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Sample records for pulmonary edema developed

  1. Pulmonary Edema

    MedlinePlus

    ... suddenly or develop over time. Sudden (acute) pulmonary edema symptoms Extreme shortness of breath or difficulty breathing ( ... fatal if not treated. Long-term (chronic) pulmonary edema symptoms Having more shortness of breath than normal ...

  2. 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 ...

  3. Reexpansion pulmonary edema.

    PubMed

    Tarver, R D; Broderick, L S; Conces, D J

    1996-01-01

    Reexpansion pulmonary edema is a rare complication attending the rapid reexpansion of a chronically collapsed lung, such as occurs after evacuation of a large amount of air or fluid from the pleural space. The condition usually appears unexpectedly and dramatically-immediately or within 1 h in 64% of patients and within 24 h in the remainder. The clinical manifestations are varied; they range from roentgenographic findings alone in asymptomatic patients to severe cardiorespiratory insufficiency. The radiographic evidence of reexpansion pulmonary edema is a unilateral alveolar filling pattern, seen within a few hours of reexpansion of the lung. The edema may progress for 24-48 h and persist for 4-5 days. Human data on the pathophysiology of reexpansion pulmonary edema derive from small series of patients, case reports, and reviews of the literature. On the other hand, a larger body of data exists on experimental reexpansion pulmonary edema in cats, monkeys, rabbits, sheep, and goats. This review examines the clinical and experimental evidence for reexpansion pulmonary edema. In addition, we detail the historical background, clinical setting, treatment, and outcome of reexpansion pulmonary edema.

  4. Postobstructive pulmonary edema.

    PubMed

    Udeshi, Ashish; Cantie, Shawn Michael; Pierre, Edgar

    2010-09-01

    Postobstructive pulmonary edema (POPE; also known as negative pressure pulmonary edema) is a potentially life-threatening complication in which pulmonary edema occurs shortly after the relief of an upper airway obstruction. The incidence of POPE has been reported to be as high as 1 in 1000 general anesthetic cases and commonly presents as acute respiratory distress that requires immediate intervention. This review examines the 2 subclasses of POPE and describes the etiologic factors, pathophysiology, clinical manifestations, diagnostic criteria, and treatment strategies associated with each. The aim of this review was to equip clinicians with the knowledge base necessary to identify patients at increased risk for POPE and to expeditiously diagnose and treat this potentially catastrophic complication.

  5. Reperfusion pulmonary edema

    SciTech Connect

    Klausner, J.M.; Paterson, I.S.; Mannick, J.A.; Valeri, C.R.; Shepro, D.; Hechtman, H.B. )

    1989-02-17

    Reperfusion following lower-torso ischemia in humans leads to respiratory failure manifest by pulmonary hypertension, hypoxemia, and noncardiogenic pulmonary edema. The mechanism of injury has been studied in the sheep lung lymph preparation, where it has been demonstrated that the reperfusion resulting in pulmonary edema is due to an increase in microvascular permeability of the lung to protein. This respiratory failure caused by reperfusion appears to be an inflammatory reaction associated with intravascular release of the chemoattractants leukotriene B{sub 4} and thromboxane. Histological studies of the lung in experimental animals revealed significant accumulation of neutrophils but not platelets in alveolar capillaries. The authors conclude that thromboxane generated and released from the ischemic tissue is responsible for the transient pulmonary hypertension. Second, it is likely that the chemoattractants are responsible for leukosequestration, and third, neutrophils, oxygen-derived free radicals, and thromboxane moderate the altered lung permeability.

  6. New Developments in the Pathogenesis of Smoke Inhalation-Induced Pulmonary Edema

    PubMed Central

    Witten, Mark L.; Quan, Stuart F.; Sobonya, Richard E.; Lemen, Richard J.

    1988-01-01

    Smoke inhalation causes most of the deaths in fire-related injuries, with pulmonary edema as a major determinant in the outcome of smoke-inhalation injury. The pathophysiology of pulmonary edema is thought to be related to the products of incomplete combustion. Damage to the integrity of the alveolar epithelium is one of the determinants of the development of smoke-induced pulmonary edema. In recent studies using lung clearance of aerosolized pentetic acid (DTPA [diethylenetriaminepentaacetic acid]) labeled with technetium Tc 99m to assess the permeability of the alveolar epithelium, several factors were identified that may increase a person's susceptibility to smoke-induced acute lung injury. These are increased initial alveolar permeability and alterations in the number and activity of alveolar macrophages. Clinical measurement of 99mTcDTPA clearance may provide a sensitive and convenient method for the early detection and serial assessment of smoke-induced alveolar epithelial permeability changes. Images PMID:3277334

  7. Negative-Pressure Pulmonary Edema.

    PubMed

    Bhattacharya, Mallar; Kallet, Richard H; Ware, Lorraine B; Matthay, Michael A

    2016-10-01

    Negative-pressure pulmonary edema (NPPE) or postobstructive pulmonary edema is a well-described cause of acute respiratory failure that occurs after intense inspiratory effort against an obstructed airway, usually from upper airway infection, tumor, or laryngospasm. Patients with NPPE generate very negative airway pressures, which augment transvascular fluid filtration and precipitate interstitial and alveolar edema. Pulmonary edema fluid collected from most patients with NPPE has a low protein concentration, suggesting hydrostatic forces as the primary mechanism for the pathogenesis of NPPE. Supportive care should be directed at relieving the upper airway obstruction by endotracheal intubation or cricothyroidotomy, institution of lung-protective positive-pressure ventilation, and diuresis unless the patient is in shock. Resolution of the pulmonary edema is usually rapid, in part because alveolar fluid clearance mechanisms are intact. In this review, we discuss the clinical presentation, pathophysiology, and management of negative-pressure or postobstructive pulmonary edema.

  8. Clinical and radiologic features of pulmonary edema.

    PubMed

    Gluecker, T; Capasso, P; Schnyder, P; Gudinchet, F; Schaller, M D; Revelly, J P; Chiolero, R; Vock, P; Wicky, S

    1999-01-01

    Pulmonary edema may be classified as increased hydrostatic pressure edema, permeability edema with diffuse alveolar damage (DAD), permeability edema without DAD, or mixed edema. Pulmonary edema has variable manifestations. Postobstructive pulmonary edema typically manifests radiologically as septal lines, peribronchial cuffing, and, in more severe cases, central alveolar edema. Pulmonary edema with chronic pulmonary embolism manifests as sharply demarcated areas of increased ground-glass attenuation. Pulmonary edema with veno-occlusive disease manifests as large pulmonary arteries, diffuse interstitial edema with numerous Kerley lines, peribronchial cuffing, and a dilated right ventricle. Stage 1 near drowning pulmonary edema manifests as Kerley lines, peribronchial cuffing, and patchy, perihilar alveolar areas of airspace consolidation; stage 2 and 3 lesions are radiologically nonspecific. Pulmonary edema following administration of cytokines demonstrates bilateral, symmetric interstitial edema with thickened septal lines. High-altitude pulmonary edema usually manifests as central interstitial edema associated with peribronchial cuffing, ill-defined vessels, and patchy airspace consolidation. Neurogenic pulmonary edema manifests as bilateral, rather homogeneous airspace consolidations that predominate at the apices in about 50% of cases. Reperfusion pulmonary edema usually demonstrates heterogeneous airspace consolidations that predominate in the areas distal to the recanalized vessels. Postreduction pulmonary edema manifests as mild airspace consolidation involving the ipsilateral lung, whereas pulmonary edema due to air embolism initially demonstrates interstitial edema followed by bilateral, peripheral alveolar areas of increased opacity that predominate at the lung bases. Familiarity with the spectrum of radiologic findings in pulmonary edema from various causes will often help narrow the differential diagnosis.

  9. [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.

  10. Sympathetic crashing acute pulmonary edema

    PubMed Central

    Agrawal, Naman; Kumar, Akshay; Aggarwal, Praveen; Jamshed, Nayer

    2016-01-01

    Sympathetic crashing acute pulmonary edema (SCAPE) is the extreme end of the spectrum of acute pulmonary edema. It is important to understand this disease as it is relatively common in the emergency department (ED) and has better outcomes when managed appropriately. The patients have an abrupt redistribution of fluid in the lungs, and when treated promptly and effectively, these patients will rapidly recover. Noninvasive ventilation and intravenous nitrates are the mainstay of treatment which should be started within minutes of the patient's arrival to the ED. Use of morphine and intravenous loop diuretics, although popular, has poor scientific evidence. PMID:28149030

  11. Sympathetic crashing acute pulmonary edema.

    PubMed

    Agrawal, Naman; Kumar, Akshay; Aggarwal, Praveen; Jamshed, Nayer

    2016-12-01

    Sympathetic crashing acute pulmonary edema (SCAPE) is the extreme end of the spectrum of acute pulmonary edema. It is important to understand this disease as it is relatively common in the emergency department (ED) and has better outcomes when managed appropriately. The patients have an abrupt redistribution of fluid in the lungs, and when treated promptly and effectively, these patients will rapidly recover. Noninvasive ventilation and intravenous nitrates are the mainstay of treatment which should be started within minutes of the patient's arrival to the ED. Use of morphine and intravenous loop diuretics, although popular, has poor scientific evidence.

  12. [A rare form of acute pulmonary edema: case report].

    PubMed

    Ricardo, José; Anaya, Maria José; Barbosa, Mário; André, Nelson; Magno, Pedro; Morais, José; Proença, Gonçalo; Rabaçal, Carlos; Gil, Victor

    2011-10-01

    We report the case of a 21-year-old man who underwent appendectomy under general anesthesia and developed acute pulmonary edema immediately after extubation. We then review the literature, focusing on the pathophysiology and the most important aspects of diagnosis and treatment of post-extubation pulmonary edema.

  13. 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

  14. [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.

  15. Unilateral pulmonary edema during laparoscopic resection of adrenal tumor

    PubMed Central

    Prakash, Smita; Nayar, Pavan; Virmani, Pooja; Bansal, Shipra; Pawar, Mridula

    2015-01-01

    Despite technological, therapeutic and diagnostic advancements, surgical intervention in pheochromocytoma may result in a life-threatening situation. We report a patient who developed unilateral pulmonary edema during laparoscopic resection of adrenal tumor. PMID:26330724

  16. Role of tidal volume, FRC, and end-inspiratory volume in the development of pulmonary edema following mechanical ventilation.

    PubMed

    Dreyfuss, D; Saumon, G

    1993-11-01

    Mechanical ventilation with high peak inspiratory pressure and large tidal volume (VT) produces permeability pulmonary edema. Whether it is mean or peak inspiratory pressure (i.e., mean or end-inspiratory volume) that is the major determinant of ventilation-induced lung injury is unsettled. Rats were ventilated with increasing tidal volumes starting from different degrees of FRC that were set by increasing end-expiratory pressure during positive-pressure ventilation. Pulmonary edema was assessed by the measurement of extravascular lung water content. The importance of permeability alterations was evaluated by measurement of dry lung weight and determination of albumin distribution space. Pulmonary edema with permeability alterations occurred regardless of the value of positive end-expiratory pressure (PEEP), provided the increase in VT was large enough. Similarly, edema occurred even during normal VT ventilation provided the increase in PEEP was large enough. Furthermore, moderate increases in VT or PEEP that were innocuous when applied alone, produced edema when combined. The effect of PEEP was not the consequence of raised airway pressure but of the increase in FRC since similar observations were made in animals ventilated with negative inspiratory pressure. However, although permeability alterations were similar, edema was less marked in animals ventilated with PEEP than in those ventilated with zero end-expiratory pressure (ZEEP) with the same end-inspiratory pressure. This "beneficial" effect of PEEP was probably the consequence of hemodynamic alterations. Indeed, infusion of dopamine to correct the drop in systemic arterial pressure that occurred during PEEP ventilation resulted in a significant increase in pulmonary edema. In conclusion, rather than VT or FRC value, the end-inspiratory volume is probably the main determinant of ventilation-induced edema. Hemodynamic status plays an important role in modulating the amount of edema during lung overinflation

  17. [Acute pulmonary edema secondary to acute upper airway obstruction].

    PubMed

    Sánchez-Ortega, J L; Carpintero-Moreno, F; Olivares-López, A; Borrás-Rubio, E; Alvarez-López, M J; García-Izquierdo, A

    1992-01-01

    We report a 72 years old woman with mild arterial hypertension and no other pathological history who presented an acute pulmonary edema due to acute obstruction of the upper airway secondary to vocal chord paralysis developing during the immediate postoperative phase of thyroidectomy. The acute pulmonary edema resolved after application of tracheal reintubation, mechanical ventilation controlled with end expiratory positive pressure, diuretics, morphine, and liquid restriction. We discuss the possible etiopathogenic possibilities of this infrequent clinical picture and we suggest that all patients who suffered and acute obstruction of the upper airways require a careful clinical surveillance in order to prevent the development of the pulmonary syndrome.

  18. Interstitial Pulmonary Edema Following Bromocarbamide Intoxication

    PubMed Central

    Sugihara, H.; Hagedorn, M.; Bōttcher, D.; Neuhof, H.; Mittermayer, Ch.

    1974-01-01

    Bromocarbamides are sleep-inducing drugs which can lead, in man, to intoxication and death due to respiratory failure. To prove whether hemodynamic factors or the changed endothelial permeability induce pulmonary edema, animal experiments were performed. The fine structural changes in pulmonary edema in rabbits were observed at 60, 90 and 120 minutes after oral administration. The major findings were a) large blebs between capillary endothelium and alveolar epithelium and b) interstitial edema of the vessel wall. The bleb contents were much less electron dense than the blood contents in the capillary. Colloidal carbon did not enter the bleb or the edematous interstitial tissue. Exogenous peroxidase uptake in pinocytotie vesicles increased in pathologic cases. The hemodynamic measurements in animal receiving artificial respiration which maintained the blood pO2 at a steady state showed similar blebs in the pulmonary vessels, indicating that anoxia is not the major cause of the vascular lesion. Moreover, pulmonary arterial pressure and pulmonary vascular resistance could be held in the normal range in artificially respirated animals under bromocarbamide intoxication. Thus, hemodynamic factors are not likely to play a pathogenetic role in bringing about pulmonary edema. The chief, early factor is the increased endothelial permeability due to increased cytoplasmic transport. From this a practical suggestion for treating patients with bromocarbamide intoxication is derived: the usual fluid replacement in shock patients should be handled with great care to avoid fluid overload of the lung. ImagesFig 1Fig 2Fig 3Fig 4Fig 5Fig 6 PMID:4835993

  19. [Negative pressure pulmonary edema: 3 case reports].

    PubMed

    Ortíz-Gómez, J R; Paja Martí, I; Sos-Ortigosa, F; Pérez-Cajaraville, J J; Arteche-Andrés, M A; Bengoechea, C; Lobo-Palanco, J; Ahmad-Al-Ghool, M

    2006-01-01

    Negative pressure pulmonary edema is a complication, described since 1977, caused by upper airway obstruction in both children and adults. Although its aetiopathogeny is multifactorial, especially outstanding is excessive negative intrathoracic pressure caused by the forced spontaneous inspiration of a patient against a closed glottis, that causes high arteriole and capillary fluid pressures that favor transudation into the alveolar space The resulting pulmonary edema can appear a few minutes after the obstruction of the airway or in a deferred way after several hours. The clinical manifestations are potentially serious, but normally respond well to treatment with supplemental oxygen, positive pressure mechanical ventilation and diuretics. Diagnostic suspicion is important for acting promptly. We report three clinical cases with acute negative pressure pulmonary edema.

  20. [Acute pulmonary edema as a nursing emergency].

    PubMed

    Navarro Aldana, M C

    2001-01-01

    The presence of Acute Pulmonary Edema represents a severe emergency condition that requires immediate and efficient treatment; otherwise, imminent death of the patient occurs. Therefore it is of utter importance to perform frequent reviews of the literature to keep up with the newest procedures to warrant the best quality nursing care of our patients. This article reviews the physiopathology, clinical manifestations, and medical treatment of the Acute Pulmonary Edema, emphasizing on the nursing aspects of the treatment and pointing out the need to treat the predisposing cardiac alteration as soon as possible.

  1. Pulmonary edema induced by intravenous ethchlorvynol.

    PubMed

    Conces, D J; Kreipke, D L; Tarver, R D

    1986-11-01

    The intravenous injection of ethchlorvynol is an uncommon cause of noncardiac pulmonary edema. Two cases of intravenous ethchlorvynol-induced pulmonary edema are presented. The patients fell asleep after injecting the liquid contents of Placydil capsules (ethchlorvynol) and awoke several hours later with severe dyspnea. Arterial blood gases demonstrated marked hypoxia. Chest radiographs revealed bilateral diffuse alveolar densities. The patients' symptoms and radiographic findings resolved after several days of supportive care. Changes in the lung caused by ethchlorvynol may be the result of direct effect of the drug on the lung.

  2. Diagnosis and management of cardiogenic pulmonary edema.

    PubMed

    Alwi, Idrus

    2010-07-01

    Acute cardiogenic pulmonary edema (ACPE) is a common cardiogenic emergency with a quite high in-hospital mortality rate. ACPE is defined as pulmonary edema with increased secondary hydrostatic capillary pressure due to elevated pulmonary venous pressure. Increased hydrostatic pressure may result from various causes including excessive administration of intravascular volume, obstruction of pulmonary venous outflow or secondary left ventricular failure due to left ventricular systolic or diastolic dysfunction. ACPE must be distinguished from pulmonary edema associated with injury of alveolar capillary membrane caused by various etiologies, i.e. direct pulmonary injury such as pneumonia and indirect pulmonary injury such as sepsis. Numerous clinical manifestations may differentiate ACPE and Non-ACPE. ACPE usually presents with a history of acute cardiac catastrophe. Physical examination reveals a low-flow state, S3 gallop, jugular venous distention and fine crepitant rales with auscultation. The diagnosis of pulmonary edema is made based on symptoms and clinical signs are found through history taking, physical examination, ECG, chest X-ray, echocardiography and laboratory tests including blood gas analysis and specific biomarkers. Medical treatment of ACPE has 3 main objectives, i.e.: (1) reduced venous return (preload reduction); (2) reduced resistance of systemic vascular (afterload reduction); and (3) inotropic support in some cases. Treatment that can be administered includes: vasodilator when there is normal or high BP, diuretics when there is volume overload or fluid retention, and inotropic drugs when there is hypotension or signs of organ hypoperfusion. Intubation and mechanical ventilation may be necessary to achieve adequate oxygenation.

  3. Neurogenic Pulmonary Edema in Aneurysmal Subarachnoid Hemorrhage.

    PubMed

    Saracen, A; Kotwica, Z; Woźniak-Kosek, A; Kasprzak, P

    2016-01-01

    Neurogenic pulmonary edema (NPE) is observed in cerebral injuries and has an impact on treatment results, being a predictor of fatal prognosis. In this study we retrospectively reviewed medical records of 250 consecutive patients with aneurysmal subarachnoid hemorrhage (SAH) for the frequency and treatment results of NPE. The following factors were taken under consideration: clinical status, aneurysm location, presence of NPE, intracranial pressure (ICP), and mortality. All patients had plain- and angio-computer tomography performed. NPE developed most frequently in case of the aneurysm located in the anterior communicating artery. The patients with grades I-III of SAH, according to the World Federation of Neurosurgeons staging, were immediately operated on, while those with poor grades IV and V had only an ICP sensor's implantation procedure performed. A hundred and eighty five patients (74.4 %) were admitted with grades I to III and 32 patients (12.8 %) were with grade IV and V each. NPE was not observed in SAH patients with grade I to III, but it developed in nine patients with grade IV and 11 patients with grade V. Of the 20 patients with NPE, 19 died. Of the 44 poor grade patients (grades IV-V) without NPE, 20 died. All poor grade patients had elevated ICP in a range of 24-56 mmHg. The patients with NPE had a greater ICP than those without NPE. Gender and age had no influence on the occurrence of NPE. We conclude that the development of neurogenic pulmonary edema in SAH patients with poor grades is a fatal prognostic as it about doubles the death rate to almost hundred percent.

  4. 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

  5. Our patients followed up with a diagnosis of neurogenic pulmonary edema

    PubMed Central

    Sarı, Mehmet Yusuf; Yıldızdaş, Rıza Dinçer; Yükselmiş, Ufuk; Horoz, Özden Ögür

    2015-01-01

    Neurogenic pulmonary edema is a clinical situation which developes as a result of central nervous system injury. It is rare in the childhood. Neurogenic pulmonary edema is a clinical diagnosis. Although the pathogenesis is not elucidated well, there is increase in pulmonary interstitial and alveolar fluid. The main principle in treatment of neurogenic pulmonary edema is supportive treatment and decreasing intracranial pressure as in acute respiratory distress syndrome. In this article, clinical properties of our two patients diagnosed with neurogenic pulmonary edema developed as a result of central nervous system injury are presented. PMID:26884694

  6. 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.

  7. 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.

  8. 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.

  9. 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.

  10. 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.

  11. Independent ventilation and ECMO for severe unilateral pulmonary edema after SLT for primary pulmonary hypertension.

    PubMed

    Badesch, D B; Zamora, M R; Jones, S; Campbell, D W; Fullerton, D A

    1995-06-01

    Single lung transplantation (SLT) is now accepted therapy for selected cases of severe pulmonary hypertension. A recognized complication is the postoperative development of reperfusion edema in the graft, a potentially fatal cause of respiratory failure. Because reperfusion edema may be a reversible process, temporizing support measures can be life-saving. We report the case of a 48-year-old woman who developed severe reperfusion edema following right SLT for primary (unexplained) pulmonary hypertension. Extracorporeal membrane oxygenation (ECMO) was instituted. Independent lung ventilation was later begun and resulted in markedly improved oxygenation allowing withdrawal of ECMO. We conclude that reperfusion edema following SLT for pulmonary hypertension may be uniquely amenable to treatment with independent lung ventilation and ECMO if needed.

  12. Drug-induced pulmonary edema and acute respiratory distress syndrome.

    PubMed

    Lee-Chiong, Teofilo; Matthay, Richard A

    2004-03-01

    Noncardiogenic pulmonary edema, and, to a lesser extent, acute respiratory distress syndrome (ARDS), are common clinical manifestations of drug-induced lung diseases. Clinical features and radiographic appearances are generally indistinguishable from other causes of pulmonary edema and ARDS. Typical manifestations include dyspnea, chest discomfort, tachypnea, and hypoxemia. Chest radiographs commonly reveal interstitial and alveolar filling infiltrates. Unlike pulmonary edema that is due to congestive heart failure, cardiomegaly and pulmonary vascular redistribution are generally absent in cases that are drug-related. Rare cases of drug-induced myocarditis with heart failure and pulmonary edema have been described. Results from laboratory evaluation and respiratory function tests are nonspecific.

  13. Pulmonary tissue volume in dogs during pulmonary edema.

    PubMed

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

    1978-05-01

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

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

    PubMed

    Kojima, Taiki; Nishisako, Ryo; Sato, Hideo

    2012-06-01

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

  15. Post-anesthetic pulmonary edema in two horses.

    PubMed

    Kaartinen, M Johanna; Pang, Daniel S J; Cuvelliez, Sophie G

    2010-03-01

    CASE 1: A two-year old, 462 kg Standard bred horse was anesthetized for arthroscopy and castration. During anesthesia, hyperemia of the mucosal membranes and urticaria were noticed. During 5 hours of anesthesia subcutaneous edema of the eyelids and neck region developed. In the recovery box, the orotracheal (OT) tube was left in situ and secured in place with tape. Following initial attempts to stand, the horse became highly agitated and signs consistent with pulmonary edema developed subsequently. Arterial hypoxemia (PaO(2): 3.7 kPa [28 mmHg]) and hypocapnia (PaCO(2): 3.1 kPa [23 mmHg]) were confirmed. Oxygen and furosemide were administered. The horse was assisted to standing with a sling. Therapy continued with bilateral intra-nasal oxygen insufflation. Ancillary medical therapy included flunixin meglumine, penicillin, gentamycin and dimethylsulfoxide. Following 7 hours of treatment the arterial oxygen tensions began to increase towards normal values. CASE 2: An 11-year old, 528 kg Paint horse was anesthetized for surgery of a submandibular mass. The 4-hour anesthetic period was unremarkable. The OT tube was left in situ for the recovery. During recovery, the horse was slightly agitated and stood after three attempts. Clinical signs consistent with pulmonary edema and arterial hypoxemia (PaO(2): 5 kPa [37.5 mmHg]) subsequently developed following extubation. Respiratory signs resolved with medical therapy, including unilateral nasal oxygen insufflation, furosemide, flunixin meglumine and dimethylsulfoxide. The diagnosis of pulmonary edema in these horses was made by clinical signs and arterial blood-gas analysis. While pulmonary radiographs were not taken to confirm the diagnosis, the clinical signs following anesthesia support the diagnosis in both cases. The etiology of pulmonary edema was most likely multifactorial.

  16. [Pulmonary edemas due to acute heroin poisoning].

