

    2008-09-01

    Knowledge of the three-dimensional structures of protein targets from genomic data has the potential to accelerate researches pertaining to drug discovery. Human beta(2) adrenergic receptor is a G-protein-coupled receptor with seven transmembrane helices, and is important in pharmaceutical targeting on pulmonary and cardiovascular diseases. The human beta(2) adrenergic receptor has been found to play a very important role in the pathogenesis of high altitude pulmonary edema (HAPE). In the present study, a high quality of protein 3D structure has been predicted for the human beta(2) adrenergic receptor sequence with primary accession number P07550. Homologous template protein sequence with known 3D structure was identified and the template-query protein sequence validation was done by multiple sequence alignment method. The homology model was performed through Modeller and depended on the quality of the sequence alignment by BLAST, template structure and the consolidated result performed by Gene silico meta-server. The statistical verification of the generated model was evaluated by PROCHECK which revealed that the structure modeled through Modeller to be of good quality with 84.1% of residues in the most favored region. Docking studies were carried out after modeling with two well known ligands namely Salmeterol and Nifedipine, and the fitness score revealed that Salmeterol has a higher fitness score than Nifedipine. Estimation of binding affinity by X-Score revealed that Salmeterol had -10.40 binding affinity while Nifedipine showed -9.62 binding affinity. From the present study, it can be concluded that the generated model of human beta(2) adrenergic receptor can be used for further studies related to this receptor and Salmeterol was found to have a high binding affinity with human beta(2) adrenergic receptor. PMID:18512086

  14. 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.

  15. 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

  16. 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. PMID:22974762

  17. 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

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

    PubMed

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

    1984-04-01

    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 A2, and prostaglandin F2 alpha. Pretreatment with catalase, a specific scavenger of hydrogen peroxide, preserved pulmonary 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 that hydrogen peroxide impaired pulmonary vasoreactivity and subsequently caused edema. Despite the fact that hydrogen peroxide stimulated lung prostaglandin production, cyclooxygenase-derived products neither caused the decrease in vasoreactivity nor the development of edema. PMID:6427146

  19. 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

  20. 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

  1. Protective effect of prostacyclin against pre-cardiac edema caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin and a thromboxane receptor agonist in developing zebrafish.

    PubMed

    Nijoukubo, Daisuke; Tanaka, Yasuaki; Okuno, Yuki; Yin, Guojun; Kitazawa, Takio; Peterson, Richard E; Kubota, Akira; Teraoka, Hiroki

    2016-08-01

    The role of prostaglandin pathways has been suggested in some toxicological responses to dioxins. Cyclooxygenase type 2b (COX2b), thromboxane synthase, and the thromboxane receptor (TP) pathway have been implicated in mediating 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced pre-cardiac edema in developing zebrafish at 55 h post fertilization (hpf). Pre-cardiac edema refers to edema located in a small cavity between the heart and body wall of zebrafish eleutheroembryos. In the present study, we assessed the role of prostacyclin, which counteracts some biological effects of thromboxane, in TCDD-induced pre-cardiac edema. Pre-cardiac edema induced by TCDD exposure (0.5 and 1 ppb) beginning at 24 hpf was markedly inhibited by exposure to beraprost (5 and 10 μM), a prostacyclin receptor (IP) agonist, beginning at 33 hpf. The preventive effect of beraprost was reduced by exposure to CAY10441 (10 μM), an IP antagonist starting at 33 hpf. Knockdowns of the IP receptor (IP-KD) with two different morpholinos caused edema by themselves and enhanced pre-cardiac edema caused by the low concentration of TCDD (0.5 ppb). On the other hand, short exposure beginning at 48 hpf to U46619 (7.5-30 μM), a thromboxane receptor agonist caused pre-cardiac edema, which was inhibited by exposure beginning at 48 hpf to both ICI-192,605 (24 μM), a TP antagonist, and beraprost. Expression of prostacyclin synthase was increased from fertilization, plateaued by 48 hpf, and was maintained until at least 96 hpf. Overall, the results demonstrate a preventive effect of prostacyclin on TCDD-induced pre-cardiac edema in developing zebrafish. PMID:27174823

  2. 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

  3. 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.…

  4. Pulmonary reactions caused by welding-induced decomposed trichloroethylene

    SciTech Connect

    Sjoegren, B.P.; Plato, N.; Alexandersson, R.; Eklund, A.; Falkenberg, C. )

    1991-01-01

    This is the report of a welder who performed argon-shielded electric arc welding in an atmosphere containing trichloroethylene. He developed immediate respiratory symptoms, pulmonary edema 12 hours after exposure, and recurring dyspnea ten days after exposure. These pulmonary reactions might be explained by inhalation of decomposition products of trichloroethylene such as dichloroacetyl chloride and phosgene.

  5. 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.

  6. Metformin Reverses Development of Pulmonary Hypertension via Aromatase Inhibition.

    PubMed

    Dean, Afshan; Nilsen, Margaret; Loughlin, Lynn; Salt, Ian P; MacLean, Margaret R

    2016-08-01

    Females are more susceptible to pulmonary arterial hypertension than males, although the reasons remain unclear. The hypoglycemic drug, metformin, is reported to have multiple actions, including the inhibition of aromatase and stimulation of AMP-activated protein kinase. Inhibition of aromatase using anastrazole is protective in experimental pulmonary hypertension but whether metformin attenuates pulmonary hypertension through this mechanism remains unknown. We investigated whether metformin affected aromatase activity and if it could reduce the development of pulmonary hypertension in the sugen 5416/hypoxic rat model. We also investigated its influence on proliferation in human pulmonary arterial smooth muscle cells. Metformin reversed right ventricular systolic pressure, right ventricular hypertrophy, and decreased pulmonary vascular remodeling in the rat. Furthermore, metformin increased rat lung AMP-activated protein kinase signaling, decreased lung and circulating estrogen levels, levels of aromatase, the estrogen metabolizing enzyme; cytochrome P450 1B1 and its transcription factor; the aryl hydrocarbon receptor. In human pulmonary arterial smooth muscle cells, metformin decreased proliferation and decreased estrogen synthesis by decreasing aromatase activity through the PII promoter site of Cyp19a1 Thus, we report for the first time that metformin can reverse pulmonary hypertension through inhibition of aromatase and estrogen synthesis in a manner likely to be mediated by AMP-activated protein kinase. PMID:27296990

  7. 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

  8. 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

  9. Notch Activation of Ca(2+) Signaling in the Development of Hypoxic Pulmonary Vasoconstriction and Pulmonary Hypertension.

    PubMed

    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; Yuan, Jason X-J

    2015-09-01

    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 Ca(2+) 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 Ca(2+) 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

  10. Development of a Measure of Attitude toward Pulmonary Disease Prevention.

    ERIC Educational Resources Information Center

    McGaghie, William C.; And Others

    1993-01-01

    Systematic scale-development procedures, reliability analyses on 2,852 medical students (3 samples), and factor analysis were used to develop and refine a scale reflecting attitudes about pulmonary disease prevention. Development and verification samples included 110 and 2,691 students, respectively. The scale is promising for health education and…

  11. Brain edema in diseases of different etiology.

    PubMed

    Adeva, María M; Souto, Gema; Donapetry, Cristóbal; Portals, Manuel; Rodriguez, Alberto; Lamas, David

    2012-07-01

    Cerebral edema is a potentially life-threatening complication shared by diseases of different etiology, such as diabetic ketoacidosis, acute liver failure, high altitude exposure, dialysis disequilibrium syndrome, and salicylate intoxication. Pulmonary edema is also habitually present in these disorders, indicating that the microcirculatory disturbance causing edema is not confined to the brain. Both cerebral and pulmonary subclinical edema may be detected before it becomes clinically evident. Available evidence suggests that tissue hypoxia or intracellular acidosis is a commonality occurring in all of these disorders. Tissue ischemia induces physiological compensatory mechanisms to ensure cell oxygenation and carbon dioxide removal from tissues, including hyperventilation, elevation of red blood cell 2,3-bisphosphoglycerate content, and capillary vasodilatation. Clinical, laboratory, and necropsy findings in these diseases confirm the occurrence of low plasma carbon dioxide partial pressure, increased erythrocyte 2,3-bisphosphoglycerate concentration, and capillary vasodilatation with increased vascular permeability in all of them. Baseline tissue hypoxia or intracellular acidosis induced by the disease may further deteriorate when tissue oxygen requirement is no longer matched to oxygen delivery resulting in massive capillary vasodilatation with increased vascular permeability and plasma fluid leakage into the interstitial compartment leading to edema affecting the brain, lung, and other organs. Causative factors involved in the progression from physiological adaptation to devastating clinical edema are not well known and may include uncontrolled disease, malfunctioning adaptive responses, or unknown factors. The role of carbon monoxide and local nitric oxide production influencing tissue oxygenation is unclear. PMID:22579570

  12. Delayed Development of Pneumothorax After Pulmonary Radiofrequency Ablation

    SciTech Connect

    Clasen, Stephan; Kettenbach, Joachim; Kosan, Bora; Aebert, Hermann; Schernthaner, Melanie; Kroeber, Stefan-Martin; Boemches, Andrea; Claussen, Claus D.; Pereira, Philippe L.