    PubMed

    Francois, G; Faizende, J; Reboul, J

    1975-01-01

    Their frequency is estimated with difficulty, although on autopsy pulmonary edema is found almost routinely. It is a major complication of overdoses (48 p. 100 of severe intoxications). Their formation can be suspected, when after the first phase of respiratory depressions, with coma, myosis, and a variable latent period, a second attack of respiratory insufficiency occurs with tachypnea, and cyanosis. The chest X-ray shows diffuse alveolar infiltration, sparing the apices. The heart being generally of normal size. Rapid disappearance of this infiltrate (24 to 48 hours) enables the elimination of two diagnoses: pneumonia due to inhalation of gastric fluid, an infectious pneumonia. Their pathogenesis remains very debatable: - in the majority of cases abrupt L.V.F. can be eliminated: -on the other hand it could be an allergic accident of the anaphylactic type, or local liberation of histamine, or a local toxic action on the pulmonary capillaries; - hypoxia, secondary to respiratory depression, could lead to pulmonary edema, by the same mechanism as at altitude; - finally, owing to the central neurological disorders a neurogenic theory can be put forward. Their treatment is essentially a combination of Nalorphine with oxygen therapy (by mask, or if necessary by assisted, controlled ventilation) with prevention of inhalation of gastric fluid (gastric emptying) or curative treatment of possible aspiration by antibiotics, and cortico-steroids. Diuretics can be useful, as well as cardiotonics.

  17. 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.

  18. 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

  19. Pulmonary edema following transcatheter closure of atrial septal defect

    PubMed Central

    Chigurupati, Keerthi; Reshmi, Liza Jose; Gadhinglajkar, Shrinivas; Venkateshwaran, S.; Sreedhar, Rupa

    2015-01-01

    We describe an incident of development of acute pulmonary edema after the device closure of a secundum atrial septal defect in a 52-year-old lady, which was treated with inotropes, diuretics and artificial ventilation. Possibility of acute left ventricular dysfunction should be considered after the defect closure in the middle-aged patients as the left ventricular compliance may be reduced due to increased elastic stiffness and diastolic dysfunction. Baseline left atrial pressure may be > 10 mmHg in these patients. Associated risk factors for the left ventricular dysfunction are a large Qp:Qs ratio, systemic hypertension, severe pulmonary hypertension and paroxysmal atrial fibrillation. PMID:26139760

  20. [The role of BDNF in brain ischemia pulmonary edema].

    PubMed

    Zhang, Yun-Hui; Wang, Ting-Hua

    2012-11-01

    Brain ischemia pulmonary edema(BIPE)is a critical type of the neurogenic pulmonary edema (NPE), with acute development and progression and high mortality. The study on mechanism of BIPE has important scientific significance and substantial practice values. NPE, as a complicated physiopathology condition, is not resulted from single factor but systemic events including the changes in nervous system, body fluid regulation and endocrine involved in central nervous system after the injury. The studies on this topic in this current issue suggested that brain-derived neurotrophic factor (BDNF) could involve in the pathogenesis procedure of NPE following brain ischemia, which indicated that the crucial role of BDNF in the NPE after BIPE. The findings of these studies pave a way for the treatment of BIPE by using BDNF administration in future clinic trail.

  1. Noncardiac Pulmonary Edema induced by Sitagliptin Treatment

    PubMed Central

    Belice, Tahir; Yuce, Suleyman; Kizilkaya, Bayram; Kurt, Aysel; Cure, Erkan

    2014-01-01

    A 74-year-old male patient with type 2 diabetes mellitus admitted to the emergency department with the complaints of progressive breathlessness, dry cough, and swollen lower extremities. Our patient had type 2 diabetes mellitus and hypertension for 3 years. His HbA1c was not within the target range so sitagliptin was added to on-going therapy. After 1 week of starting sitagliptin therapy, even though the patient had not heart failure he applied to the emergency department with a complaint of dyspnea. The cardiovascular safety and efficacy of many anti-hyperglycemic agents such as sitagliptin, saxagliptin are unclear. Our case has shown that dipeptidyl peptidase 4 inhibitors may cause pulmonary edema. Hence, it should be used with cautious, especially in patients with heart failure. PMID:25657966

  2. Glyphosate Poisoning with Acute Pulmonary Edema

    PubMed Central

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

    2014-01-01

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

  3. Exercise-Induced Pulmonary Edema in a Triathlon

    PubMed Central

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

    2015-01-01

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

  4. Acute pulmonary edema after diazepam-ketamine in a dog.

    PubMed

    Boutureira, Joseph; Trim, Cynthia M; Cornell, Karen K

    2007-09-01

    An 8-year-old mixed-breed dog was anesthetized for colonoscopy. Moderate sedation was produced by premedication with glycopyrrolate, acepromazine, and hydromorphone, and anesthesia was induced by IV injection of diazepam and ketamine. Frothy, reddish-colored fluid flowed from the endotracheal tube immediately after endotracheal intubation but ceased after several minutes. Furosemide was injected IV. Anesthesia was maintained by sevoflurane in oxygen. Ventilation and arterial blood pressure were satisfactory, however, after oxygen was administered to maintain normal hemoglobin saturation. Radiography revealed changes consistent with a diagnosis of pulmonary edema. The following day, ventricular premature contractions developed and atrial dissociation, valvular regurgitation, and pulmonary hypertension were diagnosed on echocardiography. The proposed etiology is either profound transient hypotension and/or pulmonary hypertension induced by ketamine. The cardiac abnormalities that were present the following day suggest that myocardial dysfunction after induction of anesthesia was more severe than was apparent as assessed by routine physical examination and monitoring methods.

  5. Late-onset pulmonary edema due to propofol.

    PubMed

    Inal, M T; Memis, D; Vatan, I; Cakir, U; Yildiz, B

    2008-08-01

    Pulmonary edema after the administration of propofol has rarely been reported. In this case report, we describe pulmonary edema due to the administration of propofol during a Cesarean section and while in the intensive care unit. The skin tests demonstrated strong positive weal and flare reactions to propofol. The patient was treated successfully with mechanical ventilatory support. This report emphasizes that this fatal complication may be seen with propofol and underlying mechanisms and therapeutic approach are discussed.

  6. 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

  7. Acute pulmonary edema following inflation of arterial tourniquet.

    PubMed

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

    2014-10-01

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

  8. Negative Pressure Pulmonary Edema Associated with Anterior Cervical Spine Surgery

    PubMed Central

    Yoneda, Masana; Tanaka, Yasuhito

    2014-01-01

    We report a very rare case of negative pressure pulmonary edema (NPPE) that occurred immediately after anterior cervical discectomy and fusion (ACDF). The patient was a 25-year-old man who sustained a facet fracture-dislocation of C5 during a traffic accident. After ACDF, he developed NPPE and needed mechanical ventilation. Fortunately, he recovered fully within 24 hours. NPPE is a rare postoperative complication that may occur after cervical spine surgery. The aims of this report are to present information regarding the diagnosis and emergent treatment of NPPE, and to review the previous literature regarding this serious complication. PMID:25558327

  9. Emergent Unilateral Renal Artery Stenting for Treatment of Flash Pulmonary Edema: Fact or Fiction?

    PubMed Central

    Khan, Asaad Akbar; McFadden, Eugene Patrick

    2015-01-01

    Flash pulmonary edema is characteristically sudden in onset with rapid resolution once appropriate therapy has been instituted (Messerli et al., 2011). Acute increase of left ventricular (LV) end diastolic pressure is the usual cause of sudden decompensated cardiac failure in this patient population. Presence of bilateral renal artery stenosis or unilateral stenosis in combination with a single functional kidney in the susceptible cohort is usually blamed for this condition. We describe a patient who presented with flash pulmonary edema in the setting of normal coronary arteries. Our case is distinct as our patient developed flash pulmonary edema secondary to unilateral renal artery stenosis in the presence of bilateral functioning kidneys. Percutaneous stent implantation in the affected renal artery resulted in rapid resolution of pulmonary edema. PMID:25793128

  10. Characterization of an epizootic of pulmonary edema in swine associated with fumonisin in corn screenings.

    PubMed

    Osweiler, G D; Ross, P F; Wilson, T M; Nelson, P E; Witte, S T; Carson, T L; Rice, L G; Nelson, H A

    1992-01-01

    In 1989, corn screenings were associated with acute interstitial pulmonary edema, hydrothorax, and death in swine. Attack rate was 5-50%, case fatality rate was 50-90%, and clinical course was 1-2 days. Screenings from farms with pigs affected with pulmonary edema contained 20-330 micrograms fumonisin B1 per gram. Screenings containing 92 micrograms fumonisin B1 per gram fed to weanling pigs caused pulmonary edema and death. Sterilized corn inoculated with Fusarium moniliforme and diluted 1:1 with clean corn contained fumonisin B1 (17 micrograms/g) and caused acute pulmonary edema when fed for 5 days. Survivors developed subacute hepatotoxicosis with individual hepatocellular necrosis, hepatomegalocytosis, and increased numbers of mitotic figures. Similar liver lesions occurred in pigs given fumonisin B1 intravenously at 0.8 mg/kg body weight for 14 days.

  11. Lung ultrasound for monitoring cardiogenic pulmonary edema.

    PubMed

    Cortellaro, Francesca; Ceriani, Elisa; Spinelli, Monica; Campanella, Carlo; Bossi, Ilaria; Coen, Daniele; Casazza, Giovanni; Cogliati, Chiara

    2016-07-29

    Several studies address the accuracy of lung ultrasound (LUS) in the diagnosis of cardiogenic pulmonary edema (CPE) evaluating the interstitial syndrome, which is characterized by multiple and diffuse vertical artifacts (B-lines), and correlates with extravascular lung water. We studied the potential role of LUS in monitoring CPE response to therapy, by evaluating the clearance of interstitial syndrome within the first 24 h after Emergency Department (ED) admission. LUS was performed at arrival (T0), after 3 (T3) and 24 (T24) hours. Eleven regions were evaluated in the antero-lateral chest; the B-lines burden was estimated in each region (0 = no B-lines, 1 = multiple B-lines, 2 = confluent B-lines/white lung) and a mean score (B-Score, range 0-2) was calculated. Patients received conventional CPE treatment. Blood chemistry, vital signs, blood gas analysis, diuresis at T0, T3, T24 were also recorded. A complete echocardiography was obtained during hospitalization. Forty-one patients were enrolled. Respiratory and hemodynamic parameters improved in all patients between T0 and T3 and between T3 and T24. Mean B-score significantly decreased at T3 (from 1.59 ± 0.40 to 0.73 ± 0.44, P < 0.001) and between T3 and T 24 (from 0.73 ± 0.44 to 0.38 ± 0.33, P < 0.001). B-score was higher in the lower pulmonary regions at any time. At final evaluation (T24) 75 % of apical and only 38 % of basal regions were cleared. LUS allows one to assess the clearance of interstitial syndrome and its distribution in the early hours of treatment of CPE, thus representing a possible tool to guide therapy titration.

  12. The pathogenesis of pulmonary edema in acute pancreatitis.

    PubMed Central

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

    1975-01-01

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

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

    PubMed Central

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

    2015-01-01

    Objective Pulmonary edema is frequently observed after a successful resuscitation in out-of-hospital cardiac arrest (OHCA) patients. Currently, its risk factors and prognostic implications are mostly unknown. Methods Adult OHCA patients with a presumed cardiac etiology who achieved sustained return of spontaneous circulation (ROSC) in emergency department were retrospectively analyzed. The patients were grouped according to the severity of consolidation on their initial chest X-ray (group I, no consolidation; group II, patchy consolidations; group III, consolidation involving an entire lobe; group IV, total white-out of any lung). The primary objective was to identify the risk factors of developing severe pulmonary edema (group III or IV). The secondary objective was to evaluate the association between long-term prognosis and the severity of pulmonary edema. Results One hundred and seven patients were included. Total duration of cardiopulmonary resuscitation (CPR) and initial pCO2 level were both independent predictors of developing severe pulmonary edema with their odds ratio (OR) being 1.02 (95% confidence interval [CI], 1.00 to 1.04; per 1 minute) and 1.04 (95% CI, 1.01 to 1.07; per 1 mmHg), respectively. The long term prognosis was significantly poor in patients with severe pulmonary edema with a OR for good outcome (6-month cerebral performance category 1 or 2) being 0.22 (95% CI, 0.06 to 0.79) in group III and 0.16 (95% CI, 0.04 to 0.63) in group IV compared to group I. Conclusion The duration of CPR and initial pCO2 level were both independent predictors for the development of severe pulmonary edema after resuscitation in emergency department. The severity of the pulmonary edema was significantly associated with long-term outcome. PMID:27752581

  14. Poststreptococcal glomerulonephritis with pulmonary edema presenting as respiratory distress.

    PubMed

    Chiu, Chih-Yung; Huang, Yhu-Chering; Wong, Kin-Sun; Hsia, Shao-Hsuan; Lin, Chi-Jen; Lin, Tzou-Yien

    2004-11-01

    Acute poststreptococcal glomerulonephritis(PSGN) is characterized by an abrupt onset of edema,hypertension, and hematuria. Although the association of pulmonary edema with acute glomerulonephritis has been established, it is uncommon for children with PSGN to present with respiratory distress due to pulmonary edema. We encountered six such patients, aged 6-10 years, during a 10-month period. The demographic data, clinical manifestations, laboratory data, radiographic pictures, and clinical courses were collected. All patients presented to the primary pediatricians with dyspnea and alveolar infiltrates with bilateral pleural effusions on plain chest radiographs that were misinterpreted as pneumonia initially. The diagnosis of PSGN was de-layed until the awareness of the presence of pulmonary edema complicating PSGN. Subsequent urinalysis and blood pressure measurement all showed microscopic hematuria and hypertension. Elevated serum antistreptolysin 0 titers and depressed serum complement C3 levels confirmed the diagnosis of PSGN. Two patients progressed to respiratory failure because of a delayed diagnosis of PSGN. All patients recovered without sequelae following appropriate diuresis and antihypertensive therapy. We conclude that in preschool and school-age children who present with dyspneic respirations and a chest radiograph showing radiographic features of pulmonary edema, proper evaluation including blood pressure recording and urinalysis should be performed immediately. Prompt diagnosis and early therapy of PSGNmay avoid mortality and unnecessary therapeutic intervention.

  15. Neurogenic pulmonary edema: successful treatment with IV phentolamine.

    PubMed

    Davison, Danielle L; Chawla, Lakhmir S; Selassie, Leelie; Tevar, Rahul; Junker, Christopher; Seneff, Michael G

    2012-03-01

    Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant CNS insult. The cause is believed to be a surge of catecholamines that results in cardiopulmonary dysfunction. Although there are myriad case reports describing CNS events that are associated with this syndrome, few studies have identified specific treatment modalities. We present a case of NPE caused by an intracranial hemorrhage from a ruptured arteriovenous malformation. We uniquely document a rise and fall of serum catecholamine levels correlating with disease activity and a dramatic clinical response to IV phentolamine.

  16. Asymmetric pulmonary edema after scorpion sting: a case report.

    PubMed

    Razi, Ebrahim; Malekanrad, Elaheh

    2008-01-01

    A 12-year-old boy was referred with acute asymmetric pulmonary edema (APE) four-hour after scorpion sting to Emergency department. On admission, the main clinical manifestations were: dyspnea, tachypnea, and tachycardia. Chest x-ray revealed APE predominantly on the right hemithorax. The patient was treated with oxygen, intravenous frusemide and digoxin and discharged on the sixth hospital day in a good condition. This case report emphasizes the occurrence of asymmetric pulmonary edema after severe scorpion envenomation within few hours immediately after the sting.

  17. [The x-ray diagnosis of a predisposition to nephrogenic pulmonary edema in glomerulonephritis patients].

    PubMed

    Kamenetskiĭ, M S; Pervak, M B; Tkachenko, G D; Vernikov, B L

    1995-01-01

    To develop criteria for determining predisposition to pulmonary edema in patients with glomerulonephritis, clinical, laboratory and X-ray examinations were made in 697 patients with glomerulonephritis at different stages of its development. X-ray examination included chest tele X-ray and its densitometric analysis. Twenty two patients underwent computerized tomography with histographic analysis. In 106 patients, X-ray findings were compared with the volume of circulating blood, cardiac and stroke indices. Changes in the lungs and pleural cavities were found in 22.7%, pulmonary edema was revealed in 15.7% of the patients. The prognostically unfavourable criteria for the development of pulmonary edema were found to be Stage II pulmonary venous hypertension with hypervolemia and peripheral edemas. The densitometrically detected increase in the density of the lower lungs in patients with Stage II venous hypertension suggests early manifestations of interstitial edema of the lung and the narrowing of the histogram angle limited by its ascending and descending lines is indicative of the fact that interstitial edema progresses to alveolar one.

  18. A Rare Cause of Pulmonary Edema in the Postoperative Period

    PubMed Central

    Chatterjee, Kshitij; Mittadodla, Penchala S.; Colaco, Clinton; Jagana, Rajani

    2017-01-01

    With the increasing longevity of the population, the annual rates of hip arthroplasties performed have been steadily increasing over the past decade. Given the presence of medical comorbidities in the older patients, the peri-operative care of these individuals requires multi-specialty care, now more than ever. Hip arthroplasty is generally well tolerated, with early mortality after the procedure being <1%. Bone cement implantation syndrome (BCIS) is an entity that is occasionally encountered during or after the surgery. It is characterized by hypoxemia, hypotension, cardiac arrhythmias, and cardiac arrest leading to death, in severe cases. We report a case of a middle-aged female who developed refractory hypotension and pulmonary edema while undergoing hemiarthroplasty for a pathological femoral neck fracture and experienced cardiac arrest in the immediate postoperative period. Critical care physicians must familiarize themselves with promptly diagnosing and managing BCIS. PMID:28250610

  19. A Rare Cause of Pulmonary Edema in the Postoperative Period.

    PubMed

    Chatterjee, Kshitij; Mittadodla, Penchala S; Colaco, Clinton; Jagana, Rajani

    2017-02-01

    With the increasing longevity of the population, the annual rates of hip arthroplasties performed have been steadily increasing over the past decade. Given the presence of medical comorbidities in the older patients, the peri-operative care of these individuals requires multi-specialty care, now more than ever. Hip arthroplasty is generally well tolerated, with early mortality after the procedure being <1%. Bone cement implantation syndrome (BCIS) is an entity that is occasionally encountered during or after the surgery. It is characterized by hypoxemia, hypotension, cardiac arrhythmias, and cardiac arrest leading to death, in severe cases. We report a case of a middle-aged female who developed refractory hypotension and pulmonary edema while undergoing hemiarthroplasty for a pathological femoral neck fracture and experienced cardiac arrest in the immediate postoperative period. Critical care physicians must familiarize themselves with promptly diagnosing and managing BCIS.

  20. Pulmonary edema induced by calcium-channel blockade for tocolysis.

    PubMed

    Bal, Laurence; Thierry, Stéphane; Brocas, Elsa; Adam, Marie; Van de Louw, Andry; Tenaillon, Alain

    2004-09-01

    Nicardipine is used in the treatment of premature labor. There are no previous reports in the anesthesia literature of serious side effects associated with this drug. We report a case of pulmonary edema induced by nicardipine therapy for tocolysis in a pregnant 27-yr-old patient admitted to our hospital for preterm labor with intact membranes at 27 wk of gestation.

  1. Ibuprofen prevents synthetic smoke-induced pulmonary edema

    SciTech Connect

    Shinozawa, Y.; Hales, C.; Jung, W.; Burke, J.

    1986-12-01

    Multiple potentially injurious agents are present in smoke but the importance of each of these agents in producing lung injury as well as the mechanisms by which the lung injury is produced are unknown. In order to study smoke inhalation injury, we developed a synthetic smoke composed of a carrier of hot carbon particles of known size to which a single known common toxic agent in smoke, in this case HCI, could be added. We then exposed rats to the smoke, assayed their blood for the metabolites of thromboxane and prostacyclin, and intervened shortly after smoke with the cyclooxygenase inhibitors indomethacin or ibuprofen to see if the resulting lung injury could be prevented. Smoke exposure produced mild pulmonary edema after 6 h with a wet-to-dry weight ratio of 5.6 +/- 0.2 SEM (n = 11) compared with the non-smoke-exposed control animals with a wet-to-dry weight ratio of 4.3 +/- 0.2 (n = 12), p less than 0.001. Thromboxane B, and 6-keto-prostaglandin F1 alpha rose to 1660 +/- 250 pg/ml (p less than 0.01) and to 600 +/- 100 pg/ml (p greater than 0.1), respectively, in the smoke-injured animals compared with 770 +/- 150 pg/ml and 400 +/- 100 pg/ml in the non-smoke-exposed control animals. Indomethacin (n = 11) blocked the increase in both thromboxane and prostacyclin metabolites but failed to prevent lung edema.

  2. Cardiogenic Pulmonary Edema in a Dog Following Initiation of Therapy for Concurrent Hypoadrenocorticism and Hypothyroidism.

    PubMed

    Paik, Jooyae; Kang, Ji-Houn; Chang, Dongwoo; Yang, Mhan-Pyo

    A 5 yr old intact female cocker spaniel dog weighing 7.8 kg was referred with anorexia, vomiting, and depression. At referral, the dog was diagnosed initially with typical hypoadrenocorticism, and 2 d later, concurrent primary hypothyroidism was detected. Hormonal replacement therapies, including fludrocortisone, prednisolone, and levothyroxine, were initiated, but a few days later the dog became abruptly tachypneic, and thoracic radiographs indicated the development of pulmonary edema. Echocardiography showed that there were abnormalities indicating impaired left ventricular function, although the heart valves were normal. Following treatment with pimobendan and furosemide, the pulmonary edema resolved. The dog had no recurrence of the clinical signs after 10 mo of follow-up, despite being off all cardiac medications; consequently, the cardiac failure was transient or reversible in this dog. The case report describes the stepwise diagnosis and successful treatment of cardiogenic pulmonary edema after initiation of hormonal replacement therapy for concurrent hypoadrenocorticism and hypothyroidism in a dog.

  3. Negative pressure pulmonary edema after nasal fracture reduction in an obese female patient: a case report

    PubMed Central

    Choi, Eunkyung; Yi, Junggu; Jeon, Younghoon

    2015-01-01

    Postoperative negative pressure pulmonary edema (NPPE) is a rare, but well-known life-threatening complication of acute upper airway obstruction (UAO) which develops after general anesthesia. The pronounced inspiratory efforts following UAO lead to excessive negative inspiratory pressure, which may cause acute pulmonary edema. Early recognition and prompt treatment of NPPE is necessary to prevent patient morbidity and mortality. In addition, the physician should carefully manage the patient who has risk factors of UAO to prevent this situation. We experienced a case of NPPE following laryngospasm after tracheal extubation in an obese patient who underwent open reduction of orbital wall and nasal bone surgery. PMID:26316826

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

    PubMed

    Sánchez Marteles, Marta; Urrutia, Agustín

    2014-03-01

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

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

    PubMed

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

    2014-01-01

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

  6. A delayed, unusual non-cardiogenic pulmonary edema after intravascular administration of non-ionic, low osmolar radiocontrast media for coronary angiography.

    PubMed

    Kang, Min-Ho; Nah, Jong-Chun

    2013-07-01

    Non-cardiogenic pulmonary edema (NCPE) is a rare adverse reaction to iodinated radiocontrast media (RCM), in which all previous cases were immediate reactions. A 56-year-old male was given iopamidol, a non-ionic, low osmolar RCM, during coronary artery angiography. He developed pulmonary edema and fever a day after the procedure. Despite diuretic therapy, the patient's pulmonary edema worsened and his high fever persisted. The patient's pulmonary edema was eventually resolved with intravenous steroid treatment. We interpreted the patient's condition as NCPE manifesting as a delayed reaction to RCM. To our knowledge, our case is the first to show NCPE as a delayed hypersensitivity reaction.

  7. Reexpansion pulmonary edema after chest drainage for pneumothorax: A case report and literature overview

    PubMed Central

    Verhagen, M.; van Buijtenen, J.M.; Geeraedts, L.M.G.

    2014-01-01

    Background Reexpansion pulmonary edema (RPE) is a rare complication that may occur after treatment of lung collapse caused by pneumothorax, atelectasis or pleural effusion and can be fatal in 20% of cases. The pathogenesis of RPE is probably related to histological changes of the lung parenchyma and reperfusion-damage by free radicals leading to an increased vascular permeability. RPE is often self-limiting and treatment is supportive. Case report A 76-year-old patient was treated by intercostal drainage for a traumatic pneumothorax. Shortly afterwards he developed reexpansion pulmonary edema and was transferred to the intensive care unit for ventilatory support. Gradually, the edema and dyspnea diminished and the patient could be discharged in good clinical condition. Conclusion RPE is characterized by rapidly progressive respiratory failure and tachycardia after intercostal chest drainage. Early recognition of signs and symptoms of RPE is important to initiate early management and allow for a favorable outcome. PMID:26029567

  8. Non-cardiogenic pulmonary edema complicating electroconvulsive therapy: short review of the pathophysiology and diagnostic approach.

    PubMed

    Manne, Janaki R; Kasirye, Yusuf; Epperla, Narendranath; Garcia-Montilla, Romel J

    2012-08-01

    Acute pulmonary edema complicating electroconvulsive therapy is an extremely uncommon event that has rarely been described in the literature. Different theories, including one suggesting a cardiogenic component, have been proposed to explain its genesis. The present report describes a classic presentation of this condition with review of its potential mechanisms and diagnostic approach. After successful completion of a session of electroconvulsive therapy, a 42-year-old woman with major depressive disorder developed acute systemic high blood pressure, shortness of breath, and hemoptysis. A chest radiograph demonstrated diffuse bilateral pulmonary infiltrates. Initially cardiogenic pulmonary edema was presumed, but an extensive diagnostic work-up demonstrated normal systolic and diastolic left ventricular function, and with only supportive measures, a complete clinical and radiographic recovery was achieved within 48 hours. The present case does not support any cardiogenic mechanism in the genesis of this condition.

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

    PubMed

    Blanco, Pablo A; Cianciulli, Tomás F

    2016-05-01

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

  10. [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.

  11. 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.

  12. Pulmonary Embolism Masquerading as High Altitude Pulmonary Edema at High Altitude.

    PubMed

    Pandey, Prativa; Lohani, Benu; Murphy, Holly

    2016-12-01

    Pandey, Prativa, Benu Lohani, and Holly Murphy. Pulmonary embolism masquerading as high altitude pulmonary edema at high altitude. High Alt Med Biol. 17:353-358, 2016.-Pulmonary embolism (PE) at high altitude is a rare entity that can masquerade as or occur in conjunction with high altitude pulmonary edema (HAPE) and can complicate the diagnosis and management. When HAPE cases do not improve rapidly with descent, other diagnoses, including PE, ought to be considered. From 2013 to 2015, we identified eight cases of PE among 303 patients with initial diagnosis of HAPE. Upon further evaluation, five had deep vein thrombosis (DVT). One woman had a contraceptive ring and seven patients had no known thrombotic risks. PE can coexist with or mimic HAPE and should be considered in patients presenting with shortness of breath from high altitude regardless of thrombotic risk.

  13. Pulmonary Embolism Masquerading as High Altitude Pulmonary Edema at High Altitude

    PubMed Central

    Lohani, Benu; Murphy, Holly

    2016-01-01

    Abstract Pandey, Prativa, Benu Lohani, and Holly Murphy. Pulmonary embolism masquerading as high altitude pulmonary edema at high altitude. High Alt Med Biol. 17:353–358, 2016.—Pulmonary embolism (PE) at high altitude is a rare entity that can masquerade as or occur in conjunction with high altitude pulmonary edema (HAPE) and can complicate the diagnosis and management. When HAPE cases do not improve rapidly with descent, other diagnoses, including PE, ought to be considered. From 2013 to 2015, we identified eight cases of PE among 303 patients with initial diagnosis of HAPE. Upon further evaluation, five had deep vein thrombosis (DVT). One woman had a contraceptive ring and seven patients had no known thrombotic risks. PE can coexist with or mimic HAPE and should be considered in patients presenting with shortness of breath from high altitude regardless of thrombotic risk. PMID:27768392

  14. 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

  15. Is high altitude pulmonary edema relevant to Hawai'i?

    PubMed

    Cornell, Seth Lewis

    2014-11-01

    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.

  16. Negative pressure pulmonary edema in healthy cosmetic surgery patients.

    PubMed

    Dieu, Tam; Upjohn, Edward

    2003-01-01

    Anesthetic complications are uncommon in young and healthy patients undergoing cosmetic surgery. We report 2 cases of negative pressure pulmonary edema (NPPE) in young patients, 1 who underwent rhinoplasty and another who underwent augmentation mammaplasty and suction-assisted lipoplasty of the thighs and buttocks This rare and potentially fatal complication requires admission to an intensive-care unit and delayed discharge. Although cases of NPPE have been reported in the medical and anesthetic literature, NPPE in plastic surgery has never been reported previously.

  17. 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

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

    PubMed

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

    2013-10-15

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

  19. Chest ultrasonography in emergency Cesarean delivery in multi-valvular heart disease with pulmonary edema during spinal anesthesia.

    PubMed

    Samanta, Sukhen; Samanta, Sujay; Ghatak, Tanmoy; Grover, V K

    2014-05-01

    Valvular heart disease in a parturient presenting for Cesarean section is challenging. A 25 year old primigravida parturient with severe mitral stenosis, mild mitral regurgitation, mild aortic regurgitation, and mild pulmonary arterial hypertension required Cesarean delivery after developing pulmonary edema. Low-dose spinal with hyperbaric bupivacine 0.5% 1.8 mL plus 25 μg of fentanyl was used for anesthesia. Chest ultrasonography (US) and transthoracic echocardiography (TTE) were used for monitoring purposes. Spinal-induced preload reduction improved the pulmonary edema, as evidenced by chest US. Chest US and TTE helped in fluid management.

  20. 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.

  1. A case of recurrent swimming-induced pulmonary edema in a triathlete: the need for awareness.

    PubMed

    Smith, R; Brooke, D; Kipps, C; Skaria, B; Subramaniam, V

    2016-08-03

    This report discusses a rare case of a 55-year-old female triathlete who developed recurrent episodes of swimming-induced pulmonary edema (SIPE). She had two hospital admissions with pulmonary edema after developing breathlessness while swimming, including a near-drowning experience in an open water swim. With increasing popularity of triathlon and open water sports, this case highlights the importance of a greater awareness of SIPE among health professionals, event organizers, and athletes. This report explores the previous reported cases in triathletes and those who have suffered recurrent episodes. It is paramount that an accurate diagnosis is made as these individuals may be at an increased risk of future life-threatening episodes.

  2. Takotsubo Cardiomyopathy in the Setting of Immersion Pulmonary Edema: Case Series

    PubMed Central

    Sorrentino, Dante; Azuma, Steven

    2015-01-01

    Immersion Pulmonary Edema is a unique medical condition being increasingly described in the medical literature as sudden-onset pulmonary edema in the setting of scuba diving and or swimming. Case reports have associated immersion pulmonary edema with cardiac dysfunction, but there are no known case reports describing submersion pulmonary edema resulting in Takotsubo cardiomyopathy. We report on three patients with unique presentations of immersion pulmonary edema with associated Takotsubo cardiomyopathy. All three cases occurred in O‘ahu, Hawai‘i and were seen by the same cardiologist within a span of seven years. Each patient was scuba diving with sudden dyspnea with pulmonary edema on chest X-ray. Cardiac catheterization revealed no significant epicardial stenosis. Wall motion abnormalities resolved. EKG's showed typical evolution of symmetric T wave inversion. Immersion pulmonary edema and Takotsubo cardiomyopathy may occur together and may be more common than initially thought. Dyspnea has been long known to be stressful as in “waterboarding.” Stressful events are known to trigger Takotsubo cardiomyopathy. Takotsubo cardiomyopathy should be considered as a possible complication of immersion pulmonary edema and EKG's, troponins, echocardiogram and in the appropriate situation cardiac catheterization should be considered.

  3. Acute pulmonary edema and airway hemorrhage in a goat during sevoflurane anesthesia.

    PubMed

    Adami, C; Levionnois, O; Spadavecchia, C

    2011-02-01

    A goat was scheduled for experimental surgery under general anesthesia. The first attempt of performing endotracheal intubation failed and provoked laryngeal spasm. After repeated succesful intubation of inhalation anesthesia was delivered in high concentrations of sevoflurane. Suddenly hypertension and tachycardia were observed, followed by foamy airway secretion and then severe airway hemorrhage. The authors hypothesize that laryngeal spasm provoked respiratory distress and pulmonary edema. The delivered high concentrations of sevoflurane probably enhanced a hyperadrenergic response, predisposing to the development of airway hemorrhage.

  4. Acute pulmonary edema caused by takotsubo cardiomyopathy in a pregnant woman undergoing transvaginal cervical cerclage

    PubMed Central

    Lee, Jae-Young; Kwon, Hyun-Jung; Park, Sang-Wook; Lee, Yu-Mi

    2017-01-01

    Abstract Background: The physiological changes associated with pregnancy may predispose pregnant women to pulmonary edema. Other known causes of pulmonary edema during pregnancy include tocolytic drugs, preeclampsia, eclampsia, and peripartum cardiomyopathy. Methods: We describe a rare case of pulmonary edema caused by takotsubo cardiomyopathy in a pregnant woman at 14 weeks of gestation who was undergoing emergency transvaginal cervical cerclage. Results: Intraoperative chest radiography revealed severe pulmonary edema and echocardiography indicated moderate left ventricular dysfunction with akinesia of the mid to apical left ventricular wall segment, which is reflective of takotsubo cardiomyopathy. Conclusion: With early detection and appropriate management, the patient was stabilized in a relatively short period of time. Based on her clinical signs and symptoms, we suspect that the pulmonary edema was caused by takotsubo cardiomyopathy. PMID:28072695

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

    PubMed Central

    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

  6. Delayed Pneumoperitoneum and Acute Pulmonary Edema Secondary to Acute Gastric Dilatation

    PubMed Central

    Ahn, Jae Yun; Kim, Jong Kun

    2015-01-01

    Pneumoperitoneum caused by acute gastric dilatation (AGD) is a very rare complication. We report a case of pneumoperitoneum and acute pulmonary edema caused by AGD in a patient with Parkinson’s disease. A 78-year-old woman presented with pneumonia and AGD. We inserted a nasogastric tube and administered empirical antibiotics. We performed an endoscopy, and perforation or necrosis of the stomach and pyloric stenosis were not observed. Thirty-six hours after admission, the patient suddenly developed dyspnea and shock, and eventually died. We suspected the cause of death was pneumoperitoneum and acute pulmonary edema caused by AGD during the conservative treatment period. Immunocompromised patients with chronic illness require close observation even if they do not show any symptoms suggestive of complications. Even if the initial endoscopic or abdominal radiologic findings do not show gastric necrosis or perforation, follow-up with endoscopy is essential to recognize complications of AGD early. PMID:26668807

  7. Anti-thymocyte globulin induced non-cardiogenic pulmonary edema during renal transplantation.

    PubMed

    Parikh, Beena K; Bhosale, Guruprasad P; Shah, Veena R

    2011-10-01

    Non-cardiogenic pulmonary edema (NCPE) is a clinical syndrome characterized by simultaneous presence of severe hypoxemia, bilateral alveolar infiltrates on chest radiograph, without evidence of left atrial hypertension/congestive heart failure/fluid overload. The diagnosis of drugrelated NCPE relies upon documented exclusion of other causes of NCPE like gastric aspiration, sepsis, trauma, negative pressure pulmonary edema. We describe a 28year-old, 50 kg male with ASA risk III posted for laparoscopic renal transplantation, who developed NCPE after 4 hours of administration of rabbit anti-human thymocyte immunoglobulin (ATG). He was successfully treated with mechanical ventilatory support and adjuvant therapy. This report emphasizes that this fatal complication may occur with use of ATG.

  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.

  9. Edema

    MedlinePlus

    ... Schedules Nutrient Shortfall Questionnaire Home Diseases and Conditions Edema Edema Condition Family HealthSeniors Share Edema Table of Contents1. Overview2. Causes3. Diagnosis4. Treatment5. Questions ...

  10. Basiliximab induced non-cardiogenic pulmonary edema in two pediatric renal transplant recipients.

    PubMed

    Dolan, Niamh; Waldron, Mary; O'Connell, Marie; Eustace, Nick; Carson, Kevin; Awan, Atif

    2009-11-01

    We report two cases of non-cardiogenic pulmonary edema as a complication of basiliximab induction therapy in young pediatric renal transplant patients identified following a retrospective review of all pediatric renal transplant cases performed in the National Paediatric Transplant Centre, Childrens University Hospital, Temple Street, Dublin, Ireland. Twenty-eight renal transplantations, of which five were living-related (LRD) and 23 were from deceased donors (DD), were performed in 28 children between 2003 and 2006. In six cases, transplantations were pre-emptive. Immunosuppression was induced pre-operatively using a combination of basiliximab, tacrolimus and methylprednisolone in all patients. Basiliximab induction was initiated 2 h prior to surgery in all cases and, in 26 patients, basiliximab was re-administered on post-operative day 4. Two patients, one LRD and one DD, aged 6 and 11 years, respectively, developed acute non-cardiogenic pulmonary edema within 36 h of surgery. Renal dysplasia was identified as the primary etiological factor for renal failure in both cases. Both children required assisted ventilation for between 4 and 6 days. While both grafts had primary function, the DD transplant patient subsequently developed acute tubular necrosis and was eventually lost within 3 weeks due to thrombotic microangiopathy and severe acute antibody-mediated rejection despite adequate immunosuppression. Non-cardiogenic pulmonary edema is a potentially devastating post-operative complication of basiliximab induction therapy in young pediatric patients following renal transplantation. Early recognition and appropriate supportive therapy is vital for patient and, where possible, graft survival.

  11. [Nursing assessment and management of patients with cardiogenic pulmonary edema].

    PubMed

    Wang, Yu-Jyuan; Liao, Chieh-Yin; Kao, Chi-Wen

    2012-02-01

    Cardiogenic pulmonary edema (CPE) is a clinical health problem that induces impaired gas exchange, dyspnea and hypoxia. This serious condition results in acute respiratory failure and high mortality rate. This article suggests an effective approach to CPE patient clinical symptom assessment and management. In accordance with evidence-based methods, we searched Cochrane, CINAHL and ScienceDirect and identified four Oxford Ia or Ib reports that employed a randomized controlled trial, systematic review and meta-analysis. Results suggest that prompt application of a non-invasive positive ventilator, especially continuous positive or bi-level positive airway pressure, can help patients reduce intubation risks, ICU stay days, and mortality rates. The authors hope to see more clinical trials on this topic to support evidence-based clinical nursing care.

  12. [High altitude pulmonary edema. An experiment of nature to study the underlying mechanisms of hypoxic pulmonary hypertension and pulmonary edema in humans].

    PubMed

    Schwab, Marcos; Jayet, Pierre-Yves; Allemann, Yves; Sartori, Claudio; Scherrer, Urs

    2007-01-01

    High altitude constitutes an exciting natural laboratory for medical research. Over the past decade, it has become clear that the results of high-altitude research may have important implications not only for the understanding of diseases in the millions of people living permanently at high altitude, but also for the treatment of hypoxemia-related disease states in patients living at low altitude. High-altitude pulmonary edema (HAPE) is a life-threatening condition occurring in predisposed, but otherwise healthy subjects, and, therefore, allows to study underlying mechanisms of pulmonary edema in humans, in the absence of confounding factors. Over the past decade, evidence has accumulated that HAPE results from the conjunction of two major defects, augmented alveolar fluid flooding resulting from exaggerated hypoxic pulmonary hypertension, and impaired alveolar fluid clearance related to defective respiratory transepithelial sodium transport. Here, after a brief presentation of the clinical features of HAPE, we review this novel concept. We provide experimental evidence for the novel concept that impaired pulmonary endothelial and epithelial nitric oxide synthesis and/or bioavailability may represent the central underlying defect predisposing to exaggerated hypoxic pulmonary vasoconstriction and alveolar fluid flooding. We demonstrate that exaggerated pulmonary hypertension, while possibly a condition sine qua non, may not be sufficient to cause HAPE, and how defective alveolar fluid clearance may represent a second important pathogenic mechanism. Finally, we outline how this insight gained from studies in HAPE may be translated into the management of hypoxemia related disease states in general.

  13. 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.

  14. [Continuous spectrophotometry as a method to study pulmonary edema in isolated canine pulmonary lobe].

    PubMed

    Palomar Lever, A; Furuya Meguro, M E; Gómez González, A; Martínez Guerra, M L; Gertrudiz Salvador, N; Oppenheimer, L; Sandoval Zárate, J

    1996-01-01

    The aim of this paper is to introduce the spectrophotometric method to the study of pulmonary edema in isolated ex-vivo canine pulmonary lobe preparation. This spectrophotometric method is based on the on-line measure of light transmission in a column of blood, that is proportional to hematocrit. A second light is used to follow Evans blue dyed proteins. With this method we were able to measure the amount of edema in 10 isolated canine lobes. Both the filtration and reflection coefficient of the membrane as well as the characteristics of the filtrate could be calculated. The filtration coefficient was 0.6 +/- 0.4 ml/min (1.3 +/- 0.9 ml/min/100 g pulmonary, tissue) at maximum capillary pressure and the reflection coefficient was 0.53 +/- 0.07. With the spectrophotometric method we have the capability to study different aspects of lung edema formation. This method has the advantage of being exact and independent from pressure and volume induced vascular changes. It also allows the measurement of solute transport.

  15. [Effectiveness of oxygen therapy for pulmonary edema in patients with hypertensive crisis before hospitalization].

    PubMed

    Dolgikh, V T; Epifanov, V G; Lukach, V N

    2003-01-01

    The oxygen therapy, involving the KI-3M respiratory apparatus administered in the positive pressure regimen on expiration (8-10 cm aq. c.), used, before hospitalization, within the complex therapy of patients with pulmonary edema triggered by hypertensive crisis arrests fast enough the pulmonary edema, cuts the working time of an ER crew and promotes the ER efficiency. The key clinical manifestations of pulmonary edema were found to begin to go down on minutes 5 to 10 after the administration of artificial lungs ventilation (ALV) by oxygen with the positive pressure being on expiration end; such signs were totally stopped in 20-25 minutes.

  16. 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 ...

  17. 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.

  18. [Cardiogenic pulmonary edema - truth and myths in the perspective of emergency medicine].

    PubMed

    Osterwalder, J J

    2012-09-19

    This critical analysis of the traditional pathophysiological approach to the diagnosis and treatment of cardiogenic pulmonary edema calls into question some long-established ideas and interventions that ought to be replaced by better evidence-based concepts.

  19. 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

  20. 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.

  1. Management of acute cardiogenic pulmonary edema: a literature review.

    PubMed

    Johnson, Jeremy M

    2009-01-01

    Acute cardiogenic pulmonary edema (CPE) is a pathology frequently seen in patients presenting to emergency departments (EDs) and can usually be attributed to preexisting cardiovascular disease. Heart failure alone accounts for more than 1 million hospital admissions annually and has one of the highest ED morbidity and mortality to date (). Historically, CPE has been managed by the treating clinician in a manner that is based largely on anecdotal evidence. Furosemide (Lasix), morphine, and nitroglycerin have historically been the baseline standard for drug therapy in CPE management. A lack of drastic improvement in the patient's condition over the course of the ED visit may reflect a management style that results in higher morbidity and mortality for CPE patients. Several recent articles provide evidence-based outcomes that suggest changing standard therapy along with the adjunctive use of other medications. These articles also describe treatment modalities that result in a marked improvement in the management of patients with CPE along with decreases in adverse outcomes and hospital length of stay. The goal of this article is to present a summary of the evidence regarding the management of CPE and discuss the implications for current practice.

  2. Noncardiogenic Pulmonary Edema after Amlodipine Overdose without Refractory Hypotension and Bradycardia

    PubMed Central

    Hedaiaty, M.; Eizadi-Mood, N.; Sabzghabaee, A. M.

    2015-01-01

    Amlodipine overdose can be life-threatening when manifesting as noncardiogenic pulmonary edema. Treatment remains challenging. We describe a case of noncardiogenic pulmonary edema without refractory hypotension and bradycardia after ingestion of 500 milligram amlodipine with suicidal intent. Mechanical ventilation, dexamethasone, atrovent HFA (ipratropium), pulmicort inhalation, and antibiotic therapy were used for the management. Length of hospital stay was 11 days. The patient was discharged with full recovery. PMID:26075111

  3. Profiling of ARDS Pulmonary Edema Fluid Identifies a Metabolically Distinct Subset.

    PubMed

    Rogers, Angela J; Contrepois, Kevin; Wu, Manhong; Zheng, Ming; Peltz, Gary; Ware, Lorraine B; Matthay, Michael A

    2017-03-03

    There is considerable biologic and physiologic heterogeneity among patients who meet standard clinical criteria for acute respiratory distress syndrome (ARDS). In this study, we tested the hypothesis that there exists a sub-group of ARDS patients who exhibit a metabolically distinct profile. We examined undiluted pulmonary edema fluid obtained at the time of endotracheal intubation from 16 clinically phenotyped ARDS patients and 13 control patients with hydrostatic pulmonary edema. Non-targeted metabolic profiling was carried out on the undiluted edema fluid. Univariate and multivariate statistical analyses including principal components analysis (PCA) and partial least squares discriminant analysis (PLSDA) were conducted to find discriminant metabolites. 760 unique metabolites were identified in the pulmonary edema fluid of these 29 patients. We found that a subset of ARDS patients (6/16, 38%) presented a distinct metabolic profile with the overrepresentation of 235 metabolites compared to edema fluid from the other 10 ARDS patients, whose edema fluid metabolic profile was indistinguishable from those of the 13 control patients with hydrostatic edema. This "high metabolite" endotype was characterized by higher concentrations of metabolites belonging to all of the main metabolic classes including lipids, amino acids, and carbohydrates. This distinct group with high metabolite levels in the edema fluid was also associated with a higher mortality rate. Thus, metabolic profiling of the edema fluid of ARDS patients supports the hypothesis that there is considerable biologic heterogeneity among ARDS patients who meet standard clinical and physiologic criteria for ARDS.

  4. Prevalence of pulmonary edema among the deceased cases with acute Methadone poisoning: A report from Iran

    PubMed Central

    Eizadi-Mood, Nastaran; Naeini, Seyed Amir Hossein Madani; Hedaiaty, Mahrang; Sabzghabaee, Ali Mohammad; Moudi, Maryam

    2016-01-01

    Objective: Methadone poisoning is common in our society, mainly in drug addicts. One of its lethal complications is pulmonary edema. Therefore, we evaluated the prevalence of pulmonary edema in the deceased cases with methadone poisoning and its possible relationship with some medical variables. Methods: In this cross-sectional study which was done in 2014, we have investigated the deceased patients with methadone toxicity who underwent autopsy at Isfahan Forensic Medicine Department (Iran). All variables including age, gender, and autopsy findings were recorded and analyzed. Demographic characteristics and medical complications of the patients were compared between the patients with or without pulmonary edema in the autopsy findings. Findings: There were 64 cases who died with methadone poisoning during the 1-year study period. The average age of cases (±standard deviation) was 32.1 ± 10.29 years, among which 92.2% were male. Based on the autopsy findings, 64.1% were diagnosed with pulmonary edema. There was no statistically significant relationship between pulmonary edema and age, gender, history of addiction, and hepatic or cardiovascular complications. Conclusion: Pulmonary edema is a common finding in deceased methadone poisoning cases and must be considered and ruled out in patients with acute methadone toxicity. PMID:27843967

  5. High Altitude Pulmonary Edema in an Experienced Mountaineer. Possible Genetic Predisposition

    PubMed Central

    Whitlow, Kenneth S.; Davis, Babette W.

    2014-01-01

    High altitude pulmonary edema (HAPE) is a form of high altitude illness characterized by cough, dyspnea upon exertion progressing to dyspnea at rest and eventual death, seen in patients who ascend over 2,500 meters, particularly if that ascent is rapid. This case describes a patient with no prior history of HAPE and extensive experience hiking above 2,500 meters who developed progressive dyspnea and cough while ascending to 3,200 meters. His risk factors included rapid ascent, high altitude, male sex, and a possible genetic predisposition for HAPE. PMID:25493133

  6. Transthoracic lung ultrasound in normal dogs and dogs with cardiogenic pulmonary edema: a pilot study.

    PubMed

    Rademacher, Nathalie; Pariaut, Romain; Pate, Julie; Saelinger, Carley; Kearney, Michael T; Gaschen, Lorrie

    2014-01-01

    Pulmonary edema is the most common complication of left-sided heart failure in dogs and early detection is important for effective clinical management. In people, pulmonary edema is commonly diagnosed based on transthoracic ultrasonography and detection of B line artifacts (vertical, narrow-based, well-defined hyperechoic rays arising from the pleural surface). The purpose of this study was to determine whether B line artifacts could also be useful diagnostic predictors for cardiogenic pulmonary edema in dogs. Thirty-one normal dogs and nine dogs with cardiogenic pulmonary edema were prospectively recruited. For each dog, presence or absence of cardiogenic pulmonary edema was based on physical examination, heartworm testing, thoracic radiographs, and echocardiography. A single observer performed transthoracic ultrasonography in all dogs and recorded video clips and still images for each of four quadrants in each hemithorax. Distribution, sonographic characteristics, and number of B lines per thoracic quadrant were determined and compared between groups. B lines were detected in 31% of normal dogs (mean 0.9 ± 0.3 SD per dog) and 100% of dogs with cardiogenic pulmonary edema (mean 6.2 ± 3.8 SD per dog). Artifacts were more numerous and widely distributed in dogs with congestive heart failure (P < 0.0001). In severe cases, B lines increased in number and became confluent. The locations of B line artifacts appeared consistent with locations of edema on radiographs. Findings from the current study supported the use of thoracic ultrasonography and detection of B lines as techniques for diagnosing cardiogenic pulmonary edema in dogs.

  7. 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

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

    PubMed

    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.