    2009-05-15

    Acute pneumothorax is a frequent complication after percutaneous pulmonary radiofrequency (RF) ablation. In this study we present three cases showing delayed development of pneumothorax after pulmonary RF ablation in 34 patients. Our purpose is to draw attention to this delayed complication and to propose a possible approach to avoid this major complication. These three cases occurred subsequent to 44 CT-guided pulmonary RF ablation procedures (6.8%) using either internally cooled or multitined expandable RF electrodes. In two patients, the pneumothorax, being initially absent at the end of the intervention, developed without symptoms. One of these patients required chest drain placement 32 h after RF ablation, and in the second patient therapy remained conservative. In the third patient, a slight pneumothorax at the end of the intervention gradually increased and led into tension pneumothorax 5 days after ablation procedure. Underlying bronchopleural fistula along the coagulated former electrode track was diagnosed in two patients. In conclusion, delayed development of pneumothorax after pulmonary RF ablation can occur and is probably due to underlying bronchopleural fistula, potentially leading to tension pneumothorax. Patients and interventionalists should be prepared for delayed onset of this complication, and extensive track ablation following pulmonary RF ablation should be avoided.

  13. Complete Heart Block with Diastolic Heart Failure and Pulmonary Edema Secondary to Enlarging Previously Diagnosed Thrombosed Aneurysm of Sinus of Valsalva in a Patient with History of Autosomal Dominant Polycystic Kidney Disease

    PubMed Central

    Eltawansy, Sherif Ali; Thomas, Maria Joana; Daniels, Jeffrey

    2015-01-01

    Autosomal dominant polycystic kidney disease (ADPKD) is associated with vascular aneurysms that can affect any part of the vascular tree, like ascending aorta or coronary arteries. Sinus of Valsalva is known as an anatomical dilation at the root of aorta above the aortic valve and very few cases show aneurysm at that site in patients with ADPKD. Sinus of Valsalva aneurysm (SVA) can present with rupture and acute heart failure and infective endocarditis or could be asymptomatic accidentally discovered during cardiac catheterization. We report a case of a 76-year-old male with a unique constellation of cardiovascular anomalies associated with ADPKD. Patient was previously diagnosed with aneurysms affecting ascending aorta, sinus of Valsalva, and coronary arteries. Several years later, he came with complete heart block which was discovered later to be secondary to enlargement of his previously diagnosed thrombosed SVA. His case was complicated with acute heart failure and pulmonary edema. Conclusion. Patients with ADPKD can present with extrarenal manifestations. In our case, aneurysm at sinus of Valsalva was progressively enlarging and presented with complete heart block. PMID:25861484

  14. 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

  15. 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

  16. Lung Edema Clearance: Relevance to Patients with Lung Injury

    PubMed Central

    Azzam, Zaher S.; Sznajder, Jacob I.

    2015-01-01

    Pulmonary edema clearance is necessary for patients with lung injury to recover and survive. The mechanisms regulating edema clearance from the lungs are distinct from the factors contributing edema formation during injury. Edema clearance is effected via vectorial transport of Na+ out of the airspaces which generates an osmotic gradient causing water to follow the gradient out of the cells. This Na+ transport across the alveolar epithelium is mostly effected via apical Na+ and chloride channels and basolateral Na,K-ATPase. The Na,K-ATPase pumps Na+ out of the cell and K+ into the cell against their respective gradients in an ATP-consuming reaction. Two mechanisms contribute to the regulation of the Na,K-ATPase activity:recruitment of its subunits from intracellular compartments into the basolateral membrane, and transcriptional/translational regulation. Na,K-ATPase activity and edema clearance are increased by catecholamines, aldosterone, vasopressin, overexpression of the pump genes, and others. During lung injury, mechanisms regulating edema clearance are inhibited by yet unclear pathways. Better understanding of the mechanisms that regulate pulmonary edema clearance may lead to therapeutic interventions that counterbalance the inhibition of edema clearance during lung injury and improve the lungs’ ability to clear fluid, which is crucial for patient survival. PMID:26241220

  17. Diabetic Macular Edema

    PubMed Central

    Gundogan, Fatih C.; Yolcu, Umit; Akay, Fahrettin; Ilhan, Abdullah; Ozge, Gokhan; Uzun, Salih

    2016-01-01

    Diabetic macular edema (DME), one the most prevalent causes of visual loss in industrialized countries, may be diagnosed at any stage of diabetic retinopathy. The diagnosis, treatment, and follow up of DME have become straightforward with recent developments in fundus imaging, such as optical coherence tomography. Laser photocoagulation, intravitreal injections, and pars plana vitrectomy surgery are the current treatment modalities; however, the positive effects of currently available intravitreally injected agents are temporary. At this point, further treatment choices are needed for a permanent effect. Sources of data selection: The articles published between 1985-2015 years on major databases were searched and most appropriate 40 papers were used to write this review article. PMID:27182271

  18. 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

  19. Development of the pulmonary surfactant system in two oviparous vertebrates.

    PubMed

    Johnston, S D; Orgeig, S; Lopatko, O V; Daniels, C B

    2000-02-01

    In birds and oviparous reptiles, hatching is often a lengthy and exhausting process, which commences with pipping followed by lung clearance and pulmonary ventilation. We examined the composition of pulmonary surfactant in the developing lungs of the chicken, Gallus gallus, and of the bearded dragon, Pogona vitticeps. Lung tissue was collected from chicken embryos at days 14, 16, 18 (prepipped), and 20 (postpipped) of incubation and from 1 day and 3 wk posthatch and adult animals. In chickens, surfactant protein A mRNA was detected using Northern blot analysis in lung tissue at all stages sampled, appearing relatively earlier in development compared with placental mammals. Chickens were lavaged at days 16, 18, and 20 of incubation and 1 day posthatch, whereas bearded dragons were lavaged at day 55, days 57-60 (postpipped), and days 58-61 (posthatched). In both species, total phospholipid (PL) from the lavage increased throughout incubation. Disaturated PL (DSP) was not measurable before 16 days of incubation in the chick embryo nor before 55 days in bearded dragons. However, the percentage of DSP/PL increased markedly throughout late development in both species. Because cholesterol (Chol) remained unchanged, the Chol/PL and Chol/DSP ratios decreased in both species. Thus the Chol and PL components are differentially regulated. The lizard surfactant system develops and matures over a relatively shorter time than that of birds and mammals. This probably reflects the highly precocial nature of hatchling reptiles. PMID:10666151

  20. 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

  1. 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

  2. Synthetic pulmonary surfactant preparations: new developments and future trends.

    PubMed

    Mingarro, Ismael; Lukovic, Dunja; Vilar, Marçal; Pérez-Gil, Jesús

    2008-01-01

    Pulmonary surfactant is a lipid-protein complex that coats the interior of the alveoli and enables the lungs to function properly. Upon its synthesis, lung surfactant adsorbs at the interface between the air and the hypophase, a capillary aqueous layer covering the alveoli. By lowering and modulating surface tension during breathing, lung surfactant reduces respiratory work of expansion, and stabilises alveoli against collapse during expiration. Pulmonary surfactant deficiency, or dysfunction, contributes to several respiratory pathologies, such as infant respiratory distress syndrome (IRDS) in premature neonates, and acute respiratory distress syndrome (ARDS) in children and adults. The main clinical exogenous surfactants currently in use to treat some of these pathologies are essentially organic extracts obtained from animal lungs. Although very efficient, natural surfactants bear serious defects: i) they could vary in composition from batch to batch; ii) their production involves relatively high costs, and sources are limited; and iii) they carry a potential risk of transmission of animal infectious agents and the possibility of immunological reaction. All these caveats justify the necessity for a highly controlled synthetic material. In the present review the efforts aimed at new surfactant development, including the modification of existing exogenous surfactants by adding molecules that can enhance their activity, and the progress achieved in the production of completely new preparations, are discussed. PMID:18288994

  3. Radiosurgery for brain metastases and cerebral edema.

    PubMed

    Gazit, Inbal; Har-Nof, Sagi; Cohen, Zvi R; Zibly, Zion; Nissim, Uzi; Spiegelmann, Roberto

    2015-03-01

    The objective of this study was to assess reduction in cerebral edema following linear accelerator radiosurgery (LINAC) as first line therapy for brain metastasis. We reviewed the medical records of all patients who underwent LINAC radiosurgery for brain metastasis at our institution during 2010-2012, and who had not previously undergone either surgery or whole brain radiotherapy. Data were analyzed for 55 brain metastases from 46 patients (24 males), mean age 59.9 years. During the 2 months following LINAC radiosurgery, the mean steroid dose decreased from 4.8 to 2.6 mg/day, the mean metastasis volume decreased from 3.79±4.12 cc to 2.8±4.48 cc (p=0.001), and the mean edema volume decreased from 16.91±30.15 cc to 12.85±24.47 cc (p=0.23). The 17 patients with reductions of more than 50% in brain edema volume had single metastases. Edema volume in the nine patients with two brain metastases remained stable in five patients (volume change <10%, 0-2 cc) and increased in four patients (by >10%, 2-14 cc). In a subanalysis of eight metastases with baseline edema volume greater than 40 cc, edema volume decreased from 77.27±37.21 cc to 24.84±35.6 cc (p=0.034). Reductions in brain edema were greater in metastases for which non-small-cell lung carcinoma and breast cancers were the primary diseases. Overall, symptoms improved in most patients. No patients who were without symptoms or who had no signs of increased intracranial pressure at baseline developed signs of intracranial pressure following LINAC radiosurgery. In this series, LINAC stereotactic radiosurgery for metastatic brain lesions resulted in early reduction in brain edema volume in single metastasis patients and those with large edema volumes, and reduced the need for steroids. PMID:25533053

  4. [The effect of high-frequency ventilation of the lungs on the pulmonary and systemic circulations in microembolism of the pulmonary artery].

    PubMed

    Sanotskaia, N V; Vyzhigina, M A; Matsievskiĭ, D D; Luk'ianov, M V; Aleĭnikov, S O

    1993-11-01

    The linear and volumetric blood flow velocity in the ascending aorta and pulmonary artery conus, right-left ventricular ejection balance, pulmonary and femoral arterial blood pressures, pulmonary microcirculation in fat pulmonary microembolism induced during the routine and high-frequency jet lung ventilation (HFJLV) were studied by ultrasonic techniques in acute experiments on cats with open chest under nembutal narcosis. Pulmonary microembolism was shown to resulted in 487 and 252% increases in pulmonary vascular resistance during the routine and HFJLVs, respectively. There were also 167 and 127% increases in mean pulmonary pressure and 60 and 34% decreases in the volumetric velocity of pulmonary blood flow. The linear velocity of pulmonary blood flow was unchanged with routine lung ventilation, whereas it decreased by 68% with HFJLV. Microembolism impaired the balance between right and left ventricular ejections with blood being redistributed into the greater circulation. The imbalance lasted 5-7 min during HFJLV, while with the routine lung ventilation it was preserved up to the end of the experiment, and systemic blood pressure and total peripheral vascular resistance decreased. Alveolar edema developed in interstitial pulmonary edema. The animals' death occurred 40-60 min later. PMID:8312529

  5. 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.

  6. Development of a simple and rapid diagnosis method for swine edema disease to specifically detect Stx2e protein by immunochromatographic test.

    PubMed

    Arimitsu, Hideyuki; Sasaki, Keiko; Tsuji, Takao

    2016-05-01

    Edema disease in piglets is caused by Shiga toxin 2e (Stx2e)-producing Escherichia coli. However, there is currently no available Stx2e-specific immunochromatographic test strip to differentiate Stx2e from other types of Shiga toxin 2. In the present study, to develop an Stx2e-specific immunochromatographic test strip, we isolated nine different monoclonal antibody-producing hybridoma clones from Stx2e toxoid-immunized mice and confirmed that six antibodies were A subunit-specific whereas three antibodies were B subunit-specific. Only one A subunit-specific monoclonal antibody (45B2) was cross-reactive with prototype Stx2 (Stx2a) at the same sensitivity, but the remaining eight monoclonal antibodies were not. In immunochromatographic tests using the highly sensitive antibodies, test strips using some combinations of gold colloid-conjugated monoclonal antibody with the B subunit-specific monoclonal antibody on the membrane detected Stx2e, but not other types of Shiga toxin 2. These test strips had the ability to detect Stx2e in the culture supernatant of clinically isolated Stx2e gene-positive strains, but not in those of Stx2e gene-negative strains. These results indicate that our test strip is practical for the specific detection of Stx2e to diagnose swine edema disease. PMID:26996467

  7. 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...

  8. 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. PMID:26290369

  9. 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.

  10. 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...

  11. Nestin-expressing vascular wall cells drive development of pulmonary hypertension.

    PubMed

    Saboor, Farhan; Reckmann, Ansgar N; Tomczyk, Claudia U M; Peters, Dorothea M; Weissmann, Norbert; Kaschtanow, Andre; Schermuly, Ralph T; Michurina, Tatyana V; Enikolopov, Grigori; Müller, Dieter; Mietens, Andrea; Middendorff, Ralf

    2016-03-01

    Nestin, a well-known marker of neuronal stem cells, was recently suggested to characterise stem cell-like progenitors in non-neuronal structures during development and tissue repair. Integrating novel morphological approaches (CLARITY), we investigate whether nestin expression defines the proliferating cell population that essentially drives vascular remodelling during development of pulmonary hypertension.The role of nestin was investigated in lungs of nestin-GFP (green fluorescent protein) mice, models of pulmonary hypertension (rat: monocrotaline, SU5416/hypoxia; mouse: hypoxia), samples from pulmonary hypertension patients and human pulmonary vascular smooth muscle cells (VSMCs).Nestin was solely found in lung vasculature and localised to proliferating VSMCs, but not bronchial smooth muscle cells. Nestin was shown to affect cell number and was significantly enhanced in lungs early during development of pulmonary hypertension, correlating well with increased VSMC proliferation, expression of phosphorylated (activated) platelet-derived growth factor receptor β and downregulation of the smooth muscle cell differentiation marker calponin. At later time points when pulmonary hypertension became clinically evident, nestin expression and proliferation returned to control levels. Increase of nestin-positive VSMCs was also found in human pulmonary hypertension, both in vessel media and neointima.Nestin expression seems to be obligatory for VSMC proliferation, and specifies lung vascular wall cells that drive remodelling and (re-)generation. Our data promise novel diagnostic tools and therapeutic targets for pulmonary hypertension. PMID:26699726

  12. 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

  13. 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

  14. 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.

  15. Evidence for a role of mast cells in the lung edema induced by Tityus serrulatus venom in rats.

    PubMed

    De-Matos, I M; Talvani, A; Rocha, O O; Freire-Maia, L; Teixeira, M M

    2001-06-01

    In the most severe cases of human poisoning by Tityus serrulatus, pulmonary edema is a frequent finding and can be the cause of death. Mast cells can release a range of mediators known to be involved in the development of lung edema following T. serrulatus venom injection. The present work was designed to investigate whether mast cells participated in the acute lung injury induced by T. serrulatus scorpion venom and could, thus, be an intermediate between neuropeptide release and activation of the inflammatory cascade. To this end, mast cells were depleted using compound 48/80. Pulmonary edema, as assessed by the levels of extravasation of Evans blue dye in the bronchoalveolar lavage and in the left lung, was completely inhibited in compound 48/80-treated animals. Moreover, the number of animals surviving 60min after injection of venom rose from 20 to 60%. Our results demonstrate an important role for mast cells in the development of lung injury and lethality following the intravenous administration of T. serrulatus venom. PMID:11137547

  16. Diabetic macular edema: New promising therapies

    PubMed Central

    Shamsi, Hanan N Al; Masaud, Jluwi S; Ghazi, Nicola G

    2013-01-01

    The treatment of diabetic macular edema is rapidly evolving. The era of laser therapy is being quickly replaced by an era of pharmacotherapy. Several pharmacotherapies have been recently developed for the treatment of retinal vascular diseases such as diabetic macular edema. Several intravitreal injections or sustained delivery devices have undergone phase 3 testing while others are currently being evaluated. The results of clinical trials have shown the superiority of some of these agents to laser therapy. However, with the availability of several of these newer agents, it may be difficult to individualize treatment options especially those patients respond differently to various therapies. As such, more effort is still needed in order to determine the best treatment regimen for a given patient. In this article, we briefly summarize the major new therapeutic additions for the treatment of diabetic macular edema and allude to some future promising therapies. PMID:24379924

  17. Novel imaging techniques for diabetic macular edema.

    PubMed

    Lobo, C; Bernardes, R; Faria de Abreu, J R; Cunha-Vaz, J G

    1999-01-01

    Retinal edema should be defined as any increase of water of the retinal tissue resulting in an increase in its volume. It may be of cytotoxic or vasogenic origin. Development of vasogenic macular edema is dependent on a series of factors such as blood pressure, blood-retinal barrier permeability, retinal cell damage, retinal tissue osmotic pressure and retinal tissue compliance. Objective measurements of retinal thickness are now possible using the Retinal Thickness Analyser. Localised measurements of blood-retinal barrier permeability may also be obtained using the Retinal Leakage Analyser, a modified confocal scanning laser fluorometer, while obtaining simultaneously angiographic images of the choroid and retina. These new imaging techniques show that cytotoxic and vasogenic retinal edema may occur independently in the early stages of diabetic retinopathy. These findings offer new perspectives for designing novel therapeutic strategies. PMID:10896349

  18. Effect of 5-lipoxygenase on the development of pulmonary hypertension in rats.

    PubMed

    Jones, John E; Walker, Jennifer L; Song, Yanli; Weiss, Norbert; Cardoso, Wellington V; Tuder, Rubin M; Loscalzo, Joseph; Zhang, Ying-Yi

    2004-05-01

    5-Lipoxygenase (5-LO) and its downstream leukotriene products have been implicated in the development of pulmonary hypertension. In this study, we examined the effects of 5-LO overexpression in rat lungs on pulmonary hypertension using a recombinant adenovirus expressing 5-LO (Ad5-LO). Transthoracic echocardiography and right heart catheterization data showed that 5-LO overexpression in the lung did not cause pulmonary hypertension in normal rats; however, it markedly accelerated the progression of pulmonary hypertension in rats treated with monocrotaline (MCT). An increase in pulmonary artery pressure occurred earlier in the rats treated with MCT + Ad5-LO (7-10 days) compared with those treated with control vector, MCT + adenovirus expressing green fluorescent protein (AdGFP), or MCT alone (15-18 days). The weight ratio of the right ventricle to left ventricle plus septum was higher in the MCT + Ad5-LO group than that of the MCT + AdGFP or MCT group (0.45 +/- 0.08 vs. 0.35 +/- 0.03 or 0.33 +/- 0.06). Lung tissue histological sections from MCT + Ad5-LO rats exhibited more severe inflammatory cell infiltration and pulmonary vascular muscularization than those from MCT + AdGFP- or MCT-treated rats. Administration of 5-LO inhibitors, zileuton or MK-886, to either MCT- or MCT + Ad5-LO-treated rats prevented the development of pulmonary hypertension. These data suggest that 5-LO plays a critical role in the progression of pulmonary hypertension in rats and that the detrimental effect of 5-LO is manifest only in the setting of pulmonary vascular endothelial cell dysfunction. PMID:14726295

  19. Development and Characterization of an Inducible Rat Model of Chronic Thromboembolic Pulmonary Hypertension.

    PubMed

    Arias-Loza, Paula-Anahi; Jung, Pius; Abeßer, Marco; Umbenhauer, Sandra; Williams, Tatjana; Frantz, Stefan; Schuh, Kai; Pelzer, Theo

    2016-05-01

    Chronic thromboembolic pulmonary hypertension (CTEPH) is an entity of PH that not only limits patients quality of life but also causes significant morbidity and mortality. The treatment of choice is pulmonary endarterectomy. However numerous patients do not qualify for pulmonary endarterectomy or present with residual vasculopathy post pulmonary endarterectomy and require specific vasodilator treatment. Currently, there is no available specific small animal model of CTEPH that could serve as tool to identify targetable molecular pathways and to test new treatment options. Thus, we generated and standardized a rat model that not only resembles functional and histological features of CTEPH but also emulates thrombi fibrosis. The pulmonary embolism protocol consisted of 3 sequential tail vein injections of fibrinogen/collagen-covered polystyrene microspheres combined with thrombin and administered to 10-week-old male Wistar rats. After the third embolism, rats developed characteristic features of CTEPH including elevated right ventricular systolic pressure, right ventricular cardiomyocyte hypertrophy, pulmonary artery remodeling, increased serum brain natriuretic peptide levels, thrombi fibrosis, and formation of pulmonary cellular-fibrotic lesions. The current animal model seems suitable for detailed study of CTEPH pathophysiology and permits preclinical testing of new pharmacological therapies against CTEPH. PMID:27045032

  20. 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

  1. 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

  2. Massive vulvar edema in 2 prepartum dairy cows

    PubMed Central

    Cheong, Soon Hon; Gilbert, Robert O.