  9. 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.

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

    PubMed

    Freeman, Kimberly; Shalit, Marc; Stroh, Geoffrey

    2004-01-01

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

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

    PubMed Central

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

    2016-01-01

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

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

    PubMed

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

    2016-01-01

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

  13. [Pulmonary hypertension and lung edema at high altitude. Role of endothelial dysfunction and fetal programming].

    PubMed

    Schwab, Marcos; Allemann, Yves; Rexhaj, Emrush; Rimoldi, Stefano F; Sartori, Claudio; Scherrer, Urs

    2012-01-01

    High altitude constitutes an exciting natural laboratory for medical research. While initially, the aim of high-altitude research was to understand the adaptation of the organism to hypoxia and find treatments for altitude-related diseases, over the past decade or so, the scope of this research has broadened considerably. Two important observations led to the foundation for the broadening of the scientific scope of high-altitude research. First, high-altitude pulmonary edema (HAPE) represents a unique model which allows studying fundamental mechanisms of pulmonary hypertension and lung edema in humans. Secondly, the ambient hypoxia associated with high-altitude exposure facilitates the detection of pulmonary and systemic vascular dysfunction at an early stage. Here, we review studies that, by capitalizing on these observations, have led to the description of novel mechanisms underpinning lung edema and pulmonary hypertension and to the first direct demonstration of fetal programming of vascular dysfunction in humans.

  14. High Altitude Pulmonary Edema Without Appropriate Action Progresses to Right Ventricular Strain: A Case Study.

    PubMed

    Mills, Logan; Harper, Chris; Rozwadowski, Sophie; Imray, Chris

    2016-09-01

    Mills, Logan, Chris Harper, Sophie Rozwadowski, and Chris Imray. High altitude pulmonary edema without appropriate action progresses to right ventricular strain: A case study. High Alt Med Biol. 17:228-232, 2016.-A 24-year-old male developed high altitude pulmonary edema (HAPE) after three ascents to 4061 m over 3 days, sleeping each night at 2735 m. He complained of exertional dyspnea, dry cough, chest pain, fever, nausea, vertigo, and a severe frontal headache. Inappropriate continuation of ascent despite symptoms led to functional impairment and forced a return to the valley, but dyspnea persisted in addition to new orthopnea. Hospital admission showed hypoxemia, resting tachycardia, and systemic hypertension. ECG revealed right ventricular strain and a chest X-ray revealed right lower zone infiltrates. This case demonstrates that HAPE can develop in previously unaffected individuals given certain precipitating factors, and that in the presence of HAPE, prolonged exposure to altitude with exercise (or exertion) does not confer acclimatization with protective adaptations and that rest and descent are the appropriate actions. The case additionally demonstrates well-characterized right ventricular involvement.

  15. Edema

    MedlinePlus

    ... one position for too long Eating too much salty food Premenstrual signs and symptoms Pregnancy Edema can ... Do you restrict your intake of salt and salty foods? Do you drink alcohol? Do you seem ...

  16. 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.

  17. 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

  18. 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

    2016-07-21

    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.

  19. Beta-adrenergic agonist therapy accelerates the resolution of hydrostatic pulmonary edema in sheep and rats.

    PubMed

    Frank, J A; Wang, Y; Osorio, O; Matthay, M A

    2000-10-01

    To determine whether beta-adrenergic agonist therapy increases alveolar liquid clearance during the resolution phase of hydrostatic pulmonary edema, we studied alveolar and lung liquid clearance in two animal models of hydrostatic pulmonary edema. Hydrostatic pulmonary edema was induced in sheep by acutely elevating left atrial pressure to 25 cmH(2)O and instilling 6 ml/kg body wt isotonic 5% albumin (prepared from bovine albumin) in normal saline into the distal air spaces of each lung. After 1 h, sheep were treated with a nebulized beta-agonist (salmeterol) or nebulized saline (controls), and left atrial pressure was then returned to normal. beta-Agonist therapy resulted in a 60% increase in alveolar liquid clearance over 3 h (P < 0.001). Because the rate of alveolar fluid clearance in rats is closer to human rates, we studied beta-agonist therapy in rats, with hydrostatic pulmonary edema induced by volume overload (40% body wt infusion of Ringer lactate). beta-Agonist therapy resulted in a significant decrease in excess lung water (P < 0.01) and significant improvement in arterial blood gases by 2 h (P < 0.03). These preclinical experimental studies support the need for controlled clinical trials to determine whether beta-adrenergic agonist therapy would be of value in accelerating the resolution of hydrostatic pulmonary edema in patients.

  20. 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.

  1. Platelet-rich plasma extract prevents pulmonary edema through angiopoietin-Tie2 signaling.

    PubMed

    Mammoto, Tadanori; Jiang, Amanda; Jiang, Elisabeth; Mammoto, Akiko

    2015-01-01

    Increased vascular permeability contributes to life-threatening pathological conditions, such as acute respiratory distress syndrome. Current treatments for sepsis-induced pulmonary edema rely on low-tidal volume mechanical ventilation, fluid management, and pharmacological use of a single angiogenic or chemical factor with antipermeability activity. However, it is becoming clear that a combination of multiple angiogenic/chemical factors rather than a single factor is required for maintaining stable and functional blood vessels. We have demonstrated that mouse platelet-rich plasma (PRP) extract contains abundant angiopoietin (Ang) 1 and multiple other factors (e.g., platelet-derived growth factor), which potentially stabilize vascular integrity. Here, we show that PRP extract increases tyrosine phosphorylation levels of Tunica internal endothelial cell kinase (Tie2) and attenuates disruption of cell-cell junctional integrity induced by inflammatory cytokine in cultured human microvascular endothelial cells. Systemic injection of PRP extract also increases Tie2 phosphorylation in mouse lung and prevents endotoxin-induced pulmonary edema and the consequent decreases in lung compliance and exercise intolerance resulting from endotoxin challenge. Soluble Tie2 receptor, which inhibits Ang-Tie2 signaling, suppresses the ability of PRP extract to inhibit pulmonary edema in mouse lung. These results suggest that PRP extract prevents endotoxin-induced pulmonary edema mainly through Ang-Tie2 signaling, and PRP extract could be a potential therapeutic strategy for sepsis-induced pulmonary edema and various lung diseases caused by abnormal vascular permeability.

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

    PubMed Central

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

    2015-01-01

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

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

    PubMed

    Karamchandani, Kunal; Bortz, Brandon; Vaida, Sonia

    2016-09-23

    BACKGROUND Acute pulmonary edema in a pregnant patient is associated with significant morbidity and mortality. Takotsubo syndrome, or stress-induced cardiomyopathy, is a rare cause of acute pulmonary edema in a pregnant patient, especially prior to delivery of the fetus. CASE REPORT We describe a case of a pregnant patient who presented with acute pulmonary edema and eclampsia and was found to have Takotsubo syndrome. To the best of our knowledge, eclampsia as a precipitating factor for Takotsubo syndrome has not been described in literature. CONCLUSIONS Clinicians taking care of pregnant patients should be aware of the potential link between eclampsia and Takotsubo cardiomyopathy. Prompt correction of the precipitating cause along with supportive management as described is the key to a successful outcome.

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

    PubMed Central

    Karamchandani, Kunal; Bortz, Brandon; Vaida, Sonia

    2016-01-01

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

  5. Cocaine-induced myocardial infarction associated with severe reversible systolic dysfunction and pulmonary edema.

    PubMed

    Arzola-Castañer, Daniel; Johnson, Charles

    2004-12-01

    Myocardial infarction (MI) associated to cocaine use was originally reported in 1982 and cases are being encountered more frequently in our milieu. The literature regarding this diagnosis has included mostly cases of cocaine associated chest pain and MI without serious sequelae. A lesser number of reports however focus on the clinical presentation of severe myocardial dysfunction and severe pulmonary edema, with the mechanism for pulmonary edema still being debated. Although previously described individually, these manifestations are thought to be an uncommon complication of cocaine ingestion. In this article the subject is reviewed and we report our experience with two patients that presented to our care with severe pulmonary edema and concomitant severe left ventricular systolic dysfunction that resolved spontaneously with supportive therapy. It is felt that this clinical picture after cocaine use may be more common than expected. In this article we discuss the possible mechanisms associated to this presentation as well as review the literature regarding this subject.

  6. [Cardiogenic pulmonary edema following β2 agonist infusion for acute, severe asthma].

    PubMed

    Bahloul, M; Chaari, A; Dammak, H; Medhioub, F; Abid, L; Chtourou, K; Rekik, N; Chelly, H; Kallel, H; Bouaziz, M

    2015-09-01

    We report the case of a severe acute pulmonary edema secondary to the administration of salbutamol to a patient admitted for severe asthma. The diagnosis of acute pulmonary edema was suspected on the clinical examination, chest radiography, biological (plasmatic Pro-BNP rate) and echocardiographic findings. Rapid improvement under dobutamine and mechanical ventilation argue in favour of cardiogenic pulmonary edema. The young age of our patient, the absence of history of cardiovascular disease and the chronology of this complication onset regarded to salbutamol infusion could suggest β2 agonist involvement in this event. The improvement of cardiac function on echocardiography and the normal results obtained with myocardial perfusion scintigraphy performed 35 days later show the left ventricular reversible dysfunction.

  7. A case of negative pressure pulmonary edema in an asthmatic patient after laparoscopic cholecystectomy

    PubMed Central

    Rasheed, Asim; Palaria, Urmila; Rani, Dolly; Sharma, Shatrunjay

    2014-01-01

    Negative pressure pulmonary edema is often misdiagnosed or can go clinically unrecognized by anesthesiologists. It is characterized by a markedly low intrapleural pressure which leads to exudation of fluid and red blood cells in the interstitium. Recognition of patients with predisposing factors for upper airway obstruction is important in the diagnosis which is often confused with pulmonary aspiration of gastric contents. Signs and symptoms are subtle and edema is usually self-limited. Our patient was management conservatively with maintenance of a patent airway and administration of supplemental oxygen and had a successful outcome. PMID:25886111

  8. Hypothyroidism and non-cardiogenic pulmonary edema: are we missing something here?

    PubMed Central

    Nikolla, Dhimitri; Metta, V V S Ramesh

    2015-01-01

    Summary We report the case of a 42-year-old female with a history of hypothyroidism and asthma presenting with progressive dyspnea and orthopnea after 2 days of an upper respiratory tract infection (URTI). Based on the clinical and radiological findings, the patient was admitted as a case of cardiogenic pulmonary edema secondary to possible viral myocarditis. However, a normal brain natriuretic peptide (BNP) level with a normal ejection fraction (EF) on echocardiogram changed our working diagnosis from cardiogenic to non-cardiogenic pulmonary edema. Further questioning revealed a history of nocturnal snoring, frequent awakening, and daytime fatigue, suggesting a possible sleep apnea syndrome (SAS). In conclusion, we believe that SAS was the missing link between our patient's hypothyroidism and non-cardiogenic pulmonary edema. Learning points Always keep an open mind and look for a pathology that would explain the whole clinical scenario.The involvement of the respiratory system in hypothyroidism can range from SAS, pulmonary hypertension, hypoventilation, and severe respiratory failure.Hypothyroidism and SAS should be considered in the differential diagnosis of non-cardiogenic pulmonary edema.Patients should be instructed to take levothyroxine on an empty stomach 30–60 min before food to avoid erratic absorption of the hormone. PMID:25866647

  9. Epithelial sodium channel is involved in H2S-induced acute pulmonary edema.

    PubMed

    Jiang, Lei; Wang, Yixin; Su, Chenglei; Sun, Hao; Zhang, Huazhong; Zhu, Baoli; Zhang, Hengdong; Xiao, Hang; Wang, Jun; Zhang, Jinsong

    2015-01-01

    Acute pulmonary edema is one of the major outcomes of exposure to high levels of hydrogen sulfide (H2S). However, the mechanisms involved in H2S-induced acute pulmonary edema are still poorly understood. Therefore, the present study is designed to evaluate the role of epithelial sodium channel (ENaC) in H2S-induced acute pulmonary edema. The Sprague-Dawley rats were exposed to sublethal concentrations of inhaled H2S, then the pulmonary histological and lung epithelial cell injury were evaluated by hematoxylin-eosin staining and electron microscopy, respectively. In addition to morphological investigation, our results also revealed that H2S exposure significantly decreased the alveolar fluid clearance and increased the lung tissue wet-dry ratio. These changes were demonstrated to be associated with decreased ENaC expression. Furthermore, the extracellular-regulated protein kinases 1/2 pathway was demonstrated to be implicated in H2S-mediated ENaC expression, because PD98059, an ERK1/2 antagonist, significantly mitigated H2S-mediated ENaC down-regulation. Therefore, our results show that ENaC might represent a novel pharmacological target for the treatment of acute pulmonary edema induced by H2S and other hazardous gases.

  10. New concepts about the pathophysiology of pulmonary edema.

    PubMed

    Staub, N C

    1988-07-01

    Three new concepts concerning lung liquid and protein exchange are considered. The first is that the microvascular surface area is as important as the microvascular hydrostatic pressure in assessing filtration in the lung. One of the problems in differentiating hemodynamic from increased permeability edema is the inability to determine whether the microvascular surface area has changed. Several agents, as well as exercise, affect liquid filtration. A new, dynamic procedure that is more sensitive for the detection of increased permeability than static measurements of lung water content is described, along with its limitations. The second concept is that water and electrolytes are cleared from the alveoli by a separate mechanism from protein. Water clearance is fast and occurs mainly by an active process, which can be inhibited by amiloride or phloridzin and accelerated by beta-agonists. The mechanism appears to depend on metabolically regulated sodium transport across the alveolar epithelium. Protein clearance is very slow and is relatively independent of alveolar concentration. The protein clearance mechanism is unknown but may involve transcytosis. The third concept is that during edema formation there are two pathways for liquid clearance in addition to the lymphatic system: into the pleural space and along the bronchovascular connective tissue into the mediastinum. During recovery from edema, reabsorption into blood is important if the edema liquid has a low protein osmotic pressure. Clearance into the mediastinum may be the major pathway for liquid sequestered in the loose, binding connective tissue.

  11. 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

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

    PubMed

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

    1992-05-01

    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

  13. Neurogenic pulmonary edema combined with febrile seizures in early childhood-A report of two cases.

    PubMed

    Tasaka, Keiji; Matsubara, Kousaku; Hori, Masayuki; Nigami, Hiroyuki; Iwata, Aya; Isome, Kenichi; Kawasaki, Yu; Nagai, Sadayuki

    2016-01-01

    Neurogenic pulmonary edema (NPE) is a clinical entity that can occur following central nervous system disorders. However, NPE occurs quite rarely in early childhood, and there has only been one report about pediatric NPE associated with febrile seizures. Two cases are reported here. One case involved a 2-year-old girl who presented with febrile seizures, which rapidly progressed to severe NPE. Since the NPE occurred in the emergency department room, the patient was able to be resuscitated via immediate endotracheal intubation. The other case involved an 11-month-old boy who developed respiratory distress following a 50-min episode of febrile status epilepticus. Both patients required respiratory management in the intensive care unit. However their conditions were dramatically improved within several days and fully recovered without any sequelae.

  14. Efficacy of pimobendan on survival and reoccurrence of pulmonary edema in canine congestive heart failure

    PubMed Central

    MIZUNO, Masashi; YAMANO, Shigeki; CHIMURA, Shuichi; HIRAKAWA, Atsushi; TAKUSAGAWA, Yoshimi; SAWADA, Tamotsu; MAETANI, Shigeki; TAKAHASHI, Arane; MIZUNO, Takeshi; HARADA, Kayoko; SHINODA, Asako; UCHIDA, Shuhei; TAKEUCHI, Junichiro; MIZUKOSHI, Takahiro; ENDO, Masaaki; UECHI, Masami

    2016-01-01

    The aim of this study was to evaluate the efficacy of pimobendan with conventional therapies on survival and reocurrence of pulmonary edema in dogs with congestive heart failure (CHF) caused by myxomatous mitral valve disease (MMVD). Records of 197 client-owned dogs from 14 veterinary hospitals were included in this study. Dogs were administered conventional treatments with or without pimobendan. Sixty-four dogs received a standard dose of pimobendan (0.20–0.48 mg/kg every 12 hr (q12hr)), 49 dogs received a low dose of pimobendan (0.05–0.19 mg/kg q12hr), and 84 dogs received conventional therapy alone. Dogs in the standard-dose and low-dose pimobendan groups had significantly longer median survival times than dogs in the conventional group (334, 277 and 136 days, respectively; P<0.001). The reoccurrence rate of pulmonary edema in the standard-dose group was significantly lower than in the low-dose and conventional groups (43%, 59% and 62%, respectively; P<0.05). Combination of pimobendan with a conventional treatment regimen significantly prolonged survival time after an initial episode of pulmonary edema in dogs with CHF caused by MMVD. There was no difference in survival between dogs administered standard and low doses of pimobendan, but pimobendan did prevent the reoccurrence of pulmonary edema in a dose-dependent manner. PMID:27644192

  15. 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.

  16. Efficacy of pimobendan on survival and reoccurrence of pulmonary edema in canine congestive heart failure.

    PubMed

    Mizuno, Masashi; Yamano, Shigeki; Chimura, Shuichi; Hirakawa, Atsushi; Takusagawa, Yoshimi; Sawada, Tamotsu; Maetani, Shigeki; Takahashi, Arane; Mizuno, Takeshi; Harada, Kayoko; Shinoda, Asako; Uchida, Shuhei; Takeuchi, Junichiro; Mizukoshi, Takahiro; Endo, Masaaki; Uechi, Masami

    2017-01-20

    The aim of this study was to evaluate the efficacy of pimobendan with conventional therapies on survival and reocurrence of pulmonary edema in dogs with congestive heart failure (CHF) caused by myxomatous mitral valve disease (MMVD). Records of 197 client-owned dogs from 14 veterinary hospitals were included in this study. Dogs were administered conventional treatments with or without pimobendan. Sixty-four dogs received a standard dose of pimobendan (0.20-0.48 mg/kg every 12 hr (q12hr)), 49 dogs received a low dose of pimobendan (0.05-0.19 mg/kg q12hr), and 84 dogs received conventional therapy alone. Dogs in the standard-dose and low-dose pimobendan groups had significantly longer median survival times than dogs in the conventional group (334, 277 and 136 days, respectively; P<0.001). The reoccurrence rate of pulmonary edema in the standard-dose group was significantly lower than in the low-dose and conventional groups (43%, 59% and 62%, respectively; P<0.05). Combination of pimobendan with a conventional treatment regimen significantly prolonged survival time after an initial episode of pulmonary edema in dogs with CHF caused by MMVD. There was no difference in survival between dogs administered standard and low doses of pimobendan, but pimobendan did prevent the reoccurrence of pulmonary edema in a dose-dependent manner.

  17. Global end-diastolic volume is associated with the occurrence of delayed cerebral ischemia and pulmonary edema after subarachnoid hemorrhage.

    PubMed

    Watanabe, Akihiro; Tagami, Takashi; Yokobori, Shoji; Matsumoto, Gaku; Igarashi, Yutaka; Suzuki, Go; Onda, Hidetaka; Fuse, Akira; Yokota, Hiroyuki

    2012-11-01

    Predictive variables of delayed cerebral ischemia (DCI) and pulmonary edema following subarachnoid hemorrhage (SAH) remain unknown. We aimed to determine associations between transpulmonary thermodilution-derived variables and DCI and pulmonary edema occurrence after SAH. We reviewed 34 consecutive SAH patients monitored by the PiCCO system. Six patients developed DCI at 7 days after SAH on average; 28 did not (non-DCI). We compared the variable measures for 1 day before DCI occurred (DCI day -1) in the DCI group and 6 days after SAH (non-DCI day -1) in the non-DCI group for control. The mean value of the global end-diastolic volume index (GEDI) for DCI day -1 was lower than that for non-DCI day -1 (676 ± 65 vs. 872 ± 85 mL/m, P = 0.04). Central venous pressure (CVP) was not significantly different (7.8 ± 3.1 vs. 9.4 ± 1.9 cm H2O, P = 0.45). At day -1 for both DCI and non-DCI, 11 patients (32%) had pulmonary edema. Global end-diastolic volume index was significantly higher in patients with pulmonary edema than in those without this condition (947 ± 126 vs. 766 ± 81 mL/m, P = 0.02); CVP was not significantly different (8.7 ± 2.8 vs. 9.2 ± 2.1 cm H2O, P = 0.78). Although significant correlation was found between extravascular lung water (EVLW) measures and GEDI (r = 0.58, P = 0.001), EVLW and CVP were not correlated (r = 0.03, P = 0.88). Thus, GEDI might be associated with DCI occurrence and EVLW accumulation after SAH.

  18. The characteristic of Indonesia's pre-eclampsia: From obstetric intensive care with ventilator until epidemiologic and its molecular biology profile of pulmonary edema in severe pre-eclampsia.

    PubMed

    Hermanto; Adityawarman; Sulistyono; Ardian, M; Dachlan, E G

    2014-07-01

    Pulmonary edema is among the least frequently diagnosed criteria for severe pre-eclampsia. A higher incidence of pulmonary edema was noted in older patients, multigravidas, and patients with underlying chronic hypertension that developed prior to delivery. The development of pulmonary edema was also associated with the administration of excess colloid or crystaloid infusion. Two hundreds and thirty millions people occupying Indonesia as tropical and coastal country gave rise the problem of highly maternal mortality rate of 225/100,000 deliveries where pre-eclampsia and eclampsia as most possible cause. Over 5years from the year 2005 through 2009 our 160 eclampsia study observed about significantly correlation between typical estafet referred case and maternal mortality (Odds ratio 19.1 and P=0.065). Specifically those referred eclampsia cases arriving lately to our tertiary hospital, complication of pulmonary edema also apparently became determinant factor to uphold the increased maternal mortality (Odds ratio 6.1 and P=0.083) We found at our teaching hospital Dr. Soetomo Surabaya as referral center along the year 2012, 477 pre-eclampsia-eclampsia cases which complicated by 27 cases of pulmonary from which we apply obstetric intensive care unit for tightly monitoring treatment. The majority use of ventilator were applied on 22 cases (81.4%), that most approximately 16 cases (72%) need 48h under ventilator use and the remaining 6 cases was not untill 5days of extubation. The etiology of pulmonary edema in preeclamptic patients involves multi-factors; abnormal COP-PWCP gradient, increased pulmonary capillary permeability, and left ventricular failure were identified causes. It has been well known that the pathogenesis of pulmonary edema in severe pre-eclampsia-eclampsia initiated by capillary alveolar leakage that leading increased capillary permeability and extravascular fluid oncotic as well as decreased plasma oncotic pressure. In severe pre-eclampsia appear that

  19. RADIOGRAPHIC APPEARANCE OF PRESUMED NONCARDIOGENIC PULMONARY EDEMA AND CORRELATION WITH THE UNDERLYING CAUSE IN DOGS AND CATS.

    PubMed

    Bouyssou, Sarah; Specchi, Swan; Desquilbet, Loïc; Pey, Pascaline

    2016-12-22

    Noncardiogenic pulmonary edema is an important cause of respiratory disease in dogs and cats but few reports describe its radiographic appearance. The purpose of this retrospective case series study was to describe radiographic findings in a large cohort of dogs and cats with presumed noncardiogenic pulmonary edema and to test associations among radiographic findings versus cause of edema. Medical records were retrieved for dogs and cats with presumed noncardiogenic edema based on history, radiographic findings, and outcome. Radiographs were reviewed to assess lung pattern and distribution of the edema. Correlation with the cause of noncardiogenic pulmonary edema was evaluated with a Fisher's exact test. A total of 49 dogs and 11 cats were included. Causes for the noncardiogenic edema were airway obstruction (n = 23), direct pulmonary injury (n = 13), severe neurologic stimulation (n = 12), systemic disease (n = 6), near-drowning (n = 3), anaphylaxis (n = 2) and blood transfusion (n = 1). Mixed, symmetric, peripheral, multifocal, bilateral, and dorsal lung patterns were observed in 44 (73.3%), 46 (76.7%), 55 (91.7%), 46 (76.7%), 46 (76.7%), and 34 (57.6%) of 60 animals, respectively. When the distribution was unilateral, pulmonary infiltration involved mainly the right lung lobes (12 of 14, 85.7%). Increased pulmonary opacity was more often asymmetric, unilateral, and dorsal for postobstructive pulmonary edema compared to other types of noncardiogenic pulmonary edema, but no other significant correlations could be identified. In conclusion, noncardiogenic pulmonary edema may present with a quite variable radiographic appearance in dogs and cats.

  20. 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.

  1. Update on pulmonary edema: the role and regulation of endothelial barrier function.

    PubMed

    Patterson, C E; Lum, H

    2001-01-01

    Discovery of the pathophysiologic mechanisms leading to pulmonary edema and identification of effective strategies for prevention remain significant clinical concerns. Endothelial barrier function is a key component for maintenance of the integrity of the vascular boundary in the lung, particularly since the gas exchange surface area of the alveolar-capillary membrane is large. This review is focused on new insights in the pulmonary endothelial response to injury and recovery, reversible activation by edemagenic agents, and the biochemical/structural basis for regulation of endothelial barrier function. This information is discussed in the context of fundamental concepts of lung fluid balance and pulmonary function.