    2014-01-01

    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. PMID:24790232

  3. Pathogenic role of calcium-sensing receptors in the development and progression of pulmonary hypertension.

    PubMed

    Tang, Haiyang; Yamamura, Aya; Yamamura, Hisao; Song, Shanshan; Fraidenburg, Dustin R; Chen, Jiwang; Gu, Yali; Pohl, Nicole M; Zhou, Tong; Jiménez-Pérez, Laura; Ayon, Ramon J; Desai, Ankit A; Goltzman, David; Rischard, Franz; Khalpey, Zain; Black, Stephan M; Garcia, Joe G N; Makino, Ayako; Yuan, Jason X J

    2016-05-01

    An increase in cytosolic free Ca(2+) concentration ([Ca(2+)]cyt) in pulmonary arterial smooth muscle cells (PASMC) is a major trigger for pulmonary vasoconstriction and a critical stimulation for PASMC proliferation and migration. Previously, we demonstrated that expression and function of calcium sensing receptors (CaSR) in PASMC from patients with idiopathic pulmonary arterial hypertension (IPAH) and animals with experimental pulmonary hypertension (PH) were greater than in PASMC from normal subjects and control animals. However, the mechanisms by which CaSR triggers Ca(2+) influx in PASMC and the implication of CaSR in the development of PH remain elusive. Here, we report that CaSR functionally interacts with TRPC6 to regulate [Ca(2+)]cyt in PASMC. Downregulation of CaSR or TRPC6 with siRNA inhibited Ca(2+)-induced [Ca(2+)]cyt increase in IPAH-PASMC (in which CaSR is upregulated), whereas overexpression of CaSR or TRPC6 enhanced Ca(2+)-induced [Ca(2+)]cyt increase in normal PASMC (in which CaSR expression level is low). The upregulated CaSR in IPAH-PASMC was also associated with enhanced Akt phosphorylation, whereas blockade of CaSR in IPAH-PASMC attenuated cell proliferation. In in vivo experiments, deletion of the CaSR gene in mice (casr(-/-)) significantly inhibited the development and progression of experimental PH and markedly attenuated acute hypoxia-induced pulmonary vasoconstriction. These data indicate that functional interaction of upregulated CaSR and upregulated TRPC6 in PASMC from IPAH patients and animals with experimental PH may play an important role in the development and progression of sustained pulmonary vasoconstriction and pulmonary vascular remodeling. Blockade or downregulation of CaSR and/or TRPC6 with siRNA or miRNA may be a novel therapeutic strategy to develop new drugs for patients with pulmonary arterial hypertension. PMID:26968768

  4. Monitoring pulmonary vascular permeability using radiolabeled transferrin

    SciTech Connect

    Basran, G.S.; Hardy, J.G.

    1988-07-01

    A simple, noninvasive technique for monitoring pulmonary vascular permeability in patients in critical care units is discussed. High vascular permeability is observed in patients with clinically defined adult respiratory distress syndrome (ARDS) but not in patients with hydrostatic pulmonary edema or in patients with minor pulmonary insults who are considered to be at risk of developing ARDS. The technique has been used in the field of therapeutics and pharmacology to test the effects of the putative antipermeability agents methylprednisolone and terbutaline sulfate. There appears to be a good correlation between the acute inhibitory effect of either drug on transferrin exudation and patient prognosis. Thus, a byproduct of such drug studies may be an index of survival in patients with established ARDS.

  5. Pulmonary hypertension

    MedlinePlus

    Pulmonary arterial hypertension; Sporadic primary pulmonary hypertension; Familial primary pulmonary hypertension; Idiopathic pulmonary arterial hypertension; Primary pulmonary hypertension; PPH; Secondary pulmonary ...

  6. Development of an edema factor-mediated cAMP-induction bioassay for detecting antibody-mediated neutralization of anthrax protective antigen.

    PubMed

    Zmuda, Jonathan F; Zhang, Linyi; Richards, Terri; Pham, Quyen; Zukauskas, David; Pierre, Jennifer L; Laird, Michael W; Askins, Janine; Choi, Gil H

    2005-03-01

    Intoxication of mammalian cells by Bacillus anthracis requires the coordinate activity of three distinct bacterial proteins: protective antigen (PA), edema factor (EF), and lethal factor (LF). Among these proteins, PA has become the major focus of work on monoclonal antibodies and vaccines designed to treat or prevent anthrax infection since neither EF nor LF is capable of inducing cellular toxicity in its absence. Here, we present the development of a sensitive, precise, and biologically relevant bioassay platform capable of quantifying antibody-mediated PA neutralization. This bioassay is based on the ability of PA to bind and shuttle EF, a bacterial adenylate cyclase, into mammalian cells leading to an increase in cAMP that can be quantified using a sensitive chemiluminescent ELISA. The results of this study indicate that the cAMP-induction assay possesses the necessary performance characteristics for use as both a potency-indicating release assay in a quality control setting and as a surrogate pharmacodynamic marker for ensuring the continued bioactivity of therapeutic antibodies against PA during clinical trials. PMID:15847796

  7. Historical development of the concept of a pulmonary circulation.

    PubMed

    Persaud, T V

    1989-01-01

    Philosophical speculations and theories regarding the flow of blood through the lungs are reviewed from an historical standpoint. Michael Servetus (1511-1553) described the pulmonary circulation in his book 'Christianismi Restitutio', published in 1553. From manuscripts that were rediscovered and translated in 1924 we now know that Ibn al-Nafis (1210-1288) of Damascus had made the same observations three centuries earlier. PMID:2645980

  8. 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

  9. 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

  10. Signal transduction in the development of pulmonary arterial hypertension

    PubMed Central

    Malenfant, Simon; Neyron, Anne-Sophie; Paulin, Roxane; Potus, François; Meloche, Jolyane; Provencher, Steeve; Bonnet, Sébastien

    2013-01-01

    Pulmonary arterial hypertension (PAH) is a unique disease. Properly speaking, it is not a disease of the lung. It can be seen more as a microvascular disease occurring mainly in the lungs and affecting the heart. At the cellular level, the PAH paradigm is characterized by inflammation, vascular tone imbalance, pulmonary arterial smooth muscle cell proliferation and resistance to apoptosis and the presence of in situ thrombosis. At a clinical level, the aforementioned abnormal vascular properties alter physically the pulmonary circulation and ventilation, which greatly influence the right ventricle function as it highly correlates with disease severity. Consequently, right heart failure remains the principal cause of death within this cohort of patients. While current treatment modestly improve patients’ conditions, none of them are curative and, as of today, new therapies are lacking. However, the future holds potential new therapies that might have positive influence on the quality of life of the patient. This article will first review the clinical presentation of the disease and the different molecular pathways implicated in the pathobiology of PAH. The second part will review tomorrow's future putative therapies for PAH. PMID:24015329

  11. 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

  12. 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

  13. Pulmonary Hypertension and Pulmonary Aspergilloma-Coexistence of Two Rare Sequelae of Pulmonary Embolism.

    PubMed

    Bhartiya, Manish; Saxena, Puneet; Singh, Dharmender; Sashindran, V K

    2016-06-01

    We report a 42 year old non-smoker male who presented with progressive exertional dyspnoea, productive cough with streaky hemoptysis and progressive pedal edema. His physical examination, ECG, chest X-ray and 2D-ECHO revealed features suggestive of right heart failure and pulmonary hypertension. On further evaluation for the cause of pulmonary hypertension, his CT pulmonary angiography revealed features of chronic pulmonary thromboembolism with calcified thrombus in the main pulmonary artery along with pulmonary hypertension. Incidentally the CT also revealed a cavity in the right lung with soft tissue within it. A, trans-thoracic needle aspiration of this tissue was suggestive of an aspergilloma. This is a rare case report of co-existence of two uncommon complications of pulmonary embolism-chronic thrombo-embolic pulmonary hypertension and pulmonary Aspergilloma in the same patient. PMID:27408402

  14. INTRAVITREAL CORTICOSTEROIDS IN DIABETIC MACULAR EDEMA

    PubMed Central

    Bailey, Clare; Loewenstein, Anat; Massin, Pascale

    2015-01-01

    Purpose: To review the relationship between kinetics, efficacy, and safety of several corticosteroid formulations for the treatment of diabetic macular edema. Methods: Reports of corticosteroid use for the treatment of diabetic macular edema were identified by a literature search, which focused on the pharmacokinetics, efficacy, and safety of these agents in preclinical animal models and clinical trials. Results: Available corticosteroids for diabetic macular edema treatment include intravitreal triamcinolone acetonide, dexamethasone, and fluocinolone acetonide. Because of differences in solubility and bioavailability, various delivery mechanisms are used. Bioerodible delivery systems achieve higher maximum concentrations than nonbioerodible formulations. There is a relationship between visual gains and drug persistence in the intravitreal compartment. Safety effects were more complex; level of intravitreal triamcinolone acetonide exposure is related to development of elevated intraocular pressure and cataract; this does not seem to be the case for dexamethasone, where two different doses showed similar mean intraocular pressure and incidence of cataract surgery. With fluocinolone acetonide, rates of intraocular pressure elevations requiring surgery seem to be dose related; rates of cataract extraction were similar regardless of dose. Conclusion: Available corticosteroids for diabetic macular edema exhibit different pharmacokinetic profiles that impact efficacy and adverse events and should be taken into account when developing individualized treatment plans. PMID:26352555

  15. 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

  16. [Relation of hypoxia and edema of the intestinal wall and skin to colloid osmotic pressure].

    PubMed

    Lundsgaard-Hansen, P; Blauhut, B

    1988-02-01

    Whereas the impact of colloids and crystalloids on hypoxia and edema has been extensively debated with respect to pulmonary function, their corresponding effects on the systemic circulation have been largely ignored. Manifest edema of the intestine and skin develops, however, when the serum colloid osmotic pressure (COP) is lowered to 15 mm Hg or less by crystalloid infusions. Hypoxia of wounds, which may be aggravated by crystalloids, impairs healing and antibacterial defense, and its has been speculated that edema and/or hypoxia of the intestine may be associated with postoperative gastrointestinal dysfunction. We therefore studies the relationship between lowering and restoration of the COP, the pO2 of the intestinal surface and skin, and tissue edema. We generated an acute hypoproteinemic fluid overload reducing the COP from around 20 to 10 mm Hg in 56 rabbits by means of a 50% plasma loss and excess replacement with Ringer's lactate. We measured the COP with a membrane having a cut-off level of 20,000 d, the cardiac output (with derivation of further hemodynamic data) with an electromagnetic flow probe around the ascending aorta, and the tissue pO2 (pO2t) in mm Hg with the Dortmund 8-channel surface electrode. After 30 min without infusion (Fig. 1), we assigned 14 animals each at random to 4 treatment groups: (1) no treatment (O); (2) 20% albumin 7.5 ml/kg (A); (3) furosemide 2 mg/kg i.v. given three times at 30-min intervals (F); and (4) the combination of both agents (AF). During the infusion-free interval, the cardiac output and pO2t fell by 20%-30% of baseline (Table 1).(ABSTRACT TRUNCATED AT 250 WORDS) PMID:3364664

  17. 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

  18. 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

  19. 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

  20. 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. PMID:26111581

  1. Recent developments in the diagnosis and treatment of pulmonary embolism.

    PubMed

    van der Hulle, T; Dronkers, C E A; Klok, F A; Huisman, M V

    2016-01-01

    Due to the nonspecific symptoms of the condition, a diagnosis of acute pulmonary embolism (PE) is frequently considered. However, PE will only be confirmed in 10-20% of patients. Because the imaging test of choice, computed tomography pulmonary angiography (CTPA), is costly and associated with radiation exposure and other complications, a validated diagnostic algorithm consisting of a clinical decision rule and D-dimer test should be used to safely exclude PE in 20-30% of patients without the need for CTPA. Recently, the age-adjusted D-dimer threshold has been validated, and this has increased the proportion of patients at older age in whom PE can be excluded without CTPA. Initial therapeutic management of PE depends on the risk of short-term PE-related mortality. Haemodynamically unstable patients should be closely monitored and receive thrombolytic therapy unless contraindicated because of an unacceptably high bleeding risk, whereas patients with low-risk PE may be safely discharged early from hospital or receive only outpatient treatment. The PESI score and Hestia decision rule are available to select patients in whom early discharge or outpatient treatment will be safe, although the safety of these strategies should be confirmed in additional studies. Standard PE therapy consists of low molecular weight heparin (LMWH) followed by vitamin K antagonists (VKAs). Recently, several nonvitamin K-dependent oral anticoagulants have been shown to be as effective as LMWH/VKAs, and maybe safer. Determining the optimal duration of treatment for a first unprovoked PE remains a challenge, although clinical prediction rules for estimating the risk of recurrence of venous thromboembolism and anticoagulation-associated haemorrhage are under investigation. Using these prediction rules may lead to both more standardized and more individualized long-term treatment of PE. PMID:26286356

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

    PubMed

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

    1997-09-01

    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. PMID:9292467

  3. 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.

  4. 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

  5. Development and characterization of spray dried microparticles for pulmonary delivery of antifungal drug.

    PubMed

    Mathpal, Divita; Garg, Tarun; Rath, Goutam; Goyal, Amit Kumar

    2015-01-01

    Invasive pulmonary aspergillosis is a life threatening fungal infection mainly caused by Aspergillus species. Available treatment strategy against pulmonary aspergillosis is having very limited applicability, due to its toxicity and low circulation half-life. Pulmonary drug delivery is one of the strategies that can minimize these pitfalls. In the present study, polymeric and lipidic nanoparticles of amphotericin B were prepared by spray drying technique using hydroxypropylmethylcellulose (HPMC) and stearylamine with oleic acid respectively. Formulations were characterized for particle size, zeta potential, entrapment efficiency, in-vitro release studies, uptake analysis and in-vivo bio distribution studies. Developed polymeric and nanostructured lipid carriers (NLCs) were found in submicron size (600-700nm) and spherical in shape. Studies suggested that NLCs have better entrapment efficiency (77.1±5.5 %) as compared to HPMC carrier (71.28±5.22 %). Both formulations provided sustained drug release (HPMC, 82.05% releases up to 32 hrs and NLC, 88.2 % up to 40 hrs) and reduced dose dumping that may be helpful to reduce the toxicity and improve patient compliance. In-vitro antifungal studies suggested that stearylamine formulations exhibited better antifungal activity over control and HPMC formulations. Pharmacokinetic and organ distribution studies also support our hypothesis i.e. localized drug delivery for prolong period, improving the therapeutic effectiveness of the encapsulated drug against pulmonary aspergillosis. Studies suggested that drug delivery by pulmonary route is beneficial for local action in lungs. PMID:25808185

  6. Development and Characterization of Acellular Porcine Pulmonary Valve Scaffolds for Tissue Engineering

    PubMed Central

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

    2014-01-01

    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

  7. 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

  8. Guidelines for Curriculum Development for Undergraduate Medical Education in the Prevention of Pulmonary Diseases.

    ERIC Educational Resources Information Center

    National Heart, Lung, and Blood Inst. (DHHS/NIH), Bethesda, MD. Div. of Lung Diseases.

    These guidelines for developing an undergraduate medical education curriculum in pulmonary disease prevention emphasize not only the most current scientific practice but also the active application of cognitive and behavioral skills related to patient education. Chapter 1 introduces the guidelines and the issues and trends in preventative…

  9. 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.

    PubMed Central

    Said, S I; Berisha, H I; Pakbaz, H

    1996-01-01

    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. Images Fig. 3 PMID:8643465

  10. 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.

  11. 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.

  12. Egr-1 Expression During Neointimal Development in Flow-Associated Pulmonary Hypertension

    PubMed Central

    Dickinson, Michael G.; Bartelds, Beatrijs; Molema, Grietje; Borgdorff, Marinus A.; Boersma, Bibiche; Takens, Janny; Weij, Michel; Wichers, Pieter; Sietsma, Hannie; Berger, Rolf M.F.

    2011-01-01

    In flow-associated pulmonary arterial hypertension (PAH), increased pulmonary blood flow is an essential trigger for neointimal formation. Using microarray analysis, we recently found that the early growth response protein 1 (Egr-1) transcription factor is increased in experimental flow-associated end-stage PAH. Its role in PAH development is unknown. Here, we assessed the spatiotemporal expression of Egr-1 during neointimal development in flow-associated PAH. Flow-associated PAH was produced in rats by combining monocrotaline administration with an aortocaval shunt. Animals were sacrificed 1 day before or 1 day, 1 week, or 4 to 5 weeks after flow addition. Egr-1 expression was spatiotemporally assessed using laser microdissection, quantitative real-time PCR and immunohistochemistry. In addition, Egr-1 expression was assessed in a non-neointimal pulmonary hypertension model and in human PAH associated with congenital shunt. In 4 to 5 weeks, rats subjected to increased flow developed PAH with neointimal lesions. Egr-1 mRNA was increased 1 day after flow addition and in end-stage PAH, whereas monocrotaline only did not result in increased Egr-1 mRNA. Directly after flow addition, Egr-1 was expressed in endothelial cells. During disease development, Egr-1 protein expression increased and migrated throughout the vessel wall. In PAH patients, Egr-1 was expressed in vessels with media hypertrophy and neointimal lesions, including plexiform lesions. Thus, Egr-1 may be an important regulator in the development of pulmonary neointimal lesions induced by increased pulmonary blood flow. PMID:21924231

  13. Egr-1 expression during neointimal development in flow-associated pulmonary hypertension.

    PubMed

    Dickinson, Michael G; Bartelds, Beatrijs; Molema, Grietje; Borgdorff, Marinus A; Boersma, Bibiche; Takens, Janny; Weij, Michel; Wichers, Pieter; Sietsma, Hannie; Berger, Rolf M F

    2011-11-01

    In flow-associated pulmonary arterial hypertension (PAH), increased pulmonary blood flow is an essential trigger for neointimal formation. Using microarray analysis, we recently found that the early growth response protein 1 (Egr-1) transcription factor is increased in experimental flow-associated end-stage PAH. Its role in PAH development is unknown. Here, we assessed the spatiotemporal expression of Egr-1 during neointimal development in flow-associated PAH. Flow-associated PAH was produced in rats by combining monocrotaline administration with an aortocaval shunt. Animals were sacrificed 1 day before or 1 day, 1 week, or 4 to 5 weeks after flow addition. Egr-1 expression was spatiotemporally assessed using laser microdissection, quantitative real-time PCR and immunohistochemistry. In addition, Egr-1 expression was assessed in a non-neointimal pulmonary hypertension model and in human PAH associated with congenital shunt. In 4 to 5 weeks, rats subjected to increased flow developed PAH with neointimal lesions. Egr-1 mRNA was increased 1 day after flow addition and in end-stage PAH, whereas monocrotaline only did not result in increased Egr-1 mRNA. Directly after flow addition, Egr-1 was expressed in endothelial cells. During disease development, Egr-1 protein expression increased and migrated throughout the vessel wall. In PAH patients, Egr-1 was expressed in vessels with media hypertrophy and neointimal lesions, including plexiform lesions. Thus, Egr-1 may be an important regulator in the development of pulmonary neointimal lesions induced by increased pulmonary blood flow. PMID:21924231

  14. 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. PMID:25438734

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

    PubMed

    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. PMID:2901982

  16. Proliferation of pulmonary artery smooth muscle cells in the development of ascites syndrome in broilers induced by low ambient temperature.