  2. ["Flash" pulmonary edema as a clinical manifestation of renovascular hypertension].

    PubMed

    Kalimonovska-Ostrić, Dimitra; Ivanović, Branislava; Ostrić, Vladimir; Knezivić, Vesna; Stojanov, Vesna; Simić, Dragan

    2003-01-01

    One of the clinical manifestations of renovascular hypertension (RVH) may be a recurrent pulmonary oedema both in the absence or in the presence of systolic left ventricular dysfunction. This type of pulmonary oedema characterized as "flash" pulmonary oedema is ascribed to elevated angiotensin II concentrations with consequent hypertension as well as to volume overload resulting from decreased pressor natriuresis when there are significant stenoses of both or one renal arteries. The investigation included 30 patients with RVH treated by percutaneous transluminal angioplasty of the stenosed renal artery (PTRA) and/or stent implantation (PTR-ST) and 30 patients with surgical resection of the abdominal aortic aneurysm (AAA). The first group was divided in two subgroups according to the etiology of renal artery stenosis (RAS). In the subgroup with fibromuscular dysplasia (FMD) the mean age was 37.5 years, in the subgroup with atherosclerotic renal artery stenosis (ARAS) 54.8 years and in the group with operated AAA 68.6 years. There were more females than males only in the FMD subgroup (10:3). Two patients of the first group experienced pulmonary oedema, both in the subgroup with atherosclerotic renal artery stenosis associated with atherosclerosis of other arteries. Normalization of the blood pressure following PTRA in both and an uncomplicated course after a surgical myocardial revascularization in one of them illustrates the importance of renal revascularization. Pulmonary oedema occurred preoperatively in four out of 30 patients with abdominal aortic aneurysm in whom significant renal artery stenoses coexisted. Two patients died despite surgery, one patient is clinically stable and the medicament treatment of heart failure is inevitable in the fourth with a left ventricular aneurysm following myocardial infarction. The occurrence or recurrence of pulmonary oedema in the absence of other explanation should suggest the possibility of bilateral or unilateral renal

  3. [Pulmonary edema due to venous air embolism during craniotomy: a case report].

    PubMed

    Ishida, Kumiko; Hishinuma, Miwako; Miyazawa, Mikiko; Tanaka, Toshiyuki; Iwasawa, Ken; Kitoh, Takeshi

    2008-10-01

    We present a 35-year-old healthy male patient who developed pulmonary edema (PE) probably due to venous air embolism during craniotomy in the semi-sitting position for arteriovenous malformation (AVM). Anesthesia was maintained with oxygen, nitrous oxide, propofol and fentanyl. During craniotomy, end-tidal carbon dioxide pressure decreased suddenly from 26 to 9 mmHg. Concurrently, a decrease in oxygen saturation from 99% to 91% occurred. There were no serious changes in blood pressure and heart rate. A "mill-wheel murmur" was confirmed. PE due to venous air embolism was suspected. The operation was discontinued and the patient was transferred to the intensive care unit. In the post-operative period, the patient developed PE and made a full recovery within a week. Four months later, the patient was scheduled again for surgical excision of AVM in the semi-sitting position in the same way as the first time. Anesthesia was maintained with oxygen, air, propofol and fentanyl. Transoesophageal echocardiography and pulmonary artery catheter were used. Saline was filled at the surgical site to prevent aspiration of air bubbles and surgical procedure was performed carefully without large vein injury and uneventfully. During neurosurgical intervention in the sitting position, special attention should be paid to entry of air bubbles into the venous system which may lead to PE.

  4. Concurrent early-onset peripartum cardiomyopathy in a preeclampsia patient with acute pulmonary edema.

    PubMed

    Belen, Erdal; Tipi, Fahri Fatih; Helvaci, Aysen; Bayyigit, Akif

    2015-01-01

    We herein report the case of a preeclampsia patient with comorbid peripartum cardiomyopathy (PPCMP). A 22-year-old woman in the 26th week of gestation was admitted with acute pulmonary edema. Hypertension and proteinuria were detected, and echocardiography showed an ejection fraction of 33%. It is remarkable that PPCMP particularly that associated with preeclampsia was observed in the early gestational period. In conclusion, while dyspnea and pretibial edema are often noted during normal pregnancies, the potential for PPCMP should be considered if these symptoms are excessive and/or comorbid paroxysmal nocturnal dyspnea and orthopnea are present, even in patients with preeclampsia.

  5. Nifedipine for Treatment of High Altitude Pulmonary Edema.

    DTIC Science & Technology

    1992-07-30

    cohsistent effect on spirometry. In addition, we undertook a survey of pulmonary hypertension (PHT) at high altitude, and surprisingly discovered excessive...Systems model #503), auscultation of all lung fields, and systemic blood pressure both supine and standing. Forced vital capacity, peak expiratory flow...the same chew and swallow manner. The protocol called for repeat dosing every thirty minutes, depending upon the blood pressure response of the

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

    PubMed

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

    2000-07-01

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

  7. [Acute Postoperative Negative Pressure Pulmonary Edema Caused by the Compression of Brachiocephalic Artery].

    PubMed

    Tagawa, Miki; Iwai, Hidetaka; Fukatsu, Ken; Shimada, Mami; Hirabayashi, Yoshihiro

    2016-06-01

    We report a case of negative-pressure pulmonary edema occurring by tracheal obstruction caused by the brachiocephalic artery. The patient had deformed thorax with cerebral palsy, which deformed thorax placing the brachiocephalic artery high over the trachea, resulting in close and tight contact between the artery and trachea. Additional deformity of the thorax associated with myotonic attacks after general anesthesia might shorten the distance between the sternal notch and the vertebral body, resulting in the tracheal obstruction by the artery.

  8. Acute pulmonary edema due to rosiglitazone use in a patient with diabetes mellitus.

    PubMed

    Cekmen, Nedim; Cesur, Mustafa; Cetinbas, Riza; Bedel, Pasa; Erdemli, Ozcan

    2006-01-01

    Rosiglitazone is a peroxisome proliferator active receptor. gamma agonist, which increases insulin sensitivity in adipose tissue, muscle, and liver. Rosiglitazone is a member of the thiazolidinedione group, and because of its significantly positive effect on glycemic control, it is especially preferred in type 2 diabetic patients with a high cardiovascular disease risk. This drug, because of its decreasing effect on insulin resistance, is used alone or combined with type 2 diabetic drugs. A 73-year-old female patient was admitted to the emergency department with dyspnea, pink frothing phlegm, cyanosis, and tiredness. She was lethargic, uncooperative, and had no orientation. In arterial blood gases, hypoxemia and hypercapnia were found. She was taken to the general intensive care unit, and oxygen was applied via mask. The patient had a history of 10 years of diabetes mellitus, hypertension, and atherosclerotic cardiac disease, and she was using rosiglitazone for the past 6 weeks. Her chest x-ray was taken, and acute pulmonary edema was diagnosed. In her last echocardiography, which was performed 1 year before, no signs indicating cardiac failure and pleural effusion could be found. Therefore, it was concluded that pulmonary edema occurred as a complication of rosiglitazone use. After stabilizing the patient's vital signs, blood glucose levels, and lactate levels, medical treatment of diabetes mellitus was rearranged, and she was discharged on the seventh day after her admittance. In a patient with diabetes mellitus who has been admitted to the intensive care unit because of acute pulmonary edema, for differential diagnosis, use of rosiglitazone should be kept in mind during the determination of treatment. Therefore, the authors aim to discuss the effect of rosiglitazone on creating acute pulmonary edema with a case report presentation.

  9. The Effects of Portulaca oleracea on Hypoxia-Induced Pulmonary Edema in Mice

    PubMed Central

    Yue, Tan; Xiaosa, Wen; Ruirui, Qi; Wencai, Shi; Hailiang, Xin

    2015-01-01

    Abstract Tan Yue, Wen Xiaosa, Qi Ruirui, Shi Wencai, Xin Hailiang, and Li Min. The effects of Portulaca oleracea on hypoxia-induced pulmonary edema in mice. High Alt Med Biol 16:43–51, 2015—Portulaca oleracea L. (PO) is known as “a vegetable for long life” due to its antioxidant, anti-inflammatory, and other pharmacological activities. However, the protective activity of the ethanol extract of PO (EEPO) against hypoxia-induced pulmonary edema has not been fully investigated. In this study, we exposed mice to a simulated altitude of 7000 meters for 0, 3, 6, 9, and 12 h to observe changes in the water content and transvascular leakage of the mouse lung. It was found that transvascular leakage increased to the maximum in the mouse lung after 6 h exposure to hypobaric hypoxia. Prophylactic administration of EEPO before hypoxic exposure markedly reduced the transvascular leakage and oxidative stress, and inhibited the upregulation of NF-kB in the mouse lung, as compared with the control group. In addition, EEPO significantly reduced the levels of proinflammatory cytokines and cell adhesion molecules in the lungs of mice, as compared with the hypoxia group. Our results show that EEPO can reduce initial transvascular leakage and pulmonary edema under hypobaric hypoxia conditions. PMID:25761168

  10. Pattern of fluid accumulation in NO2-induced pulmonary edema in dogs. A morphometric study.

    PubMed Central

    Vassilyadi, M.; Michel, R. P.

    1988-01-01

    To ascertain whether the pattern of fluid accumulation could be altered by an agent introduced through the airways, the authors studied the physiology and morphology of 11 dogs exposed to 150-494 ppm.hr NO2 and compared them with 3 new and 5 previously reported control dogs. NO2 caused a partly reversible decrease in systemic arterial pressure and cardiac output, a fall in arterial PO2, and rapid shallow breathing, while pulmonary arterial and wedge pressures remained normal. Post mortem, lower (LL) and middle (ML) lobes were frozen, sections fixed for light microscopy by freeze-substitution, and wet weight/dry weight (W/D) ratios were measured. Alveolar edema was graded, and the distribution of interstitial edema around arteries and veins and within bronchovascular bundles was studied with morphometry: edema ratios (ER) were calculated as area of interstitium/area of vessel or airway. We found that NO2 produced an exposure-dependent increase in lung water (r = 0.73), and that both LL and ML had similar W/D ratios (7.77 and 8.39, respectively) and percent alveolar edema (30% and 34%). Morphometry of interstitial edema showed that the ER for vessels and airways of edematous LL were essentially similar to controls, while those of the ML were markedly increased. It is concluded that NO2 produces exposure-related lung edema and preferential alveolar flooding with probable secondary interstitial accumulation. The discrepancies in interstitial edema between middle and lower lobes may be due to differences in lung volume or in ventilation. Images Figure 6 Figure 9 PMID:3337206

  11. Angiotensin II receptor 1 gene variants are associated with high-altitude pulmonary edema risk.

    PubMed

    Jin, Tianbo; Ren, Yongchao; Zhu, Xikai; Li, Xun; Ouyang, Yongri; He, Xue; Zhang, Zhiying; Zhang, Yuan; Kang, Longli; Yuan, Dongya

    2016-11-22

    Previous studies demonstrated that Angiotensin II Receptor 1 (AGTR1) may play an important role in the development of high-altitude pulmonary edema. We envisaged a role for AGTR1 gene variants in the pathogenesis of HAPE and investigated their potential associations with HAPE in a Han Chinese population. We genotyped seven AGTR1 polymorphisms in 267 patients with diagnosed HAPE and 304 controls and evaluated their association with risk of HAPE. Statistically significant associations were found for the single nucleotide polymorphisms (SNPs) rs275651 (p = 0.017; odds ratio [OR] = 0.65) and rs275652 (p = 0.016; OR = 0.64). Another SNP rs10941679 showed a marginally significant association after adjusting for age and sex in the additive genetic model (adjusted OR = 1.44, 95% CI = 1.01-2.04, p = 0.040). Haplotype analysis confirmed that the haplotype "AG" was associated with a 35% reduction in the risk of developing HAPE, while the haplotype "AA" increased the risk of developing HAPE by 44%. These results provide the first evidence linking genetic variations in AGTR1 with HAPE risk in Han Chinese individuals.

  12. Angiotensin II receptor 1 gene variants are associated with high-altitude pulmonary edema risk

    PubMed Central

    Zhu, Xikai; Li, Xun; Ouyang, Yongri; He, Xue; Zhang, Zhiying; Zhang, Yuan; Kang, Longli; Yuan, Dongya

    2016-01-01

    Previous studies demonstrated that Angiotensin II Receptor 1 (AGTR1) may play an important role in the development of high-altitude pulmonary edema. We envisaged a role for AGTR1 gene variants in the pathogenesis of HAPE and investigated their potential associations with HAPE in a Han Chinese population. We genotyped seven AGTR1 polymorphisms in 267 patients with diagnosed HAPE and 304 controls and evaluated their association with risk of HAPE. Statistically significant associations were found for the single nucleotide polymorphisms (SNPs) rs275651 (p = 0.017; odds ratio [OR] = 0.65) and rs275652 (p = 0.016; OR = 0.64). Another SNP rs10941679 showed a marginally significant association after adjusting for age and sex in the additive genetic model (adjusted OR = 1.44, 95% CI = 1.01-2.04, p = 0.040). Haplotype analysis confirmed that the haplotype “AG” was associated with a 35% reduction in the risk of developing HAPE, while the haplotype “AA” increased the risk of developing HAPE by 44%. These results provide the first evidence linking genetic variations in AGTR1 with HAPE risk in Han Chinese individuals. PMID:27732943

  13. 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

  14. Three-view bedside ultrasound for the differentiation of acute respiratory distress syndrome from cardiogenic pulmonary edema.

    PubMed

    Mantuani, Daniel; Nagdev, Arun; Stone, Michael

    2012-09-01

    Bedside ultrasound is being increasingly used by emergency physicians (EPs) for the differentiation of acute dyspnea in critically ill patients. Lung ultrasound is emerging as a highly sensitive tool in diagnosing alveolar interstitial edema with the presence of diffuse “B-lines” arising from the pleural line. However, when used independently, lung ultrasound is unable to differentiate between cardiogenic and noncardiogenic causes of pulmonary edema. This case report describes a rapid 3-view or “triple scan” sonographic examination to differentiate acute respiratory distress syndrome (ARDS) from cardiogenic pulmonary edema.

  15. 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

  16. An analysis of and new risk factors for reexpansion pulmonary edema following spontaneous pneumothorax

    PubMed Central

    Kawabata, Tsutomu; Ichi, Takaharu; Yohena, Tomofumi; Kawasaki, Hidenori; Ishikawa, Kiyoshi

    2014-01-01

    Background The major risk factor for reexpansion pulmonary edema (RPE) following the treatment of spontaneous pneumothorax is thought to be chronic lung collapse. However, a long-term collapsed lung does not always cause RPE. The purpose of this study was to define other risk factors for RPE among patients undergoing drainage for the treatment of spontaneous pneumothorax. Methods We retrospectively reviewed all the patients with spontaneous pneumothorax who had been treated at our hospital during a 5-year period. The duration of symptoms, location and size of the pneumothorax, size of the chest tube, and pleural effusion, which can occur coincidentally with pneumothorax, were compared in patients who did and did not experience RPE. Results Forty patients were underwent drainage for the treatment of a spontaneous pneumothorax between January 2007 and December 2012. RPE developed in 13 of the 40 (32.5%) patients. In the multivariate analysis, the presence of pleural effusion coincident with pneumothorax contributed to the risk for RPE [odds ratios (OR), 1.557; 95% confidence intervals (CI), 1.290-1.880]. The duration of symptoms, location and size of the pneumothorax and size of the chest tube were similar between the groups. Symptomatic RPE was associated with a larger pneumothorax size. Conclusions The rate of RPE following spontaneous pneumothorax is higher than was previously reported. Our findings suggest the presence of pleural effusion coincidentally with pneumothorax may therefore be a new risk factor for RPE. PMID:25276359

  17. 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

  18. 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

  19. 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

  20. Therapeutic efficacy of milrinone in the management of enterovirus 71-induced pulmonary edema.

    PubMed

    Wang, Shih-Min; Lei, Huan-Yao; Huang, Mei-Chih; Wu, Jing-Min; Chen, Chun-Ta; Wang, Jieh-Neng; Wang, Jen-Ren; Liu, Ching-Chuan

    2005-03-01

    Hand, foot, and mouth disease and herpangina are the major clinical manifestations of enterovirus 71 (EV71) infections. Brain-stem encephalitis and pulmonary edema are severe complications that can lead to death. This study was designed to evaluate the potential therapeutic effect of milrinone, a phosphodiesterase (PDE) inhibitor, in the treatment of patients with EV71-induced pulmonary edema. We conducted a historically controlled trial of 24 children with severe EV71-induced pulmonary edema from April 1998-June 2003 in southern Taiwan. Patients were divided into groups treated before and after the introduction of milrinone therapy. Etiological diagnosis was established by viral cultures and confirmed by specific immunofluorescence and neutralization tests. All 24 patients were below 5 years of age. The mortality was lower in the milrinone-treated vs. nontreated group (36.4% vs. 92.3%, P=0.005). Sympathetic tachycardia was decreased in patients treated with milrinone compared to controls (144 +/- 17/min vs. 206 +/- 26/min, P=0.004). A marked decrease in IL-13 (77 +/- 9 pg/ml vs. 162 +/- 88 pg/ml, P=0.001) was observed in milrinone-treated patients compared to controls. There was a significant reduction in white blood cell (10,838 +/- 4,537/mm3 vs. 19,475 +/- 7,798/mm3, P=0.009) and platelet (257 +/- 45 x 10(3)/mm3 vs. 400 +/- 87 x 10(3)/mm3, P=0.001) counts in milrinone-treated patients compared to controls. These results were associated with improvement in sympathetic regulation and decrease in IL-13 production. Milrinone therapy may provide a useful therapeutic approach for this highly lethal disorder.

  1. Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil

    PubMed Central

    Moon, Richard E.; Martina, Stefanie D.; Peacher, Dionne F.; Potter, Jennifer F.; Wester, Tracy E.; Cherry, Anne D.; Natoli, Michael J.; Otteni, Claire E.; Kernagis, Dawn N.; White, William D.; Freiberger, John J.

    2016-01-01

    Background Swimming-induced pulmonary edema (SIPE) occurs during swimming or scuba diving, often in young individuals with no predisposing conditions, and its pathophysiology is poorly understood. This study tested the hypothesis that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise compared to the general population and are reduced by sildenafil. Methods and Results Ten study subjects with a history of SIPE (mean age 41.6 years) and 20 control subjects (mean age 36.2 years) were instrumented with radial artery and pulmonary artery catheters and performed moderate cycle ergometer exercise for 6–7 minutes while submersed in 20°C water. SIPE-susceptible subjects repeated the exercise 150 minutes after oral administration of 50 mg sildenafil. Work rate and mean arterial pressure during exercise were similar in controls and SIPE-susceptibles. Average VO2 and cardiac output (CO) in SIPE-susceptibles and controls were: VO2 2.42 L.min−1 vs. 1.95 L.min−1, P=0.2; CO 17.9 L.min−1 vs. 13.8 L.min−1, P=0.01). Accounting for differences in CO between groups, mean pulmonary artery pressure (MPAP) at CO=13.8 L.min−1 was 22.5 mmHg in controls vs. 34.0 mmHg in SIPE-susceptibles (P=0.004) and the corresponding pulmonary artery wedge pressure (PAWP) 11.0 mmHg vs. 18.8 mmHg (P=0.028). After sildenafil, there were no statistically significant differences in MPAP or PAWP between SIPE-susceptibles and controls. Conclusions These observations confirm that SIPE is a form of hemodynamic pulmonary edema. The reduction in pulmonary vascular pressures after sildenafil with no adverse effect on exercise hemodynamics suggests that it may be useful in SIPE prevention. Clinical Trial Registration Information ClinicalTrials.gov. Identifier: NCT00815646. PMID:26882910

  2. Delayed renal dysfunction and flash pulmonary edema post endovascular abdominal aneurysm repair.

    PubMed

    Carron, Pierre-Louis; Piliero, Nicolas; Heitz, Morgane; Kribs, Marc; Rodière, Mathieu; Jousse, Patrick; Gunther-Calvino, Silvia; Thony, Frédéric

    2016-04-01

    After endovascular aortic repair (EVAR), the deterioration in long-term renal function is probably multifactorial. Preoperative renal failure is an independent risk factor. Postoperative renal dysfunction can be associated with inadvertent renal artery occlusion, renal artery complications as stenosis, plaque dislodgement, or dissection. Ischemic nephropathy can accelerate hypertension and circulatory congestion. We report a case of coverage of the renal arteries symptomatic with flash pulmonary edema and renal failure 15 months after EVAR, suggesting a delayed endograft migration. The patient had complete resolution of symptoms and renal function after renal artery stenting with placement between endograft and aneurysm to the left renal artery.

  3. A Case of Salicylate Intoxication Complicated by Coagulopathy, Pulmonary Edema, and Pancreatitis.

    PubMed

    Ayalon, Itay; Alder, Matthew Noble; Langner, Travis Ryan; Hafberg, Einar Thor; Miethke, Alexander Gerhard; Kaplan, Jennifer Melissa

    The large availability of salicylic acid products makes them an often encountered source of poisoning in the emergency department. Even though in most cases the prognosis is good, with a low incidence of long-term morbidity and mortality, complications do occur, and some of those can be life threatening. We present an unusual case of salicylate intoxication in an adolescent in which several uncommon complications (severe coagulopathy, pulmonary edema, and pancreatitis) conjoined together. We review the literature and discuss the complications pathogenesis and differential diagnosis. We suggest that these potentially life-threatening complications be acknowledged, investigated, and rapidly treated.

  4. An Unusual Type of Localized Hypertrophic Cardiomyopathy With Wolf Parkinson White Syndrome Presenting With Pulmonary Edema

    PubMed Central

    Vatan, Mehmet Bulent; Gunduz, Huseyin; Gurel, Safiye; Kocayigit, Ibrahim; Vural, Ahmet; Demirtas, Saadet; Cakar, Mehmet Akif; Gunduz, Yasemin

    2012-01-01

    Hypertrophic cardiomyopathy (HCM) is an autosomal dominant heart disease that is the most common genetic cardiac disorder. The disease is characterized by excessive thickening of the left ventricular myocardium. The anterior portion of the interventricular ventricular septum is often involved. Asymmetric hypertrophy of apical site, left ventricular free wall, and right ventricle are less common in hypertrophic cardiomyopathy that occur in 1% cases. We report a case of a patient with an unusual type of hypertrophic cardiomyopathy and Wolf Parkinson White (WPW) presenting with pulmonary edema.

  5. 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

  6. 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.

  7. Unilateral pulmonary edema: a rare initial presentation of cardiogenic shock due to acute myocardial infarction.

    PubMed

    Shin, Jeong Hun; Kim, Seok Hwan; Park, Jinkyu; Lim, Young-Hyo; Park, Hwan-Cheol; Choi, Sung Il; Shin, Jinho; Kim, Kyung-Soo; Kim, Soon-Gil; Hong, Mun K; Lee, Jae Ung

    2012-02-01

    Cardiogenic unilateral pulmonary edema (UPE) is a rare clinical entity that is often misdiagnosed at first. Most cases of cardiogenic UPE occur in the right upper lobe and are caused by severe mitral regurgitation (MR). We present an unusual case of right-sided UPE in a patient with cardiogenic shock due to acute myocardial infarction (AMI) without severe MR. The patient was successfully treated by percutaneous coronary intervention and medical therapy for heart failure. Follow-up chest Radiography showed complete resolution of the UPE. This case reminds us that AMI can present as UPE even in patients without severe MR or any preexisting pulmonary disease affecting the vasculature or parenchyma of the lung.

  8. Effect of partial liquid ventilation on pulmonary vascular permeability and edema after experimental acute lung injury.

    PubMed

    Lange, N R; Kozlowski, J K; Gust, R; Shapiro, S D; Schuster, D P

    2000-07-01

    We evaluated the effects of partial liquid ventilation (PLV) with two different dosages of the perfluorocarbon LiquiVent (perflubron) on pulmonary vascular permeability and edema formation after oleic acid (OA)-induced acute lung injury in dogs. We used imaging with positron emission tomography to measure fractional pulmonary blood flow, lung water concentration (LWC), and the pulmonary transcapillary escape rate (PTCER) of (68)Ga-labeled transferrin at 5 and 21 h after lung injury in five dogs undergoing conventional mechanical ventilation (CMV), five dogs undergoing low-dose PLV (perflubron at 10 ml/kg), and four dogs undergoing high dose PLV (perflubron at 30 ml/kg). A positive end-expiratory pressure of 7.5 cm H(2)O was used in all dogs. After OA (0.08 ml/kg)- induced lung injury, there were no significant differences or trends for PTCER or LWC at any time when the PLV groups were compared with the CMV group. However, lung tissue myeloperoxidase activity was significantly lower in the combined PLV group than in the CMV group (p = 0.016). We conclude that after OA-induced lung injury, the addition of PLV to CMV does not directly attenuate pulmonary vascular leak or lung water accumulation. Rather, the benefits of such treatment may be due to modifications of the inflammatory response.