    PubMed

    Wang, J; Qiao, J; Zhao, L H; Li, K; Wang, H; Xu, T; Tian, Y; Gao, M; Wang, X

    2007-12-01

    Pulmonary vascular remodelling, mainly characterized by arterial medial thickening, is an important pathological feature of broiler ascites syndrome (AS). Since vascular smooth muscle cells (VSMC) form the major cellular component of arterial medial layer, we speculate that VSMC proliferation is one of the causes of pulmonary arterial medial thickening in ascitic broilers. Hence, the present study was designed to investigate the role of VSMC proliferation in pulmonary vascular remodelling in development of AS induced by low ambient temperature. Broilers in control group (22 +/- 1.5 degrees C) and low temperature group (11 +/- 2 degrees C) were sampled every week at 15-50 days of age. Proliferative indexes of VSMC in pulmonary arteries were assessed with proliferating cell nuclear antigen, and the relative medial thickness (RMT) and relative wall area (RWA), as indexes of pulmonary vascular remodelling, were examined by computer-image analysing system. The results showed that the high incidence (18.75%) of AS was induced by low temperature, and a significantly increased VSMC proliferation was observed in pulmonary arteries in the low temperature group at 22-50 days of age (P < 0.05). In addition, RMT and RWA in pulmonary arteries were significantly elevated in the low temperature group from 36 days of age (P < 0.05), indicating that pulmonary vascular remodelling occurred following VSMC proliferation in AS. Our data suggest that proliferation of VSMC may facilitate pulmonary vascular remodelling and have a pivotal role in AS induced by low ambient temperature. PMID:18045340

  17. Role of ASIC1 in the development of chronic hypoxia-induced pulmonary hypertension

    PubMed Central

    Nitta, Carlos H.; Osmond, David A.; Herbert, Lindsay M.; Beasley, Britta F.; Resta, Thomas C.; Walker, Benjimen R.

    2013-01-01

    Chronic hypoxia (CH) associated with respiratory disease results in elevated pulmonary vascular intracellular Ca2+ concentration, which elicits enhanced vasoconstriction and promotes vascular arterial remodeling and thus has important implications in the development of pulmonary hypertension (PH). Store-operated Ca2+ entry (SOCE) contributes to this elevated intracellular Ca2+ concentration and has also been linked to acute hypoxic pulmonary vasoconstriction (HPV). Since our laboratory has recently demonstrated an important role for acid-sensing ion channel 1 (ASIC1) in mediating SOCE, we hypothesized that ASIC1 contributes to both HPV and the development of CH-induced PH. To test this hypothesis, we examined responses to acute hypoxia in isolated lungs and assessed the effects of CH on indexes of PH, arterial remodeling, and vasoconstrictor reactivity in wild-type (ASIC1+/+) and ASIC1 knockout (ASIC1−/−) mice. Restoration of ASIC1 expression in pulmonary arterial smooth muscle cells from ASIC1−/− mice rescued SOCE, confirming the requirement for ASIC1 in this response. HPV responses were blunted in lungs from ASIC1−/− mice. Both SOCE and receptor-mediated Ca2+ entry, along with agonist-dependent vasoconstrictor responses, were diminished in small pulmonary arteries from control ASIC−/− mice compared with ASIC+/+ mice. The effects of CH to augment receptor-mediated vasoconstrictor and SOCE responses in vessels from ASIC1+/+ mice were not observed after CH in ASIC1−/− mice. In addition, ASIC1−/− mice exhibited diminished right ventricular systolic pressure, right ventricular hypertrophy, and arterial remodeling in response to CH compared with ASIC1+/+ mice. Taken together, these data demonstrate an important role for ASIC1 in both HPV and the development of CH-induced PH. PMID:24186095

  18. 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

  19. 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

  20. The von Hippel–Lindau Chuvash mutation promotes pulmonary hypertension and fibrosis in mice

    PubMed Central

    Hickey, Michele M.; Richardson, Theresa; Wang, Tao; Mosqueira, Matias; Arguiri, Evguenia; Yu, Hongwei; Yu, Qian-Chun; Solomides, Charalambos C.; Morrisey, Edward E.; Khurana, Tejvir S.; Christofidou-Solomidou, Melpo; Simon, M. Celeste

    2010-01-01

    Mutation of the von Hippel–Lindau (VHL) tumor suppressor protein at codon 200 (R200W) is associated with a disease known as Chuvash polycythemia. In addition to polycythemia, Chuvash patients have pulmonary hypertension and increased respiratory rates, although the pathophysiological basis of these symptoms is unclear. Here we sought to address this issue by studying mice homozygous for the R200W Vhl mutation (VhlR/R mice) as a model for Chuvash disease. These mice developed pulmonary hypertension independently of polycythemia and enhanced normoxic respiration similar to Chuvash patients, further validating VhlR/R mice as a model for Chuvash disease. Lungs from VhlR/R mice exhibited pulmonary vascular remodeling, hemorrhage, edema, and macrophage infiltration, and lungs from older mice also exhibited fibrosis. HIF-2α activity was increased in lungs from VhlR/R mice, and heterozygosity for Hif2a, but not Hif1a, genetically suppressed both the polycythemia and pulmonary hypertension in the VhlR/R mice. Furthermore, Hif2a heterozygosity resulted in partial protection against vascular remodeling, hemorrhage, and edema, but not inflammation, in VhlR/R lungs, suggesting a selective role for HIF-2α in the pulmonary pathology and thereby providing insight into the mechanisms underlying pulmonary hypertension. These findings strongly support a dependency of the Chuvash phenotype on HIF-2α and suggest potential treatments for Chuvash patients. PMID:20197624

  1. The von Hippel-Lindau Chuvash mutation promotes pulmonary hypertension and fibrosis in mice.

    PubMed

    Hickey, Michele M; Richardson, Theresa; Wang, Tao; Mosqueira, Matias; Arguiri, Evguenia; Yu, Hongwei; Yu, Qian-Chun; Solomides, Charalambos C; Morrisey, Edward E; Khurana, Tejvir S; Christofidou-Solomidou, Melpo; Simon, M Celeste

    2010-03-01

    Mutation of the von Hippel-Lindau (VHL) tumor suppressor protein at codon 200 (R200W) is associated with a disease known as Chuvash polycythemia. In addition to polycythemia, Chuvash patients have pulmonary hypertension and increased respiratory rates, although the pathophysiological basis of these symptoms is unclear. Here we sought to address this issue by studying mice homozygous for the R200W Vhl mutation (VhlR/R mice) as a model for Chuvash disease. These mice developed pulmonary hypertension independently of polycythemia and enhanced normoxic respiration similar to Chuvash patients, further validating VhlR/R mice as a model for Chuvash disease. Lungs from VhlR/R mice exhibited pulmonary vascular remodeling, hemorrhage, edema, and macrophage infiltration, and lungs from older mice also exhibited fibrosis. HIF-2alpha activity was increased in lungs from VhlR/R mice, and heterozygosity for Hif2a, but not Hif1a, genetically suppressed both the polycythemia and pulmonary hypertension in the VhlR/R mice. Furthermore, Hif2a heterozygosity resulted in partial protection against vascular remodeling, hemorrhage, and edema, but not inflammation, in VhlR/R lungs, suggesting a selective role for HIF-2alpha in the pulmonary pathology and thereby providing insight into the mechanisms underlying pulmonary hypertension. These findings strongly support a dependency of the Chuvash phenotype on HIF-2alpha and suggest potential treatments for Chuvash patients. PMID:20197624

  2. 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

  3. Vitamin A-retinoid signaling in pulmonary development and disease.

    PubMed

    Marquez, Hector A; Cardoso, Wellington V

    2016-12-01

    Retinoic acid (RA), the active form of vitamin A, regulates key developmental processes in multiple organs. In the developing lung, RA is crucial for normal growth and differentiation of airways. Disruption in RA signaling or vitamin A deficiency (VAD) has been linked to aberrant development of the lung including alterations in the airway smooth muscle (SM) differentiation, development, and function. These alterations have been linked to disease states including asthma in both human and animal models. PMID:27480876

  4. [Hereditary angioneurotic edema in children].

    PubMed

    Farkas, H; Harmat, G; Füst, G; Varga, L; Visy, B

    2000-11-19

    Hereditary angioneurotic edema results from the deficiency of C1-esterase inhibitor. The clinical picture of this autosomal dominant disorder is characterized by recurrent attacks of edema formation in the subcutis and/or the submucosa. The clinical records of 21 children with established hereditary angioneurotic edema were reviewed. Follow-up care included laboratory check-ups and abdominal ultrasound. Clinical manifestations of the disease first occurred in 2.5 to 12 years of age. Mechanical trauma was the most common precipitating factor. Pedigree-analysis revealed 19 patients with afflicted relatives. Long-term prophylaxis was initiated with tranexamic acid and danazol in 10 cases; 2 children required short-term prophylaxis. Therapy improved serum complement parameters significantly and reduced the frequency and severity of clinical manifestations. Acute, life-threatening edematous attacks were treated by the administration of C1-inhibitor concentrate, which achieved the resolution of the edema within several hours. Abdominal ultrasonography performed during the attack invariably demonstrated transitory ascites that resolved spontaneously after treatment. Adequate prophylaxis and follow-up care can spare pediatric patients from edematous attacks. Undesirable adverse effects can be avoided and the patient's quality of life can be enhanced considerably by administering the lowest effective drug dose. PMID:11143287

  5. 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. PMID:27101784

  6. 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 ...

  7. Two cases of familial primary pulmonary hypertension.

    PubMed

    Yamashita, Kazuhito; Tasaki, Hiromi; Kubara, Takahiro; Nakashima, Yasuhide

    2004-12-01

    Case 1, a 28-year-old woman (third daughter of Case 2) delivered her first child in September 2000, but leg edema and dyspnea on exertion appeared the following January. At the time of our first examination of the patient in May 2001, a chest X-ray showed cardiomegaly and pulmonary artery enlargement. Echocardiography demonstrated enlargement of the right ventricle and small left ventricular dimensions, and an electrocardiogram revealed right ventricle hypertrophy. After perfusion-ventilation lung scintigraphy and cardiac catheterization, she was diagnosed as having primary pulmonary hypertension (PPH). Although she was discharged with prescriptions for a diuretic, warfarin and beraprost sodium, she died of a pulmonary hypertensive crisis twenty days after readmission. Case 2, a 60-year-old woman(mother of Case 1) developed the same symptoms as those in Case 1, in May 2001, but recovered after medication. PPH is a rare disease and only a few familial cases are reported. In this family, the eldest daughter of Case 2 had also died of pulmonary hypertension ten years ago, several months after her first delivery. In contrast to the daughters, the mother's symptoms developed gradually. PMID:15624356

  8. Inflammatory sequences in acute pulmonary radiation injury.

    PubMed Central

    Slauson, D. O.; Hahn, F. F.; Benjamin, S. A.; Chiffelle, T. L.; Jones, R. K.

    1976-01-01

    The histopathologic events in the developing acute pulmonary inflammatory reaction to inhaled particles of Yttrium 90 are detailed. In animals that died or were sacrificed during the first year after inhalation exposure, microscopic findings of acute inflammation predominated and included vascular congestion; stasis, focal hemorrhage; edema; various inflammatory cell infiltrates; cytolysis and desquamation of bronchiolar and alveolar epithelium followed by regeneration; vascular injury and repair; and the eventual development of pulmonary fibrosis. Accumulation of alveolar fibrin deposits was an additional characteristic, though not a constant feature of the early stages of radiation pneumonitis. In addition to the direct effects of radiation on pulmonary cell populations, the histopathologic findings were suggestive of diverse activation of various cellular and humoral mediation systems in their pathogenesis. The potential interrelationships of systems responsible for increased vascular permeability, coagulation and fibrinolysis, chemotaxis, and direct cellular injury were discussed and related to the pathogenesis of the microscopic findings characteristic of early pulmonary radiation injury. Images Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 7 Figure 8 Figure 9 Figure 10 PMID:1258976

  9. 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

  10. Development of the chronic obstructive pulmonary disease activity rating scale: reliability, validity and factorial structure.

    PubMed

    Morimoto, Michiko; Takai, Kenichi; Nakajima, Kazuo; Kagawa, Koujiro

    2003-03-01

    The purpose of the present study was to develop the Chronic Obstructive Pulmonary Disease (COPD) Activity Rating Scale (CARS) to measure life-related activity in patients with COPD, and to confirm its reliability and constructive validity in a factorial structure model. The subjects consisted of 114 patients with COPD. An 88-item life-related activity list, generated previously from a literature review, was administered. The secondary structural model consisted of four factors with 12 items. The results of the confirmatory factor analysis by structural equation modeling showed the fit criteria to be statistically significant. The internal consistency of the 12 items was highly reliable (Cronbach's alpha = 0.924). The CARS score was correlated with pulmonary function tests, breathlessness, and the health-related quality of life (QOL) scales in Pearson correlation coefficient. The results suggest that the COPD Activity Rating Scale is a valid scale for the assessment of life-related activity in patients with COPD. PMID:12603718

  11. Pulmonary accumulation of polymorphonuclear leukocytes in the adult respiratory distress syndrome

    SciTech Connect

    Powe, J.E.; Short, A.; Sibbald, W.J.; Driedger, A.A.

    1982-11-01

    The polymorphonuclear leukocyte (PMN) plays an integral role in the development of permeability pulmonary edema associated with the adult respiratory distress syndrome (ARDS). This report describes 3 patients with ARDS secondary to systemic sepsis who demonstrated an abnormal diffuse accumulation of Indium (/sup 111/In)-labeled PMNs in their lungs, without concomitant clinical or laboratory evidence of a primary chest infection. In one patient, the accumulation of the pulmonary activity during an initial pass suggested that this observation was related to diffuse leukoaggregation within the pulmonary microvasculature. A 4th patient with ARDS was on high-dose corticosteroids at the time of a similar study, and showed no pulmonary accumulation of PMNs, suggesting a possible reason for the reported beneficial effect of corticosteroids in human ARDS.

  12. [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

  13. Inactivation of p53 Is Sufficient to Induce Development of Pulmonary Hypertension in Rats

    PubMed Central

    Jacquin, S.; Rincheval, V.; Mignotte, B.; Richard, S.; Humbert, M.; Mercier, O.; Londoño-Vallejo, A.; Fadel, E.; Eddahibi, S.

    2015-01-01

    Objective Pulmonary artery smooth muscle cells (PA-SMCs) in pulmonary arterial hypertension (PAH) show similarities to cancer cells. Due to the growth-suppressive and pro-apoptotic effects of p53 and its inactivation in cancer, we hypothesized that the p53 pathway could be altered in PAH. We therefore explored the involvement of p53 in the monocrotaline (MCT) rat model of pulmonary hypertension (PH) and the pathophysiological consequences of p53 inactivation in response to animal treatment with pifithrin-α (PFT, an inhibitor of p53 activity). Methods and Results PH development was assessed by pulmonary arterial pressure, right ventricular hypertrophy and arterial wall thickness. The effect of MCT and PFT on lung p53 pathway expression was evaluated by western blot. Fourteen days of daily PFT treatment (2.2 mg/kg/day), similar to a single injection of MCT (60 mg/kg), induced PH and aggravated MCT-induced PH. In the first week after MCT administration and prior to PH development, p53, p21 and MDM2 protein levels were significantly reduced; whereas PFT administration effectively altered the protein level of p53 targets. Anti-apoptotic and pro-proliferative effects of PFT were revealed by TUNEL and MTT assays on cultured human PA-SMCs treated with 50 μM PFT. Conclusions Pharmacological inactivation of p53 is sufficient to induce PH with a chronic treatment by PFT, an effect related to its anti-apoptotic and pro-proliferative properties. The p53 pathway was down-regulated during the first week in the rat MCT model. These in vivo experiments implicate the p53 pathway at the initiation stages of PH pathogenesis. PMID:26121334

  14. Pulmonary vascular and alveolar development in tetralogy of Fallot: a recommendation for early correction.

    PubMed

    Johnson, R J; Haworth, S G

    1982-12-01

    Using quantitative morphometric techniques, we analysed pulmonary arterial and alveolar development in the lungs of seven children aged 1.2-12 years who died during or soon after repair of tetralogy of Fallot. One child had a residual ventricular septal defect and survived for five months. One other child had had a previous Waterston-Cooley anastomosis (Waterston shunt). Postmortem lung volume in relation to body surface area was generally below normal for age, the alveoli were small, and the total alveolar number was below normal in five of the seven cases. Microscopically, airway and alveolar structure appeared normal. The preacinar arteries were larger and the intra-acinar arteries were smaller than normal for age. The preacinar elastic pulmonary arteries appeared to contain less elastin and in both preacinar and intra-acinar muscular arteries the media was thinner than normal, although muscle was normally distributed along the arterial pathway. Eccentric areas of intimal fibrosis were small and uncommon. The bronchial arteries were generally more prominent than usual both macroscopically and microscopically, but no abnormal bronchopulmonary connections were present. After corrective surgery a residual ventricular septal defect and pulmonary hypertension were associated with arterial medial hypertrophy, and this change was also found in the right lung of a normotensive patient who had had a Waterston shunt. This group probably represents the most favourable clinical picture of tetralogy in patients who usually survive but, even so, pulmonary arterial and alveolar development was abnormal. The structural findings are discussed in relation to the functional outcome in patients with tetralogy who have survived. Repair of the abnormality during the first two to three years of life is recommended. PMID:7170679

  15. Bosentan for pulmonary hypertension secondary to idiopathic pulmonary fibrosis

    PubMed Central

    Onda, Naomi; Tanaka, Yosuke; Hino, Mitsunori; Gemma, Akihiko

    2014-01-01

    Pulmonary hypertension is a poor prognostic factor in patients with interstitial lung disease. No established treatment exists for pulmonary hypertension secondary to interstitial pneumonia. We describe the case of an 81-year-old woman with idiopathic pulmonary fibrosis (IPF), who was admitted to our hospital due to aggravation of dyspnea and decreased oxygen saturation, as well as onset of orthopnea and rapidly progressing edema. The transthoracic echocardiography and right heart catheterization showed the mean pulmonary artery pressure was 39 mmHg and the mean pulmonary capillary wedge pressure was 9 mmHg. After various examinations, the diagnoses of pulmonary hypertension (PH) due to IPF and of congestive heart failure secondary to PH were established. Diuretic therapy was started, but the patient's condition showed poor improvement. Subsequent initiation of oral bosentan therapy led to improvement in symptoms and findings. At the follow-up assessment one year later her pulmonary function showed no significant changes and no apparent worsening of arterial blood gases, with evident improvement of PH, WHO functional class, maximum exercise tolerance on treadmill exercise testing, right heart catheterization, and transthoracic echocardiography. This report describes a case of successful treatment with bosentan for severe pulmonary hypertension in a patient with idiopathic pulmonary fibrosis. We also present a review of the literature on treatment of pulmonary hypertension in patients with chronic lung disease. Bosentan appears to be efficacious in some patients with pulmonary hypertension secondary to idiopathic interstitial pneumonitis. PMID:26029570

  16. Pulmonary Complications of Drug Abuse

    PubMed Central

    Gottlieb, Leon S.; Boylen, Thomas C.