  9. Molecular Pathology of Pulmonary Edema in Forensic Autopsy Cases with Special Regard to Fatal Methamphetamine Intoxication.

    PubMed

    Du, Yu; Jin, Hong-Nian; Zhao, Rui; Zhao, Dong; Xue, Ye; Zhu, Bao-Li; Guan, Da-Wei; Xie, Xiao-Li; Wang, Qi

    2016-11-01

    Pulmonary edema is a common finding in fatal methamphetamine intoxication. However, the underlying mechanism remains poorly understood. This study investigated the molecular pathology of alveolar damage involving pulmonary edema in forensic autopsy cases. Seven candidate reference genes (RPL13A, YWHAZ, GUSB, SDHA, GAPDH, B2M, and ACTB) were evaluated in the lung by the geNorm module in qBase(plus) software. RPL13A, YWHAZ, and GUSB were identified as the most stable reference genes. Using these validated reference genes, intrapulmonary mRNA 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 METH intoxication cases. These findings suggested alveolar damage and compensatory response in fatal METH intoxication cases. Systematic analysis of gene expressions using real-time qPCR is a useful tool in forensic death investigation.

  10. [Re-expansion pulmonary edema as a complication of a spontaneous pneumothorax drainage--a case review].

    PubMed

    Toporcer, T; Il'ková, J; Lakyová, L; Belák, J; Radonak, J

    2008-07-01

    Reexpansion pulmonary edema is an iatrogenic complication occurring after reinflation of the collapsed lung of a patient with pneumothorax or fluidothorax. The following risk factors have been associated with reexpansion pulmonary edema: younger age, longer duration of a lung collapse, its large extend and a quick lung reexpansion. We report a case of 26-years-old man. The patient was admited to the second surgical clinic FNLP, Kosice because of a spontaneous pneumothorax. A chest tube was inserted in local anesthesia in the right anterior axilar line and the fourth intercostal space. An active negative pressure of 20 cm H2O was applied. Dyspnea, decrease of blood pressure, tachycardia, tachypnoe and expectoration of pink sputum were recorded after negative pressure application. Oxygen saturation decreased to 90% despite the addition of oxygen. Glucocorticoids, diuretic stimulants, analgesic and bronchodilatators were administered. Chest X-rays and computer tomography showed a strong ipsilateral pulmonary edema and an incipient contralateral pulmonary edema. The patient was stabilized and after 16 hours continuous oxygen administration was not longer needed. Because of continuous pneumothorax, a video assisted thoracoscopic surgery was performed on the seventh day after the chest tube insertion. After 13 days of hospitalization the patient was discharged in good condition without any further complications to the ambulatory care. Reexpansion pulmonary edema is a rare complication of the chest tube insertion and thoracocentesis because of pneumothorax and fluidothorax. The mortality of reexpansion pulmonary edema reaches up to 20%. Chest tube insertion and thoracocentesis are therapeutic procedures to be performed solely on medical department which can provide artificial lung ventilation.

  11. Lethal Factor, but Not Edema Factor, Is Required to Cause Fatal Anthrax in Cynomolgus Macaques after Pulmonary Spore Challenge

    PubMed Central

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

    2015-01-01

    Inhalational anthrax is caused by inhalation of Bacillus anthracis spores. The ability of B. anthracis to cause anthrax is attributed to the plasmid-encoded A/B-type toxins, edema toxin (edema factor and protective antigen) and lethal toxin (lethal factor and protective antigen), and a poly-d-glutamic acid capsule. To better understand the contribution of these toxins to the disease pathophysiology in vivo, we used B. anthracis Ames strain and isogenic toxin deletion mutants derived from the Ames strain to examine the role of lethal toxin and edema toxin after pulmonary spore challenge of cynomolgus macaques. Lethal toxin, but not edema toxin, was required to induce sustained bacteremia and death after pulmonary challenge with spores delivered via bronchoscopy. After intravenous challenge with bacilli to model the systemic phase of infection, lethal toxin contributed to bacterial proliferation and subsequent host death to a greater extent than edema toxin. Deletion of protective antigen resulted in greater loss of virulence after intravenous challenge with bacilli than deletion of lethal toxin or edema toxin alone. These findings are consistent with the ability of anti–protective antigen antibodies to prevent anthrax and suggest that lethal factor is the dominant toxin that contributes to the escape of significant numbers of bacilli from the thoracic cavity to cause anthrax after inhalation challenge with spores. PMID:25285720

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

    PubMed

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

    2014-12-01

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

  13. 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

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

    PubMed

    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.

  15. Experience of step-wise protocol using noninvasive positive pressure ventilation for treating cardiogenic pulmonary edema.

    PubMed

    Momii, Hidetoshi; Tashima, Yuki; Kadokami, Toshiaki; Narita, Sumito; Yoshida, Masayoshi; Ando, Shin-ichi

    2012-08-01

    Initiating and weaning procedure of noninvasive positive pressure ventilation (NIPPV) on acute cardiogenic pulmonary edema (ACPE) has been determined empirically, and the total time of its use has been sometimes prolonged unnecessarily. A simple protocol for its use may facilitate initiation and avoids prolongation of the NIPPV treatment. We designed a step-wise protocol for NIPPV use and retrospectively examined the clinical outcome of our protocol for initiation and weaning of NIPPV in 45 patients with ACPE. Almost all patients recovered from respiratory distress successfully. There was no intubation nor complication related to NIPPV. In most of the cases, maximal-end expiratory pressure was less than 7-cm H2O. The mean duration of NIPPV was 19.5±28.0 h and the median duration was 8.0 h (interquartile range=14.0 h). This simple step-wise NIPPV protocol for ACPE can facilitate quick and safe initiation and termination of the treatment.

  16. Radiation induced endothelial cell retraction in vitro: correlation with acute pulmonary edema.

    PubMed

    Onoda, J M; Kantak, S S; Diglio, C A

    1999-01-01

    We determined the effects of low dose radiation (<200 cGy) on the cell-cell integrity of confluent monolayers of pulmonary microvascular endothelial cells (PMEC). We observed dose- and time-dependent reversible radiation induced injuries to PMEC monolayers characterized by retraction (loss of cell-cell contact) mediated by cytoskeletal F-actin reorganization. Radiation induced reorganization of F-actin microfilament stress fibers was observed > or =30 minutes post irradiation and correlated positively with loss of cell-cell integrity. Cells of irradiated monolayers recovered to form contact inhibited monolayers > or =24 hours post irradiation; concomitantly, the depolymerized microfilaments organized to their pre-irradiated state as microfilament stress fibers arrayed parallel to the boundaries of adjacent contact-inhibited cells. Previous studies by other investigators have measured slight but significant increases in mouse lung wet weight >1 day post thoracic or whole body radiation (> or =500 cGy). Little or no data is available concerning time intervals <1 day post irradiation, possibly because of the presumption that edema is mediated, at least in part, by endothelial cell death or irreversible loss of barrier permeability functions which may only arise 1 day post irradiation. However, our in vitro data suggest that loss of endothelial barrier function may occur rapidly and at low dose levels (< or =200 cGy). Therefore, we determined radiation effects on lung wet weight and observed significant increases in wet weight (standardized per dry weight or per mouse weight) in < or =5 hours post thoracic exposure to 50 200 cGy x-radiation. We suggest that a single fraction of radiation even at low dose levels used in radiotherapy, may induce pulmonary edema by a reversible loss of endothelial cell-cell integrity and permeability barrier function.

  17. 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

  18. Neonatal high-permeability pulmonary edema based on serial cytokine profiles and KL-6 in serum: case report.

    PubMed

    Nakamura, Toshihiko; Nakamura, Mari; Takahashi, Naoto

    2017-03-22

    A newborn male with pulmonary edema was delivered at term by elective Caesarian section. Cytokine profiles of 17 cytokines and KL-6 in cord blood and serial serum values were investigated. The cord blood values of all 17 cytokines and KL-6 were within normal limits. Subsequently, IL-6, IL-8, IL-10, IL-13, IL-17, and IFNγ rapidly elevated during the first several hours after birth and dramatically decreased thereafter, whereas KL-6 rose to 611 U/ml on the 3(rd) day of life and then gradually decreased. These cytokines may induce pulmonary permeability, and KL-6 secreted in lining fluid could result in influx into the bloodstream. This is the first report that we have differentiated neonatal pulmonary edema from TTN by the measurement of serial cytokine profiles and KL-6 in serum.

  19. Non-cardiogenic pulmonary edema, rhabdomyolysis and myocardial injury following heroin inhalation: a case report

    PubMed Central

    Bazoukis, G; Spiliopoulou, A; Mourouzis, K; Grigoropoulou, P; Yalouris, A

    2016-01-01

    Background: Heroin use by non-injecting routes of administration (snorting, swallowing, “chasing the dragon”) is considered to be safer but is not risk-free for fatal overdose or serious side effects. We report the case of an adolescent who was transferred unconscious to the emergency department after heroin inhalation. Description of the case: A 17-year-old male was transferred to the emergency department unconscious (Glasgow coma scale: 6/15) after heroin inhalation. He was treated with non-rebreather mask and intravenous infusion of naloxone with gradual improvement of consciousness and arterial blood gasses. The chest computed tomography showed signs of acute respiratory distress syndrome. Laboratory exams on the second day of hospitalization showed elevated creatine kinase (CK) and troponin-I levels while his electrocardiography (ECG) showed J-point elevation in V1, V2, and V3 precordial leads. On the second day of hospitalization the pulmonary infiltrates were not present in his chest X-ray while on the eighth day, troponin-I and CK levels were normalized without dynamic ECG changes and the patient was discharged uneventfully. Conclusion: Heroin inhalation may cause severe complications, such as non-cardiogenic pulmonary edema, rhabdomyolysis or myocardial injury. Hippokratia 2016, 20(1): 84-87 PMID:27895451

  20. 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

    2016-05-23

    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.

  1. 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

  2. Susceptibility To High Altitude Pulmonary Edema Is Associated With A More Uniform Distribution Of Regional Specific Ventilation.

    PubMed

    Patz, Michael D; Sá, Rui Carlos; Darquenne, Chantal; Elliott, Ann R; Assadi, Amran K; Theilmann, Rebecca J; Dubowitz, David J; Swenson, Erik Richard; Prisk, Gordon Kim; Hopkins, Susan Roberta

    2017-01-05

    High altitude pulmonary edema (HAPE) is a potentially fatal condition affecting high altitude sojourners. The biggest predictor of HAPE development is a history of prior HAPE. Magnetic resonance imaging (MRI) shows HAPE-susceptible, with a history of HAPE, but not HAPE-resistant (a history of repeated ascents without illness) individuals develop greater heterogeneity of regional pulmonary perfusion breathing hypoxic gas (O2=12.5%), consistent with uneven hypoxic pulmonary vasoconstriction (HPV). Why HPV is uneven in HAPE-susceptibles is unknown, but may arise from regionally heterogeneous ventilation resulting in an uneven stimulus to HPV. We tested the hypothesis that ventilation is more heterogeneous in HAPE-susceptible subjects (n=6) compared to HAPE-resistant controls (n=7). MRI Specific Ventilation Imaging (SVI), was used to measure regional specific ventilation and the relative dispersion (SD/mean) of SVI used to quantify baseline heterogeneity. Ventilation heterogeneity from conductive and respiratory airways was measured in normoxia and hypoxia (O2=12.5%) using multiple breath washout and heterogeneity quantified from the indices Scond and Sacin, respectively. Contrary to our hypothesis, HAPE-susceptibles had significantly lower relative dispersion of specific ventilation than the HAPE-resistant controls (Susceptible=1.33±0.67, Resistant=2.36±0.98, p=0.05) and Sacin tended to be more uniform (Susceptible=0.085±0.009, Resistant=0.113±0.030, p=0.07). Scond was not significantly different between groups (Susceptible=0.019±0.007, Resistant=0.020±0.004, p=0.67). Sacin and Scond did not change significantly in hypoxia (p=0.56, 0.19, respectively). In conclusion, ventilation heterogeneity does not change with short-term hypoxia irrespective of HAPE susceptibility and lesser rather than greater ventilation heterogeneity is observed in HAPE-susceptible subjects. This suggests the basis for uneven HPV in HAPE involves vascular phenomena.

  3. A rare presentation of patent ductus arteriosus in an adult patient with normal pulmonary hypertension and limb edema

    PubMed Central

    Pishgoo, Bahram; Saburi, Amin; Khosravi, Arezoo

    2014-01-01

    BACKGROUND Patent ductus arteriosus (PDA) at childhood is one of the five major and frequent congenital abnormalities, but it can be rarely seen in adults. Pulmonary hypertension (PHTN) and other presentations such as heart failure and edema are the identified complications of longstanding PDA, but adult case with no permanent heart symptoms and PHTN was rare. We reported a rare case of with an obvious PDA and normal pulmonary pressure. CASE REPORT A 61-year-old woman presented with dyspnea (New York Heart Association class 2), chest pain, and lower limb edema. Echocardiogram showed; normal left ventricular chamber size and function, normal size of both atria. Furthermore, an obvious PDA (diameter = 6-7 mm) connecting the aortic arch to the pulmonary artery was reported in echocardiography. No lung congestion and evidence for PHTN was reported by computed tomographic angiography [Pulmonary capillary wedge pressure (PCWP) = 30 mmHg]. The patient was treated with antihypertensive drugs and after 1 and 3 months follow-up, edema and other symptoms were resolved. CONCLUSION Finally, we conclude that PDA in adulthood can present with nonspecific cardiovascular symptoms, and it seems that PHTN is not a fixed echocardiographic finding in these patients. PMID:25477985

  4. Managing High-Altitude Pulmonary Edema with Oxygen Alone: Results of a Randomized Controlled Trial.

    PubMed

    Yanamandra, Uday; Nair, Velu; Singh, Surinderpal; Gupta, Amul; Mulajkar, Deepak; Yanamandra, Sushma; Norgais, Konchok; Mukherjee, Ruchira; Singh, Vikrant; Bhattachar, Srinivasa A; Patyal, Sagarika; Grewal, Rajan; Chopra, Bhushan

    2016-12-01

    Yanamandra, Uday, Velu Nair, Surinderpal Singh, Amul Gupta, Deepak Mulajkar, Sushma Yanamandra, Konchok Norgais, Ruchira Mukherjee, Vikrant Singh, Srinivasa A. Bhattachar, Sagarika Patyal, and Rajan Grewal. High-altitude pulmonary edema management: Is anything other than oxygen required? Results of a randomized controlled trial. High Alt Med Biol. 17:294-299, 2016.-Treatment strategies for management of high-altitude pulmonary edema (HAPE) are mainly based on the observational studies with only two randomized controlled trials, thus the practice is very heterogeneous and individualized as per the choice of treating physician. To compare the response to different modalities of therapy in patients with HAPE in a randomized controlled manner. We conducted an open-label, randomized noninferiority trial to compare three modalities of therapy (Therapy 1: supplemental O2 with oral dexamethasone 8 mg q8 hours [n = 42], Therapy 2: supplemental O2 with sustained release oral nifedipine 20 mg q8 hours [n = 41], and Therapy 3: only supplemental O2 [n = 50]). Bed rest was mandated in all patients. The study was conducted in a cohort of previously healthy young lowlander males at an altitude of 3500 m. Baseline characteristics of the patients were comparable in the study arms. Complete response was defined as clinical and radiological resolution of features of HAPE, no oxygen dependency, a normal 6-minute walk test (6MWT) on 2 consecutive days, and normal two-dimensional echocardiography. Results were compared by analysis of variance using SPSS version 16.0. There was no statistical difference in duration of therapy to complete response between the three groups (Therapy 1: 8.1 ± 4.0 days, Therapy 2: 6.7 ± 3.9 days, Therapy 3: 6.8 ± 3.2 days; p = 0.15). There were no deaths in any of the groups. We conclude that oxygen and bed rest alone are adequate therapy for HAPE and that adjuvant pharmacotherapy with either dexamethasone or nifedipine

  5. A new view of pulmonary edema and acute respiratory distress syndrome.

    PubMed

    Ketai, L H; Godwin, J D

    1998-07-01

    The old division of lung edema into two categories--cardiogenic (hydrostatic) and noncardiogenic (increased permeability)--is no longer adequate. For instance, it fails to distinguish between the capillary leak caused by acute respiratory distress syndrome from that caused by interleukin-2 treatment. Further, it fails to account for the capillary leak ('stress-failure') that may accompany edema. A modern view of edema must recognize the natural barriers to the formation and spread of edema. These barriers are the capillary endothelium and the alveolar epithelium. Varying degrees of damage to them can account for the varying radiographic and clinical manifestations of lung edema. Thus, interleukin-2 administration causes increased endothelial permeability without causing alveolar epithelial damage. The result is lung edema that is largely confined to the interstitium, causing little hypoxia and clearing rapidly. However, acute respiratory distress syndrome, which is characterized by extensive alveolar damage, causes air-space consolidation, severe hypoxia, and slow resolution. Thus, a reasonable classification of lung edema requires at least four categories: 1) hydrostatic edema; 2) acute respiratory distress syndrome (permeability edema caused by diffuse alveolar damage); 3) permeability edema without alveolar damage; and (4) mixed hydrostatic and permeability edema. The authors emphasize the importance of the barriers provided by the capillary endothelium and the alveolar epithelium in determining the clinical and radiographic manifestations of edema. In general, when the alveolar epithelium is intact, the radiographic manifestations are those of interstitial (not air-space) edema; this radiographic pattern predicts a mild clinical course and prompt resolution.

  6. Transcatheter closure of atrial septal defect protects from pulmonary edema: septal occluder device gradually reduces LR shunt.

    PubMed

    Murakami, Tsutomu; Nakazawa, Gaku; Horinouchi, Hitomi; Torii, Sho; Ijichi, Takeshi; Ohno, Yohei; Amino, Mari; Shinozaki, Norihiko; Ogata, Nobuhiko; Yoshimachi, Fuminobu; Yoshioka, Koichiro; Ikari, Yuji

    2017-01-01

    A 56-year-old woman was diagnosed as atrial septal defect (ASD) with pulmonary hypertension; pulmonary blood flow/systemic blood flow (Qp/Qs) of 2.3, pulmonary artery pressure (PAP) of 71/23(39) mmHg and diastolic dysfunction of left ventricle. PAP was improved after medical therapy; therefore, transcatheter ASD closure was performed. Seven days later, left-sided heart failure occurred, however, the improvement of Qp/Qs (1.7) and PAP of 51/21(32) was confirmed. Diuretic therapy was introduced which led to further decrease of PAP 40/12(25) and Qp/Qs (1.1). Because of gradual decrease of Qp/Qs, this patient appeared to be protected from acute pulmonary edema.

  7. Combination of constant-flow and continuous positive-pressure ventilation in canine pulmonary edema.

    PubMed

    Sznajder, J I; Becker, C J; Crawford, G P; Wood, L D

    1989-08-01

    Constant-flow ventilation (CFV) maintains alveolar ventilation without tidal excursion in dogs with normal lungs, but this ventilatory mode requires high CFV and bronchoscopic guidance for effective subcarinal placement of two inflow catheters. We designed a circuit that combines CFV with continuous positive-pressure ventilation (CPPV; CFV-CPPV), which negates the need for bronchoscopic positioning of CFV cannula, and tested this system in seven dogs having oleic acid-induced pulmonary edema. Addition of positive end-expiratory pressure (PEEP, 10 cmH2O) reduced venous admixture from 44 +/- 17 to 10.4 +/- 5.4% and kept arterial CO2 tension (PaCO2) normal. With the innovative CFV-CPPV circuit at the same PEEP and respiratory rate (RR), we were able to reduce tidal volume (VT) from 437 +/- 28 to 184 +/- 18 ml (P less than 0.001) and elastic end-inspiratory pressures (PEI) from 25.6 +/- 4.6 to 17.7 +/- 2.8 cmH2O (P less than 0.001) without adverse effects on cardiac output or pulmonary exchange of O2 or CO2; indeed, PaCO2 remained at 35 +/- 4 Torr even though CFV was delivered above the carina and at lower (1.6 l.kg-1.min-1) flows than usually required to maintain eucapnia during CFV alone. At the same PEEP and RR, reduction of VT in the CPPV mode without CFV resulted in CO2 retention (PaCO2 59 +/- 8 Torr). We conclude that CFV-CPPV allows CFV to effectively mix alveolar and dead spaces by a small bulk flow bypassing the zone of increased resistance to gas mixing, thereby allowing reduction of the CFV rate, VT, and PEI for adequate gas exchange.

  8. Involvement of water channel Aquaporin 5 in H2S-induced pulmonary edema.

    PubMed

    Xu, Chunyang; Jiang, Lei; Zou, Yuxia; Xing, Jingjing; Sun, Hao; Zhu, Baoli; Zhang, Hengdong; Wang, Jun; Zhang, Jinsong

    2017-01-01

    Acute exposure to hydrogen sulfide (H2S) poses a significant threat to life, and the lung is one of the primary target organs of H2S. However, the mechanisms involved in H2S-induced acute pulmonary edema are poorly understood. This study aims to investigate the effects of H2S on the expression of water channel aquaporin 5 (AQP5) and to elucidate the signaling pathways involved in AQP5 regulation. In an in vivo study, C57BL6 mice were exposed to sub-lethal concentrations of inhaled H2S, and histological injury of the lungs and ultrastructure injury of the epithelial cells were evaluated. With real-time PCR and western blot assays, we found that H2S exposure contributed to a significant decrease in AQP5 expression both in murine lung tissue and the A549 cell line, and the ERK1/2 and p38 MAPK signaling pathways were demonstrated to be implicated in AQP5 regulation. Therefore, adjusting AQP5 protein levels could be considered a therapeutic strategy for the treatment of APE induced by H2S and other hazardous gases.

  9. 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

  10. 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.

  11. Hemorrhagic onset of hemangioblastoma located in the dorsal medulla oblongata presenting with tako-tsubo cardiomyopathy and neurogenic pulmonary edema: a case report.

    PubMed

    Gekka, Masayuki; Yamaguchi, Shigeru; Kazumata, Ken; Kobayashi, Hiroyuki; Motegi, Hiroaki; Terasaka, Shunsuke; Houkin, Kiyohiro

    2014-01-01

    Here, we present a case of dorsal medulla oblongata hemangioblastoma with fourth ventricular hemorrhage. A 23-year-old female developed sudden consciousness disturbance, and CT revealed hemorrhage in all cerebral ventricles and a hyperdense mass in the cisterna magna. Although the reddish tumor located in the dorsal medulla oblongata was successfully removed, she suffered from severe tako-tsubo cardiomyopathy (TTC) and neurogenic pulmonary edema (NPE) because of baroreflex failure and damage to the solitary tract nuclei. After intensive care for 12 weeks following surgery, she was discharged without any neurological or radiological deficits. Pathogenesis of TTC/NPE is discussed in this paper.

  12. A Peptide to Reduce Pulmonary Edema in a Rat Model of Lung Transplantation

    PubMed Central

    Finsterwalder, Richard; Friedl, Heinz P.; Rauscher, Sabine; Gröger, Marion; Kocher, Alfred; Wagner, Christine; Wagner, Stephan N.; Fischer, Gottfried; Schultz, Marcus J.; Wiedemann, Dominik; Petzelbauer, Peter

    2015-01-01

    Background Despite significant advances in organ preservation, surgical techniques and perioperative care, primary graft dysfunction is a serious medical problem in transplantation medicine in general and a specific problem in patients undergoing lung transplantation. As a result, patients develop lung edema, causing reduced tissue oxygenation capacity, reduced lung compliance and increased requirements for mechanical ventilatory support. Yet, there is no effective strategy available to protect the grafted organ from stress reactions induced by ischemia/reperfusion and by the surgical procedure itself. Methods We assessed the effect of a cingulin-derived peptide, XIB13 or a random peptide in an established rat model of allogeneic lung transplantation. Donor lungs and recipients received therapeutic peptide at the time of transplantation and outcome was analyzed 100min and 28 days post grafting. Results XIB13 improved blood oxygenation and reduced vascular leak 100min post grafting. Even after 28 days, lung edema was significantly reduced by XIB13 and lungs had reduced fibrotic or necrotic zones. Moreover, the induction of an allogeneic T cell response was delayed indicating a reduced antigen exchange between the donor and the host. Conclusions In summary, we provide a new tool to strengthen endothelial barrier function thereby improving outcomes in lung transplantation. PMID:26536466

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

    PubMed Central

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

    2015-01-01

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

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

    PubMed

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

    2015-05-12

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

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

    PubMed Central

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

    2015-01-01

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

  16. Negative-pressure pulmonary edema complicated by acute respiratory distress syndrome in an orangutan (Pongo pygmaeus abelii).