    1974-01-01

    Complications resulting from drug abuse more frequently affect the lung than any other organ. The spectrum of pulmonary complications associated with drug abuse is wide. The current practice of using mixtures of drugs is mainly responsible for the increase in pulmonary complications. The chief complications observed in a series of 241 drug abuse patients were aspiration pneumonitis (12.9 percent), pulmonary edema (10.0 percent), and pneumonia (7.5 percent). ImagesFigure 1.Figure 2.Figure 3.Figure 4.Figure 5.Figure 6.Figure 7.Figure 8.Figure 9.Figure 10. PMID:4812215

  17. Anatomical considerations for the development of a new transcatheter aortopulmonary shunt device in patients with severe pulmonary arterial hypertension

    PubMed Central

    2013-01-01

    Abstract Morbidity from pulmonary arterial hypertension (PAH) ensues when the pulmonary pressure reaches suprasystemic levels. A transcatheter alternative to the Potts shunt would allow decompression of the right heart without the surgical risks. To aid development of a transcatheter aortopulmonary shunt (TAPS) device, we described the anatomic relationship between the left pulmonary artery (LPA) and the descending aorta (dAO) in adults with severe pulmonary hypertension. Adults with severe PAH (peak systolic pulmonary arterial pressure [PASP] ≥80 mmHg) who had computed tomography of the chest were enrolled. Measurements were taken on the axial plane at the level of the pulmonary artery bifurcation. Forty patients (male sex, 9 patients; median age ± standard deviation [SD], years; median PASP ± SD, mmHg) were identified. The mean distance (±SD) between the LPA and dAO was mm. The mean luminal dAO and LPA diameters (±SD) were mm and mm, respectively. The LPA and dAO approximated in 93% of patients, with 38% having aortic calcification at the contact site. The mean “landing zone” width and height (defining an area with distance <4 mm between the outer borders) of the two arteries were mm and mm, respectively, at a mean distance of mm from the main pulmonary artery bifurcation. This study shows that the landing zone is able to accommodate a TAPS device of up to 15 mm in diameter in the majority of patients with severe PAH. PMID:24618548

  18. 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

  19. [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

  20. Development of the Pulmonary Vein and the Systemic Venous Sinus: An Interactive 3D Overview

    PubMed Central

    van den Berg, Gert; Moorman, Antoon F. M.

    2011-01-01

    Knowledge of the normal formation of the heart is crucial for the understanding of cardiac pathologies and congenital malformations. The understanding of early cardiac development, however, is complicated because it is inseparably associated with other developmental processes such as embryonic folding, formation of the coelomic cavity, and vascular development. Because of this, it is necessary to integrate morphological and experimental analyses. Morphological insights, however, are limited by the difficulty in communication of complex 3D-processes. Most controversies, in consequence, result from differences in interpretation, rather than observation. An example of such a continuing debate is the development of the pulmonary vein and the systemic venous sinus, or “sinus venosus”. To facilitate understanding, we present a 3D study of the developing venous pole in the chicken embryo, showing our results in a novel interactive fashion, which permits the reader to form an independent opinion. We clarify how the pulmonary vein separates from a greater vascular plexus within the splanchnic mesoderm. The systemic venous sinus, in contrast, develops at the junction between the splanchnic and somatic mesoderm. We discuss our model with respect to normal formation of the heart, congenital cardiac malformations, and the phylogeny of the venous tributaries. PMID:21779373

  1. 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

  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. Methylene blue-related corneal edema and iris discoloration.

    PubMed

    Timucin, Ozgur Bulent; Karadag, Mehmet Fatih; Aslanci, Mehmet Emin; Baykara, Mehmet

    2016-04-01

    We report the case of a 70-year-old female patient who developed corneal edema and iris discoloration following the inadvertent use of 1% methylene blue instead of 0.025% trypan blue to stain the anterior capsule during cataract phacoemulsification surgery. Copious irrigation was performed upon realization of incorrect dye use. Corneal edema and iris discoloration developed during the early postoperative period and persisted at 24-months follow-up. However, keratoplasty was not required. The intracameral use of 1% methylene blue has a cytotoxic effect on the corneal endothelium and iris epithelium. Copious irrigation for at least 30 min using an anterior chamber maintainer may improve outcomes. PMID:27224079

  4. Redox regulation of epidermal growth factor receptor signaling during the development of pulmonary hypertension.

    PubMed

    Rafikova, Olga; Rafikov, Ruslan; Kangath, Archana; Qu, Ning; Aggarwal, Saurabh; Sharma, Shruti; Desai, Julin; Fields, Taylor; Ludewig, Britta; Yuan, Jason X-Y; Jonigk, Danny; Black, Stephen M

    2016-06-01

    The development of pulmonary hypertension (PH) involves the uncontrolled proliferation of pulmonary smooth muscle cells via increased growth factor receptor signaling. However, the role of epidermal growth factor receptor (EGFR) signaling is controversial, as humans with advanced PH exhibit no changes in EGFR protein levels and purpose of the present study was to determine whether there are post-translational mechanisms that enhance EGFR signaling in PH. The EGFR inhibitor, gefinitib, significantly attenuated EGFR signaling and prevented the development of PH in monocrotaline (MCT)-exposed rats, confirming the contribution of EGFR activation in MCT induced PH. There was an early MCT-mediated increase in hydrogen peroxide, which correlated with the binding of the active metabolite of MCT, monocrotaline pyrrole, to catalase Cys377, disrupting its multimeric structure. This early oxidative stress was responsible for the oxidation of EGFR and the formation of sodium dodecyl sulfate (SDS) stable EGFR dimers through dityrosine cross-linking. These cross-linked dimers exhibited increased EGFR autophosphorylation and signaling. The activation of EGFR signaling did not correlate with pp60(src) dependent Y845 phosphorylation or EGFR ligand expression. Importantly, the analysis of patients with advanced PH revealed the same enhancement of EGFR autophosphorylation and covalent dimer formation in pulmonary arteries, while total EGFR protein levels were unchanged. As in the MCT exposed rat model, the activation of EGFR in human samples was independent of pp60(src) phosphorylation site and ligand expression. This study provides a novel molecular mechanism of oxidative stress stimulated covalent EGFR dimerization via tyrosine dimerization that contributes into development of PH. PMID:26928584

  5. Pulmonary arteriovenous fistula

    MedlinePlus

    Pulmonary arteriovenous fistula is an abnormal connection between an artery and vein in the lungs. As a result, blood passes ... Pulmonary arteriovenous fistulas are usually the result of abnormal development of the blood vessels of the lung. Most occur in ...

  6. The Role of Hyperglycemia and Insulin Resistance in the Development and Progression of Pulmonary Arterial Hypertension

    PubMed Central

    Grinnan, Daniel; Farr, Grant; Fox, Adam; Sweeney, Lori

    2016-01-01

    Pulmonary hypertension is a progressive disorder which often leads to right ventricular failure and death. While the existing classification system for pulmonary hypertension does not account for the impact of diabetes mellitus, evidence is emerging that suggests that diabetes is associated with pulmonary hypertension and that diabetes modifies the course of pulmonary hypertension. There is also growing radiographic, hemodynamic, biochemical, and pathologic data supporting an association between diabetes and pulmonary hypertension. More robust epidemiologic studies are needed to confirm an association between diabetes and pulmonary hypertension and to show that diabetes is a disease modifier in pulmonary hypertension. In addition, evaluating the effects of glucose control in animals with pulmonary hypertension and diabetes (as well as in humans) is warranted. PMID:27376089

  7. 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.

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

    PubMed

    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

  9. 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

  10. [MODELING INFLAMMATORY EDEMA: ARE THE MODELS INTERCHANGEABLE].

    PubMed

    Hanh, Cong Hong; Khaziakhmetova, V N; Ziganshina, L E

    2015-01-01

    Experimental modeling of inflammatory edema by sub-plantar injection of carrageenan and formalin in mice and rats is widely used to evaluate potential anti-inflammatory activity of new drugs. This systematic analysis of published data showed that carrageenan induced paw edema model is used for evaluating the anti-inflammatory activity mostly in rats rather than mice. Formalin induced paw edema in rats and mice is used primarily for evaluation of the analgesic activity of drugs. Taken together, the results of this systematic review of available literature on edema modeling substantiate recommendation to use carrageenan paw edema in rats and formalin paw edema in mice as complementary, but not interchangeable models of inflammation. PMID:26591204