    PubMed

    Kenny, David E; Knightly, Felicia; Haas, Bradley; Hergott, Lawrence; Kutinsky, Ilana; Eller, Jimmie L

    2003-12-01

    A 22-yr-old, 86-kg, morbidly obese female orangutan (Pongo pygmaeus abelii) was immobilized and transported to the Denver Zoological Gardens hospital for a routine physical examination. Immediately after arriving at the hospital, cyanosis and apparent inadequate ventilatory efforts were noted. Clinically significant hypoxia occurred despite attempts to ventilate the orangutan through face mask, and attempts to place an endotracheal tube began. A large volume of pink-tinged frothy fluid flowed from the trachea when the laryngoscope was inserted into the oropharynx. Severe pulmonary edema due to negative-pressure pulmonary edema, precipitating life-threatening hypoxia was suspected. The orangutan was maintained on a mechanical ventilator using the neuromuscular blocking agent cisatracurium besylate and sedation with periodic doses of isoflurane and midazolam for 48 hr. Positive end-expiratory pressure was used while the orangutan was ventilated mechanically to improve respiratory function. The edema and hypoxia improved, but respiratory arrest ensued 30 min after extubation, when the orangutan was removed from mechanical ventilation. Necropsy and histopathology demonstrated that serious lung injury had led to acute respiratory distress syndrome.

  17. [Epidemiology and development of macular edema in the diabetic].

    PubMed

    Zghal-Mokni, I; Jeddi, A; Boujemaa, C; Ben Hadj Alouane, W; Gaigi, S; Ayed, S

    2001-12-01

    Macular edema is the first cause of blindness in diabetics. Macular edema is defined by macular thickening or deposits of hard exudates. On 1000 diabetics examined over 2 years, 60 patients had a macular edema of which we retained 38 cases(54 eyes). All the patients had an ophthalmologic examination with a retinal angiography. Laser photocoagulation with green Argon laser was instituted in 50 eyes. 63% had background rethinopathy. Total or partial regression of the edema happened in 84.4%. Laser photocoagulation decrease by the half vision loss risk. Interest of early detection and treatment to decrease blindness incidence of macular edema in diabetics.

  18. [Acute pulmonary edema occurred during tocolytic treatment using nicardipine in a twin pregnancy. Report of three cases].

    PubMed

    Philippe, H-J; Le Trong, A; Pigeau, H; Demeure, D; Desjars, P; Esbelin, J; Caroit, Y; Winer, N

    2009-02-01

    We report three cases of acute pulmonary edema that occurred during treatment by intravenous tocolysis using nicardipine in twin pregnancy patients with no previous heart problems. The three patients were admitted into our unit on account of the risk of premature birth after 29 to 32 weeks of amenorrhea. The treatment by intravenous tocolysis using nicardipine combined with glucocorticoids therapy had been undertaken in the previous maternity ward. The three patients presented symptoms of acute dyspnea 48 hours after the beginning of the treatment. Paraclinical examinations eliminated the diagnosis of pulmonary embolism. The patients'condition improved rapidly with appropriate diuretic treatment and by modifying the tocolysis. There are currently few studies proving the benefits of nicardipine in tocolysis treatment. Few similar cases of acute pulmonary edema have been noted in twin pregnancy patients treated with nicardipine. Haemodynamic modifications specific to twin pregnancy, intravenous hydratation and glucocorticoid maturation may explain a part of this complication. Therefore, it is appropriated to limit the use of intravenous nicardipine in the sole indication of tocolysis in twin pregnancy, and to prefer the use of nifedipine and atosiban, that have proven their effectiveness in this indication.

  19. Inhibition of secretory phospholipase A2 activity attenuates acute cardiogenic pulmonary edema induced by isoproterenol infusion in mice after myocardial infarction.

    PubMed

    Kawabata, Kenichi; Fujioka, Daisuke; Kobayashi, Tsuyoshi; Saito, Yukio; Obata, Jun-Ei; Nakamura, Takamitsu; Yano, Toshiaki; Watanabe, Kazuhiro; Watanabe, Yosuke; Mishina, Hideto; Kugiyama, Kiyotaka

    2010-10-01

    Several types of secretory phospholipase A2 (sPLA2) are expressed in lung tissue, yielding various eicosanoids that might cause pulmonary edema. This study examined whether inhibition of sPLA2 activity attenuates acute cardiogenic pulmonary edema in mice. Acute cardiogenic pulmonary edema was induced in C57BL/6J male mice by an increase in heart rate with continuous intravenous infusion of isoproterenol (ISP) (10 mg/kg/h) at 2 weeks after the creation of myocardial infarction by left coronary artery ligation. Just before ISP infusion, a single intraperitoneal injection of 100 mg/kg LY374388, a prodrug of LY329722 that inhibits sPLA2 activity, or vehicle was administered. The ISP infusion after myocardial infarction induced interstitial and alveolar edema on lung histology. Furthermore, it increased the lung-to-body weight ratio, pulmonary vascular permeability evaluated by the Evans blue extravasation method, lung activity of sPLA2, and lung content of thromboxane A2 and leukotriene B4. These changes were significantly attenuated by LY374388 treatment. In Kaplan-Meier analysis, the survival rate during the ISP infusion after myocardial infarction was significantly higher in LY374388- than in vehicle-treated mice. Similar results were obtained with another inhibitor of sPLA2 activity, para-bromophenacyl bromide. In conclusion, inhibition of sPLA2 activity suppressed acute cardiogenic pulmonary edema.

  20. Postoperative negative pressure pulmonary edema following repetitive laryngospasm even after reversal of neuromuscular blockade by sugammadex: a case report

    PubMed Central

    Lee, Jae Ho; Lee, Min Hyun; Cho, Hyun Oh; Park, Soon Eun

    2017-01-01

    Laryngospasm, an occlusion of the glottis, can occur at any time during anesthesia, and is associated with serious perioperative complications such as hypoxia, hypercabia, aspiration, bronchospasm, arrhythmia, prolonged recovery, cardiac collapse, and eventually catastrophic death. Importantly, postoperative negative pressure pulmonary edema (NPPE) is a rare, but well described life-threatening complication related to acute and chronic upper airway obstruction. Sugammadex well known for affirmatively reducing the postoperative pulmonary complications associated with residual neuromuscular blockade may have an indirect role in triggering the negative intrathoracic pressure by raising a rapid and efficacious respiratory muscle strength in acute upper airway obstruction. Herein, we report a case of postoperative NPPE following repetitive laryngospasm even after reversal of rocuronium-induced neuromuscular blockade using sugammadex. PMID:28184275

  1. Postoperative negative pressure pulmonary edema following repetitive laryngospasm even after reversal of neuromuscular blockade by sugammadex: a case report.

    PubMed

    Lee, Ji Hyeon; Lee, Jae Ho; Lee, Min Hyun; Cho, Hyun Oh; Park, Soon Eun

    2017-02-01

    Laryngospasm, an occlusion of the glottis, can occur at any time during anesthesia, and is associated with serious perioperative complications such as hypoxia, hypercabia, aspiration, bronchospasm, arrhythmia, prolonged recovery, cardiac collapse, and eventually catastrophic death. Importantly, postoperative negative pressure pulmonary edema (NPPE) is a rare, but well described life-threatening complication related to acute and chronic upper airway obstruction. Sugammadex well known for affirmatively reducing the postoperative pulmonary complications associated with residual neuromuscular blockade may have an indirect role in triggering the negative intrathoracic pressure by raising a rapid and efficacious respiratory muscle strength in acute upper airway obstruction. Herein, we report a case of postoperative NPPE following repetitive laryngospasm even after reversal of rocuronium-induced neuromuscular blockade using sugammadex.

  2. Donor smoking is associated with pulmonary edema, inflammation and epithelial dysfunction in ex vivo human donor lungs

    PubMed Central

    Ware, Lorraine B.; Lee, Jae W.; Wickersham, Nancy; Nguyen, John; Matthay, Michael A.; Calfee, Carolyn S.

    2014-01-01

    Although recipients of donor lungs from smokers have worse clinical outcomes, the underlying mechanisms are unknown. We tested the association between donor smoking and the degree of pulmonary edema (as estimated by lung weight), the rate of alveolar fluid clearance (measured by airspace instillation of 5% albumin) and biomarkers of lung epithelial injury and inflammation (bronchoalveolar lavage surfactant protein-D and IL-8) in ex vivo lungs recovered from 298 organ donors. The extent of pulmonary edema was higher in current smokers (n=127) compared to non-smokers (median 408g, IQR 364-500 vs. 385g, IQR 340 - 460, p=0.009). Oxygenation at study enrollment was worse in current smokers versus non-smokers (median PaO2/FiO2 214 mmHg, IQR 126-323 vs. 266 mmHg, IQR 154-370, p=0.02). Current smokers with the highest exposure (≥20 pack-years) had significantly lower rates of alveolar fluid clearance, suggesting that the effects of cigarette smoke on alveolar epithelial fluid transport function may be dose related. BAL IL-8 was significantly higher in smokers while surfactant protein-D was lower. These findings indicate that chronic exposure to cigarette smoke has important effects on inflammation, gas exchange, lung epithelial function and lung fluid balance in the organ donor that could influence lung function in the lung transplant recipient. PMID:25146497

  3. 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.

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

    PubMed

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

    2015-08-01

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

  5. 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

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

    PubMed

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

    2016-10-01

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

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

    PubMed Central

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

    2016-01-01

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

  8. [Case report of re-expansion pulmonary edema in a patient with anorexia nervosa after removal of a huge ovarian tumor].

    PubMed

    Hari, Junko; Arai, Masayasu; Kosaka, Yasuharu; Toda, Masaya; Kuroiwa, Masayuki; Okamoto, Hirotsugu

    2014-04-01

    We described a case of 19-year-old female who developed re-expansion pulmonary edema (RPE) after removal of a huge ovarian tumor. Altered lung volume after the surgery was observed by chest X-ray. Preoperatively, the lung was highly compressed by the tumor. Patient was intubated under general anesthesia and was ventilated by pressure controlled mode with only 5 cmH2O of positive end-expiratory pressure (PEEP). P/F ratio was changed from 163 to 444 after removal of the tumor. At the end of the surgery, P/F ratio decreased to 263 with yellow frothy sputum in the endotracheal tube and we diagnosed re-expansion pulmonary edema based on appearing yellow frothy sputum and chest X-ray. No recruitment procedure was carried out through the course except positive pressure ventilation with 5 cmH2O of PEEP in the intensive care unit after surgery. Twelve hours after the surgery, we could not confirm the recovery of lung volume on chest X-ray; however the patient was extubated because of P/F ratio increasing to 507. After 8 days of the surgery, the chest X-ray showed recovery of the lung volume to almost normal size. In this case, the compressed lung needed almost 1 week to recover the lung volume. This change in chest X-ray might indicate inadequate recovery of lung volume by recruitment maneuver and this should be avoided in order not to allow development of unfavorable clinical course of RPE.

  9. Inhaled nitric oxide for the brain dead donor with neurogenic pulmonary edema during anesthesia for organ donation: a case report

    PubMed Central

    Park, Eun Sun; Lee, A-Ran; Lee, Sang Hyun; Kim, An Suk; Park, Soon Eun; Cho, Young Woo

    2014-01-01

    Neurogenic pulmonary edema (NPE) in brain dead organ donors occurring after an acute central nervous system insult threatens organ preservation of potential organ donors and the outcome of organ donation. Hence the active and immediate management of NPE is critical. In this case, a 50-year-old male was admitted to the intensive care unit (ICU) for organ donation. He was hypoxic due to NPE induced by spontaneous intracerebral hemorrhage and intraventricular hemorrhage. Protective ventilatory management, intermittent recruitment maneuvers, and supportive treatment were maintained in the ICU and the operating room (OR). Despite this management, the hypoxemia worsened after the OR admission. So inhaled nitric oxide (NO) therapy was performed during the operation, and the hypoxic phenomena showed remarkable improvement. The organ retrieval was successfully completed. Therefore, NO inhalation can be helpful in the improvement of hypoxemia caused by NPE in brain dead organ donors during anesthesia for the organ donation. PMID:25237451

  10. Hydrothorax with alveolar-pleural fistula mimicking re-expansion pulmonary edema during liver transplantation: a case report

    PubMed Central

    2015-01-01

    We present a case of an alveolar-pleural fistula with hepatic hydrothorax in a patient undergoing orthotropic liver transplantation, which was detected by drainage of transudate through an endotracheal tube during operation. A standard endotracheal tube was changed to a double-lumen tube to provide differential lung ventilation. The patient was diagnosed with an alveolar-pleural fistula by direct vision of an air leak during positive-pressure ventilation through a diaphragmatic incision. There was still a concern about worsening his ventilation due to persistent aspiration of pleural effusion towards the ipsilateral lung during the remaining operation period. Surgeon repaired the defect on the exposed lung surface via diaphragmatic opening. Anesthesiologists should consider an alveolar-pleural fistula as a possible differential diagnosis with re-expansion pulmonary edema when transudate emanating from the endotracheal tube is obtained in patients with massive hydrothorax. PMID:25844139

  11. Selective HDAC6 inhibition prevents TNF-α-induced lung endothelial cell barrier disruption and endotoxin-induced pulmonary edema.

    PubMed

    Yu, Jinyan; Ma, Zhongsen; Shetty, Sreerama; Ma, Mengshi; Fu, Jian

    2016-07-01

    Lung endothelial damage contributes to the pathogenesis of acute lung injury. New strategies against lung endothelial barrier dysfunction may provide therapeutic benefits against lung vascular injury. Cell-cell junctions and microtubule cytoskeleton are basic components in maintaining endothelial barrier integrity. HDAC6, a deacetylase primarily localized in the cytoplasm, has been reported to modulate nonnuclear protein function through deacetylation. Both α-tubulin and β-catenin are substrates for HDAC6. Here, we examined the effects of tubastatin A, a highly selective HDAC6 inhibitor, on TNF-α induced lung endothelial cell barrier disruption and endotoxin-induced pulmonary edema. Selective HDAC6 inhibition by tubastatin A blocked TNF-α-induced lung endothelial cell hyperpermeability, which was associated with increased α-tubulin acetylation and microtubule stability. Tubastatin A pretreatment inhibited TNF-α-induced endothelial cell contraction and actin stress fiber formation with reduced myosin light chain phosphorylation. Selective HDAC6 inhibition by tubastatin A also induced β-catenin acetylation in human lung endothelial cells, which was associated with increased membrane localization of β-catenin and stabilization of adherens junctions. HDAC6 knockdown by small interfering RNA also prevented TNF-α-induced barrier dysfunction and increased α-tubulin and β-catenin acetylation in endothelial cells. Furthermore, in a mouse model of endotoxemia, tubastatin A was able to prevent endotoxin-induced deacetylation of α-tubulin and β-catenin in lung tissues, which was associated with reduced pulmonary edema. Collectively, our data indicate that selective HDAC6 inhibition by tubastatin A is a potent approach against lung endothelial barrier dysfunction.

  12. Benzo(a)pyrene-induced pulmonary inflammation, edema, surfactant dysfunction, and injuries in rats: alleviation by farnesol.

    PubMed

    Qamar, Wajhul; Khan, Abdul Quaiyoom; Khan, Rehan; Lateef, Abdul; Tahir, Mir; Rehman, Muneeb U; Ali, Farrah; Sultana, Sarwat

    2012-02-01

    Benzo(a)pyrene (B(a)P) is a well-known environmental contaminant and carcinogen. Its sources include tobacco smoke, automobile exhaust, forest fire, and other combustion processes. Farnesol, an active principle of Vachellia farnesiana and other aromatic plants, possesses preventive properties against various toxicities. Present study was designed to estimate chemopreventive effects of farnesol against B(a)P-induced pulmonary injuries. To determine the protective effects of farnesol, it was administered orally at 2 doses (100 and 200 mg/kg body weight [b.w.]) once daily for 14 days. Rats were exposed intratracheally to B(a)P, 5 mg/kg b.w. on days 12 and 14, thereafter assessed for pulmonary toxicities 24 hours post last dose of B(a)P. B(a)P-induced edema, inflammation, oxidative stress, and consequent damages in lungs were assessed in terms of total protein, total cell count, nitric oxide (NO), lactate dehydrogenase (LDH), alkaline phosphatase, and in bronchoalveolar lavage fluid (BALF). B(a)P also reduced the levels of phospholipids (lung surfactants) in BALF. However, pretreatment with farnesol at both the doses significantly reduced the lung injuries and inflammatory responses. Farnesol also protected the levels of phospholipids to normal when compared with control. It also modified the activities of B(a)P metabolizing enzymes NADPH-cytochrome P450 reductase, microsomal epoxide hydrolase (mEH), and glutathione S-transferase (GST) in lung tissue of rats. Present findings suggest a prominent role of farnesol against B(a)P-induced lung inflammation, edema, surfactant dysfunction, and epithelial damages in Wistar rats. In conclusion, farnesol shows lung protection against B(a)P toxicities in Wistar rats.

  13. 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

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

    SciTech Connect

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

    1992-11-01

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

  15. Clara Cell Protein (CC16), a Marker of Lung Epithelial Injury, Is Decreased in Plasma and Pulmonary Edema Fluid From Patients With Acute Lung Injury

    PubMed Central

    Kropski, Jonathan A.; Fremont, Richard D.; Calfee, Carolyn S.; Ware, Lorraine B.

    2009-01-01

    Background: Acute lung injury (ALI) and ARDS are common clinical syndromes that are underdiagnosed. Clara cell secretory protein (CC16) is an antiinflammatory protein secreted by the Clara cells of the distal respiratory epithelium that has been proposed as a biomarker of lung epithelial injury. We tested the diagnostic and prognostic utility of CC16 in patients with non–trauma-related ALI/ARDS compared to a control group of patients with acute cardiogenic pulmonary edema (CPE). Methods: Plasma and pulmonary edema fluid samples were obtained from medical and surgical patients with ALI/ARDS or CPE requiring intubation for mechanical ventilation. The etiology of pulmonary edema was determined using consensus clinical criteria for ALI/ARDS and CPE and the edema fluid-to-plasma protein ratio. Plasma and edema fluid CC16 levels were measured by sandwich enzyme-linked immunosorbent assay. CC16 levels were log transformed for analysis, and comparisons were made by the Student t test or χ2 as appropriate. Results: Compared to patients with CPE (n = 9), patients with ALI/ARDS (n = 23) had lower median CC16 levels in plasma (22 ng/mL [interquartile range (IQR), 9 to 44 ng/mL] vs 55 ng/mL [IQR, 18 to 123 ng/mL], respectively; p = 0.053) and pulmonary edema fluid (1,950 ng/mL [IQR, 1,780 to 4,024 ng/mL] vs 4,835 ng/mL [IQR, 2,006 to 6,350 ng/mL], respectively; p = 0.044). Relative to total pulmonary edema fluid protein concentration, the median CC16 level was significantly lower in patients with ALI/ARDS (45 ng CC16/mg total protein [IQR, 4 to 64 ng CC16/mg total protein] vs 120 ng CC16/mg total protein [IQR, 87 to 257 ng CC16/mg total protein], respectively; p = 0.005). Neither plasma nor edema fluid CC16 levels predicted mortality, the number of days of unassisted ventilation, or ICU length of stay. Conclusion: CC16 is a promising diagnostic biomarker for helping to discriminate ALI from CPE. Larger scale validation is warranted to better characterize the utility of CC16

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

    PubMed

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

    2001-12-01

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

  17. 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

  18. Incidence of high altitude pulmonary edema in low-landers during re-exposure to high altitude after a sojourn in the plains

    PubMed Central

    Apte, C.V.; Tomar, R.K.S.; Sharma, D.

    2015-01-01

    Background There is uncertainty whether acclimatized low-landers who return to high altitude after a sojourn at low altitude have a higher incidence of pulmonary edema than during the first exposure to high altitude. Methods This was a prospective cohort study consisting of men ascending to 3400 m by road (N = 1003) or by air (N = 4178). The study compared the incidence of high altitude pulmonary edema during first exposure vs the incidence during re-exposure in each of these cohorts. Results Pulmonary edema occurred in 13 of the 4178 entries by air (Incidence: 0.31%, 95% CI: 0.18%–0.53%). The incidence during first exposure was 0.18% (0.05%–0.66%) and 0.36% (0.2%–0.64%) during re-exposure (Fisher Exact Test for differences in the incidence (two-tailed) p = 0.534). The relative risk for the re-exposure cohort was 1.95 (95% CI, 0.43%–8.80%). Pulmonary edema occurred in 3 of the 1003 road entrants (Incidence: 0.30%, 95% CI: 0.08%–0.95%). All three cases occurred in the re-exposure cohort. Conclusion The large overlap of confidence intervals between incidence during first exposure and re-exposure; the nature of the confidence interval of the relative risk; and the result of the Fisher exact test, all suggest that this difference in incidence could have occurred purely by chance. We did not find evidence for a significantly higher incidence of HAPE during re-entry to HA after a sojourn in the plains. PMID:26288488

  19. Enhanced expression of Fas and FasL modulates apoptosis in the lungs of severe P. falciparum malaria patients with pulmonary edema

    PubMed Central

    Punsawad, Chuchard; Viriyavejakul, Parnpen; Setthapramote, Chayanee; Palipoch, Sarawoot

    2015-01-01

    Apoptosis mediated by Fas/FasL has been implicated in pulmonary disorders. However, little is known about the relationship between Fas and FasL in the process of lung injury during malaria infection. Paraffin-embedded lung tissues from malaria patients were divided into two groups: those with pulmonary edema (PE) and those without pulmonary edema (non-PE). Normal lung tissues were used as the control group. Cellular expression of Fas, FasL, and the markers of apoptotic caspases, including cleaved caspase-3 and cleaved caspase-8 in the lung tissues were investigated by the immunohistochemistry (IHC) method. Semi-quantitative analysis of IHC staining revealed that cellular expression of Fas, FasL, cleaved caspase-8, and cleaved caspase-3 were significantly increased in the lungs of patients with PE compared with the lungs of patients with non-PE and control groups (all P < 0.05). In addition, significant positive correlations were obtained between Fas and apoptosis (rs = 0.937, P < 0.001) and FasL and apoptosis (rs = 0.808, P < 0.001). Significant positive correlations were found between Fas and FasL expression (rs = 0.827, P < 0.001) and between cleaved caspase-8 and cleaved caspase-3 expression (rs = 0.823, P < 0.001), which suggests that Fas-dependent initiator and effector caspases, including cleaved caspase-8 and caspase-3, are necessary for inducing apoptosis in the lungs of patients with severe P. falciparum malaria. The Fas/FasL system and downstream activation of caspases are important mediators of apoptosis and may be involved in the pathogenesis of pulmonary edema in severe P. falciparum malaria patients. The proper regulation of the Fas/FasL pathway can be a potential treatment for pulmonary complications in falciparum malaria patients. PMID:26617708

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

    PubMed

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

    2013-12-01

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

  1. Mitochondrial haplogroup D4 confers resistance and haplogroup B is a genetic risk factor for high-altitude pulmonary edema among Han Chinese.

    PubMed

    Luo, Y J; Gao, W X; Li, S Z; Huang, X W; Chen, Y; Liu, F Y; Huang, Q Y; Gao, Y Q

    2012-10-09

    High-altitude pulmonary edema (HAPE) is a life-threatening condition caused by acute exposure to high altitude. Accumulating evidence suggests that genetic factors play an important role in the etiology of HAPE. However, conclusions from association studies have been hindered by limited sample size due to the rareness of this disease. It is known that mitochondria are critical for hypoxic adaptation, and mitochondrial malfunction can be an important factor in HAPE development. Therefore, we tested the hypothesis that mitochondrial DNA haplotypes and polymorphisms affect HAPE susceptibility. We recruited 204 HAPE patients and 174 healthy controls in Tibet (3658 m above sea level), all Han Chinese, constituting the largest sample size of all HAPE vulnerability studies. Among mtDNA haplogroups, we found that haplogroup D4 is associated with resistance to HAPE, while haplogroup B is a genetic risk factor for this condition. Haplogroup D4 (tagged by 3010A) may enhance the stability of 16S rRNA, resulting in reduced oxidative stress and protection against HAPE. Within haplogroup B, subhaplogroup B4c (tagged by 15436A and 1119C) was associated with increased risk for HAPE, while subhaplogroup B4b may protect against HAPE. We indicate that there are differences in HAPE susceptibility among mtDNA haplogroups. We conclude that mitochondria are involved in adverse reactions to acute hypoxic exposure; our finding of differences in susceptibility as a function of mitochondrial DNA haplotype may shed light on the pathogenesis of other disorders associated with hypoxia, such as chronic obstructive pulmonary disease.

  2. The susceptibility gene screening in a Chinese high-altitude pulmonary edema family by whole-exome sequencing.

    PubMed

    Yingzhong, Yang; Yaping, Wang; Jin, Xu; Rili, Ge

    2017-02-20

    High-altitude pulmonary edema (HAPE) is one of idiopathic mountain sicknesses that occur in healthy lowlanders when they quickly ascend to altitudes exceeding 2500 m above sea levels within 1-7 days. Growing evidence suggests that genetics plays an important role in the risk of HAPE. In this study, we recruited a Chinese HAPE family and screened genetic variations in the 7 family members (including 6 family members with a medical history of HAPE and the propositus's mother) by whole-exome sequencing. The results showed 18 genetic variations (9 SNVs and 9 Indels) were related to HAPE. Two SNV sites (CFHR4 (p.L85F) and OXER1 (p.R176C)) were predicted to be damaging and alter protein functions by SIFT, PolyPhen-2 and PROVEAN software. The biological function of OXER1 was highly related to the hypoxia-inducible factor pathway. Therefore, those two sites were identified as candidate pathological variations. Moreover, other SNVs (NMB p.S150P, APOB p.I4194T, EIF4ENIF1 p.Q763P) and Indels (KCNJ12 p.EE333-334E, ANKRD31 p.LMN251-253LN, OR2A14 p.HFFC175-178HFC) were also predicted to be damaging as well, which also might be considered as potential candidate pathological variations related to HAPE. Collectively we firstly screened the susceptibility genes in a Chinese HAPE family by whole-exome sequencing, which will provide new clues for further mechanistic studies of HAPE.

  3. Acidemia in severe acute cardiogenic pulmonary edema treated with noninvasive pressure support ventilation: a single-center experience.

    PubMed

    Lazzeri, Chiara; Gensini, Gian F; Picariello, Claudio; Attanà, Paola; Mattesini, Alessio; Chiostri, Marco; Valente, Serafina

    2015-09-01

    In clinical practice, acidotic patients with acute cardiogenic pulmonary edema (ACPE) are commonly considered more severe in comparison with nonacidotic patients, and data on the outcome of these patients treated with noninvasive pressure support ventilation (NIV) are lacking.The present investigation was aimed at assessing whether acidosis on admission (pH < 7.35) was associated with adverse outcome in 65 consecutive patients with ACPE treated with NIV and admitted to our Intensive Cardiac Care Unit (ICCU).In our population, 28 patients were acidotic (28 of 65, 43.1%), whereas 41 patients were not (37 of 65, 56.9%). According to the Repeated Measures General Linear Model, pCO2 values significantly changed throughout the 2-h NIV treatment (P = 0.019) in both groups (P = 0001). In acidotic patients, pCO2 significantly decreased (51.9 ± 15.3 → 47.0 ± 12.8 → 44.8 ± 12.7), whereas they increased in the nonacidotic subgroup (36.8 ± 6.5 → 36.9 ± 7.2 → 37.6 ± 6.4). No difference was observed in intubation rate between acidotic (eight patients, 28.6%) and nonacidotic patients (12 patients, 32.4%) (P = 0.738). In-ICCU mortality rate did not differ between (13 patients, 35.1%) and nonacidotic patients (nine patients, 32.1%) (P = 0.801).Our data strongly suggest that in patients with severe ACPE treated with NIV, the presence of acidosis is not associated with adverse outcomes (early mortality and intubation rates) in these patients.

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

    PubMed

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

    2016-05-01

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

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

    PubMed Central

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

    2015-01-01

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

  6. Successful management of severe unilateral re-expansion pulmonary edema after mitral valve repair with mini-thoracotomy using extracorporeal membrane oxygenation.

    PubMed

    Kitahara, Hiroto; Okamoto, Kazuma; Kudo, Mikihiko; Yoshitake, Akihiro; Hayashi, Kanako; Inaba, Yu; Ai, Kimiaki; Suzuki, Takeshi; Morisaki, Hiroshi; Shimizu, Hideyuki

    2017-03-01

    A 60-year-old man received mitral valve repair via right mini-thoracotomy, which was followed by unilateral re-expansion pulmonary edema on the right side and severe hemoptysis just after the surgery. Despite differential lung ventilation with unilateral high positive end expiratory pressure was initiated for the affected right lung, respiratory function did not improved and hemodynamics was collapsed in the next day. Veno-venous extracorporeal membrane oxygenation was initiated by cannulation of the right jugular and the left femoral vein. After pulmonary function recovered gradually, veno-venous extracorporeal membrane oxygenation was terminated on the fifth postoperative day. He was discharged in ambulatory condition on postoperative day 52.

  7. The Impact of Moderate-Altitude Staging on Pulmonary Arterial Hemodynamics after Ascent to High Altitude

    DTIC Science & Technology

    2010-01-01

    et al., 1956; Sime et al., 1974). The magnitude of the PAP in- crease plays an important role in the development of high altitude pulmonary edema ...implications for travelers to high altitude. High altitude pulmonary edema (HAPE) is an important cause of high altitude morbidity and mortality, and...P., and Oelz O. (1991). Prevention of high-altitude pulmonary edema by nifedipine. N. Engl. J. Med. 325:1284–1289. Beidleman B.A., Fulco C.S., Muza

  8. Non-cardiogenic pulmonary edema and life-threatening shock due to calcium channel blocker overdose: a case report and clinical review.

    PubMed

    Siddiqi, Tauseef Afaq; Hill, Jennifer; Huckleberry, Yvonne; Parthasarathy, Sairam

    2014-02-01

    Calcium channel blockers (CCBs) overdose can be life-threatening when manifest as catastrophic shock and non-cardiogenic pulmonary edema. We describe a case of massive overdose of multiple medications, including sustained-release verapamil, which was resistant to conventional support. Initial treatment for CCB overdose is primarily supportive, and includes fluid resuscitation. The mechanism of non-cardiogenic pulmonary edema is not well known, and reported cases have been successfully treated with mechanical ventilation. Circulatory shock may fail to respond to atropine, glucagon, and calcium in severely poisoned patients, and vasopressors are usually required. Attempting to overcome calcium-channel antagonism with the supra-therapeutic doses of calcium salts is clinically indicated to reverse hypotension and bradycardia. There is evidence that hyperinsulinemia-euglycemia therapy is superior to other therapies for CCB poisoning, and the mechanism is thought to be the insulin-mediated active transport of glucose into the cells, which counters the CCB-induced intra-cellular carbohydrate-deficient state. Conventional decontamination measures are ineffective in accelerating clearance of CCB. Experience with intravenous lipid emulsion for lipophilic drug overdose, such as verapamil, is limited, but has been proposed as a rescue therapy and might improve cardiac inotropy through intravascular sequestration of the lipophilic CCB.

  9. 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

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

    PubMed Central

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

    2016-01-01

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

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

    PubMed

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

    2016-06-01

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

  12. Gpr177 regulates pulmonary vasculature development.

    PubMed

    Jiang, Ming; Ku, Wei-yao; Fu, Jiang; Offermanns, Stefan; Hsu, Wei; Que, Jianwen

    2013-09-01

    Establishment of the functional pulmonary vasculature requires intimate interaction between the epithelium and mesenchyme. Previous genetic studies have led to inconsistent conclusions about the contribution of epithelial Wnts to pulmonary vasculature development. This discrepancy is possibly due to the functional redundancy among different Wnts. Here, we use Shh-Cre to conditionally delete Gpr177 (the mouse ortholog of Drosophila Wntless, Wls), a chaperon protein important for the sorting and secretion of Wnt proteins. Deletion of epithelial Gpr177 reduces Wnt signaling activity in both the epithelium and mesenchyme, resulting in severe hemorrhage and abnormal vasculature, accompanied by branching defects and abnormal epithelial differentiation. We then used multiple mouse models to demonstrate that Wnt/β-catenin signaling is not only required for the proliferation and differentiation of mesenchyme, but also is important for the maintenance of smooth muscle cells through the regulation of the transcription factor Kruppel-like factor 2 (Klf2). Together, our studies define a novel mechanism by which epithelial Wnts regulate the normal development and maintenance of pulmonary vasculature. These findings provide insight into the pathobiology of congenital lung diseases, such as alveolar capillary dysplasia (ACD), that have abnormal alveolar development and dysmorphic pulmonary vasculature.

  13. Magnetic Resonance investigation into the mechanisms involved in the development of high-altitude cerebral edema

    PubMed Central

    Sagoo, Ravjit S; Hutchinson, Charles E; Wright, Alex; Handford, Charles; Parsons, Helen; Sherwood, Victoria; Wayte, Sarah; Nagaraja, Sanjoy; Ng’Andwe, Eddie; Wilson, Mark H

    2016-01-01

    Rapid ascent to high altitude commonly results in acute mountain sickness, and on occasion potentially fatal high-altitude cerebral edema. The exact pathophysiological mechanisms behind these syndromes remain to be determined. We report a study in which 12 subjects were exposed to a FiO2 = 0.12 for 22 h and underwent serial magnetic resonance imaging sequences to enable measurement of middle cerebral artery velocity, flow and diameter, and brain parenchymal, cerebrospinal fluid and cerebral venous volumes. Ten subjects completed 22 h and most developed symptoms of acute mountain sickness (mean Lake Louise Score 5.4; p < 0.001 vs. baseline). Cerebral oxygen delivery was maintained by an increase in middle cerebral artery velocity and diameter (first 6 h). There appeared to be venocompression at the level of the small, deep cerebral veins (116 cm3 at 2 h to 97 cm3 at 22 h; p < 0.05). Brain white matter volume increased over the 22-h period (574 ml to 587 ml; p < 0.001) and correlated with cumulative Lake Louise scores at 22 h (p < 0.05). We conclude that cerebral oxygen delivery was maintained by increased arterial inflow and this preceded the development of cerebral edema. Venous outflow restriction appeared to play a contributory role in the formation of cerebral edema, a novel feature that has not been observed previously. PMID:26746867

  14. Dexmedetomidine alleviates pulmonary edema by upregulating AQP1 and AQP5 expression in rats with acute lung injury induced by lipopolysaccharide.

    PubMed

    Jiang, Yuan-xu; Dai, Zhong-liang; Zhang, Xue-ping; Zhao, Wei; Huang, Qiang; Gao, Li-kun

    2015-10-01

    This study aims to elucidate the mechanisms by which dexmedetomidine alleviates pulmonary edema in rats with acute lung injury induced by lipopolysaccharide (LPS). Male Wistar rats were randomly divided into five groups: normal saline control (NS) group, receiving intravenous 0.9% normal saline (5 mL/kg); LPS group, receiving intravenous LPS (10 mg/kg); small-dose dexmedetomidine (S) group, treated with a small dose of dexmedetomidine (0.5 μg · kg(-1) · h(-1)); medium-dose dexmedetomidine (M) group, treated with a medium dose of dexmedetomidine (2.5 μg · kg(-1) · h(-1)); high-dose dexmedetomidine (H) group, treated with a high dose of dexmedetomidine (5 μg · kg(-1) · h(-1)). The rats were sacrificed 6 h after intravenous injection of LPS or NS, and the lungs were removed for evaluating histological characteristics and determining the lung wet/dry weight ratio (W/D). The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in the lung tissues were assessed by enzyme- linked immunosorbent assay (ELISA). The mRNA and protein expression levels of aquaporin-1 (AQP1) and aquaporin-5 (AQP5) were detected by RT-PCR, immunohistochemistry, and Western blotting. The lung tissues from the LPS groups were significantly damaged, which were less pronounced in the H group but not in the small-dose dexmedetomidine group or medium-dose dexmedetomidine group. The W/D and the concentrations of TNF-α and IL-1β in the pulmonary tissues were increased in the LPS group as compared with those in NS group, which were reduced in the H group but not in S group or M group (P<0.01). The expression of AQP1 and AQP5 was lower in the LPS group than in the NS group, and significantly increased in the H group but not in the S group or M group (P<0.01). Our findings suggest that dexmedetomidine may alleviate pulmonary edema by increasing the expression of AQP-1 and AQP-5.

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

    PubMed Central

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

    2015-01-01

    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

  16. What Is Macular Edema?

    MedlinePlus Videos and Cool Tools

    ... Español Eye Health / Eye Health A-Z Macular Edema Sections What Is Macular Edema? What Causes Macular ... Edema Diagnosis Macular Edema Treatment What Is Macular Edema? Dec. 01, 2010 Macular edema is swelling or ...

  17. Drug-induced pulmonary disease

    MedlinePlus

    ... mediastinitis ) Abnormal buildup of fluid in the lungs ( pulmonary edema ) Buildup of fluid between the layers of tissue ... reactions Cardiovascular Chemotherapy Interstitial lung disease Pleural effusion Pulmonary edema Respiratory Systemic lupus erythematosus Patient Instructions Interstitial lung ...

  18. Association between single nucleotide polymorphisms in ADRB2, GNB3 and GSTP1 genes and high-altitude pulmonary edema (HAPE) in the Chinese Han population.

    PubMed

    He, Yongjun; Liu, Lijun; Xu, Pengcheng; He, Na; Yuan, Dongya; Kang, Longli; Jin, Tianbo

    2017-02-14

    High altitude pulmonary edema (HAPE) occurs mainly under conditions such as high altitude, rapid ascent, or hypoxia. Previous studies suggest that ADRB2, GNB3, TH, and GSTP1 polymorphisms are associated with various lung diseases. We evaluated whether those polymorphisms are associated with the risk of HAPE in a Chinese Han population. ADRB2, GNB3, TH and GSTP1 polymorphisms were genotyped using a Sequenom MassARRAY. Logistic regression, adjusted for age and gender, was used to evaluate the association between the genotypes and the risk of HAPE by computing odds ratios (ORs) and 95% confidence intervals (95% CIs). The results revealed that GNB3 rs4963516 allele ''G'' (G vs T: OR = 0.70, 95% CI = 0.55-0.90, p = 0.006) was associated with HAPE risk. The ADRB2 rs1042718 alleles had a 1.29-fold (95%CI = 1.00-1.66; p = 0.045) increased risk of HAPE, and the GSTP1 rs749174 alleles had a 0.71-fold (95%CI = 0.52-0.99; p = 0.042) decreased risk of HAPE. Co-dominant and dominant models of GNB3 rs4963516 decreased the risk of HAPE (p = 0.023 and p = 0.008, respectively). Our results indicate GNB3 and GSTP1 polymorphisms may protect against HAPE progression, while ADRB2 polymorphisms are associated with an increased risk of HAPE.

  19. Developing treatments for pulmonary arterial hypertension

    PubMed Central

    Wilkins, Martin R.

    2013-01-01

    Developing new treatments for pulmonary arterial hypertension (PAH) is a challenge. We have enjoyed success with regulatory approvals for three drug classes—prostanoids, endothelin receptor antagonists and phosphodiesterase type 5 inhibitors. But we have also seen some disappointing results, for example, from studies with vasoactive intestinal polypeptide, statins and tergolide. Animal models are an unreliable predictor of efficacy in humans. The best model for the disease is the patient. This review discusses three major issues facing the evaluation of drugs in PAH patients—target validation, choosing the right dose, and early trial design. PMID:23662193

  20. 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

  1. Transient Idiopathic Primary Penoscrotal Edema

    PubMed Central

    Namir, Sody A; Trattner, Akiva

    2013-01-01

    We present the case of a male born prematurely at 32 weeks gestation by cesarean section following overt symptoms of maternal preeclampsia. He developed severe penoscrotal edema anew one month from birth. No remarkable exposure or trauma was identified. This unexplained swelling remained uniform till 4 months of age, while the penile edema resolved spontaneously. A small benign hydrocele remained unchanged, since onset of the edema and continued after the edema subsided. This is the first report of persistent, but transient penoscrotal edema resolving in a 3 months course, without any apparent explanation, a possible pathogenetic mechanism was suggested. PMID:24082210

  2. Methylprednisolone prevents the development of autotomy and neuropathic edema in rats, but has no effect on nociceptive thresholds.

    PubMed

    Kingery, W S; Castellote, J M; Maze, M

    1999-04-01

    Corticosteroids are probably an effective treatment for some types of neuropathic pain and complex regional pain syndromes. This study examined the effects of systemic methylprednisolone (MP) on acute nociception and on pain behavior and hyperalgesia in normal and neuropathic rats. There was no dose-response to intraperitoneal MP (up to 12 mg/kg) for nociceptive thresholds to heat (Peltier) or mechanical (analgesy-meter and von Frey fibers) stimuli in normal rats. Chronic high dose MP (3 mg/kg per day for 21 days) also had no effect on acute nociceptive thresholds in normal rats. After sciatic nerve section in rats a saphenous nerve mediated hyperalgesia to heat and mechanical stimuli gradually developed over 21 days. High dose MP (3 mg/kg per day for 21 days) had no effect on this adjacent neuropathic hyperalgesia. When systemic MP was started immediately after bilateral sciatic and saphenous nerve transection there was a dose-dependent reduction in autotomy behavior. Substance P has been proposed as a mediator of neuropathic pain and edema. Single dose MP (12 mg/kg) slightly reduced the substance P mediated extravasation induced with electrical stimulation of the saphenous nerve. Chronic MP (3.4 mg/kg per day for 28 days) severely reduced the neurogenic extravasation induced with saphenous nerve stimulation. Sciatic sectioned rats developed hindpaw edema between 7 and 14 days after surgery, and this neuropathic edema did not develop in rats chronically treated with MP (3.4 mg/kg per day). These results demonstrate that corticosteroids did not affect nociceptive thresholds in normal or neuropathic hyperalgesic rats. Chronic steroid treatment did prevent the development of autotomy and neuropathic edema, and completely blocked neurogenic extravasation, findings consistent with the hypothesis that primary afferent substance P release mediates autotomy pain behavior and neuropathic edema. This may be a relevant model for examining the effects of corticosteroids on

  3. Objective criteria for diagnosing high altitude pulmonary edema in acclimatized patients at altitudes between 2700 m and 3500 m

    PubMed Central

    Chawla, Anuj; Tripathi, K.K.

    2015-01-01

    Background The criteria used for diagnosing high altitude illnesses are largely based on Western literature. This study was undertaken to define objective, simple and reliable diagnostic criteria for high altitude pulmonary edema (HAPE) in Indian soldiers at altitudes between 2700 m and 3500 m. Methods Clinical data of 235 cases of HAPE that occurred between 2700 m and 3500 m were analysed. Receiver operator characteristic (ROC) curve analysis was used to select simple clinical parameters suitable for the diagnosis of HAPE at peripheral medical facilities. Cut-off values and their reliability for the diagnosis of HAPE were defined. Results HAPE occurred 2.8 ± 2.2 days after arrival at altitudes between 2700 m and 3500 m. Breathlessness, cough, chest discomfort and headache were the commonest symptoms. Low pulse oximetry (SPO2) values than normal for this altitude were seen in 89% of patients. ROC analysis of clinical parameters identified a heart rate more than 95 beats per minute (bpm), respiratory rate more than 21 per minute and SPO2 less than 86% while breathing ambient air at this altitude as diagnostic of HAPE. The sensitivity and specificity of these cut-offs was 0.66, 0.83 and 0.82 and 0.94, 0.95 and 0.93 respectively. Conclusion A heart rate of more than 95 bpm, respiratory rate more than 21 per minute and SPO2 less than 86% breathing room air in individuals complaining of breathlessness, cough, chest discomfort or headache within the first 5 days of arrival at altitudes between 2700 m and 3500 m is highly suggestive of HAPE. PMID:26663962

  4. Accuracy of point-of-care lung ultrasonography for the diagnosis of cardiogenic pulmonary edema in dogs and cats with acute dyspnea.

    PubMed

    Ward, Jessica L; Lisciandro, Gregory R; Keene, Bruce W; Tou, Sandra P; DeFrancesco, Teresa C

    2017-03-15

    OBJECTIVE To determine the accuracy of a point-of-care lung ultrasonography (LUS) protocol designed to diagnose cardiogenic pulmonary edema (CPE) in dyspneic dogs and cats. DESIGN Diagnostic test evaluation. ANIMALS 76 dogs and 24 cats evaluated for dyspnea. PROCEDURES Dogs and cats were evaluated by LUS; B lines were counted at 4 anatomic sites on each hemithorax. A site was scored as positive when > 3 B lines were identified. Animals with ≥ 2 positive sites identified on each hemithorax were considered positive for CPE. Medical records were evaluated to obtain a final diagnosis (reference standard) for calculation of the sensitivity and specificity of LUS and thoracic radiography for the diagnosis of CPE. RESULTS Dogs and cats with a final diagnosis of CPE had a higher number of positive LUS sites than did those with noncardiac causes of dyspnea. Overall sensitivity and specificity of LUS for the diagnosis of CPE were 84% and 74%, respectively, and these values were similar to those of thoracic radiography (85% and 87%, respectively). Use of LUS generally led to the misdiagnosis of CPE (ie, a false-positive result) in animals with diffuse interstitial or alveolar disease. Interobserver agreement on LUS results was high (κ > 0.85). CONCLUSIONS AND CLINICAL RELEVANCE LUS was useful for predicting CPE as the cause of dyspnea in dogs and cats, although this technique could not be used to differentiate CPE from other causes of diffuse interstitial or alveolar disease. Point-of-care LUS has promise as a diagnostic tool for dyspneic dogs and cats.

  5. 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.

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

    PubMed

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

    2014-12-01

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

  7. Dysfunction of pulmonary vascular endothelium in chronic obstructive pulmonary disease: basic considerations for future drug development.

    PubMed

    Yang, Qin; Underwood, Malcolm J; Hsin, Michael K Y; Liu, Xiao-Cheng; He, Guo-Wei

    2008-09-01

    Chronic obstructive pulmonary disease (COPD) is one of the leading health problems worldwide and continues to be a major cause of morbidity and mortality in developed countries. The clinical features of COPD are chronic obstructive bronchiolitis and emphysema. Pulmonary vascular endothelial dysfunction is a characteristic pathological finding of COPD at different stages of the disease. Functional changes of pulmonary endothelial cells in COPD include antiplatelet abnormalities, anticoagulant disturbances, endothelial activation, atherogenesis, and compromised regulation of vascular tone which may adversely affect the ventilation-perfusion match in COPD. As the most important risk factor of COPD, cigarette smoking may initiate pulmonary vascular impairment through direct injury of endothelial cells or release of inflammatory mediators. Morphological changes such as denudation of endothelium and endothelial cell apoptosis have been observed in the pulmonary vasculature in COPD patients as well as functional alterations. Changes in the expression of tissue factor pathway inhibitor (TFPI), thrombomodulin, selectins, and adhesion molecules in pulmonary endothelial cells as well as complex regulation and interaction of vasoactive substances and growth factors released from endothelium may underlie the mechanisms of pulmonary endothelial dysfunction in COPD. The mechanism of endothelial repair/regeneration in COPD, although not fully understood, may involve upregulation of vascular endothelial growth factors in the early stages along with an increased number of bone marrow-derived progenitor cells. These factors should be taken into account when developing new strategies for the pharmacological therapy of patients with COPD.

  8. 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.…

  9. 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

  10. 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

  11. Agents Which Mediate Pulmonary Edema

    DTIC Science & Technology

    1990-12-01

    varying fractions of the LD50 and the plate was incubated at 370C for 4 hours. Control wells of endothelial cells plhs medium/ diluent were established. All...measured by incubation of the targets in culture medium/ diluent without challenge. Specific cytolysis was calculated by: Experimental Counts - Spontaneous...and is an important bactericidal mechanism employed by the AM. In Figures 3 and 4, production of SOA (as measured by ferricytochrome C reduction) by

  12. [Pathopshysiological mechanisms in macular edema].

    PubMed

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

    2014-01-01

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

  13. Molecular Pathogenesis of Rickettsioses and Development of Novel Anti-Rickettsia Treatment by Comginatorial Peptide-Based Libraries

    DTIC Science & Technology

    2005-02-01

    and non- cardiogenic pulmonary edema . The mechanisms responsible for increased microvascular permeability are completely unknown. Methods: Sarcoma-virus...are the development of severe cerebral and pulmonary edema leading to permanent neurologic sequelae or death owing to respiratory failure (3,4). The...therapeutic targets to prevent or ameliorate both cerebral and pulmonary edema during the acute phase of the various rickettsioses. Our plans to continue with

  14. 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.

  15. 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.

  16. Doxycycline Inhibits Vascular Leakage and Prevents the Development of Pulmonary Edema

    DTIC Science & Technology

    2008-12-01

    K., G. M. Longo, W. G. Mayhan, E. A. Waltke, B. Fleckten, R. W. Thompson, and B. T. Baxter, 2002: Doxycycline in patients with abdominal aortic ...reaction in a mouse model of contact dermatitis. Mice were sensitized by applying the hapten oxazolone to their abdominal skin, and then were treated... aneurysms and in mice: comparison of serum levels and effect on aneurysm growth in mice. J Vasc Surg, 35, 923-9. Streit, M., P. Velasco, L. Riccardi

  17. S-Nitrosylation and the Development of Pulmonary Hypertension

    DTIC Science & Technology

    2009-02-14

    transducing this signal into changes in protein expression to alter pulmonary physiology are unclear. The role S-nitrosothiols ( SNO ) play in the...development of PAH is examined in this research project. In the pulmonary circulation, erythrocytes deliver SNOs to recipient target proteins on the...oxygen saturation to deliver SNOs to the vascular endothelium. We have developed a model in which N- acetyl cysteine (NAC) is used as a tracer to 1

  18. Development of pulmonary arterial hypertension in women: interplay of sex hormones and pulmonary vascular disease

    PubMed Central

    Pugh, Meredith E; Hemnes, Anna R

    2010-01-01

    Pulmonary arterial hypertension (PAH) is a progressive disease of the pulmonary vasculature, ultimately resulting in right heart failure and death. This disease is strongly predominant in females, although little is known regarding how sex influences disease development. Recent developments highlighting the importance of estrogen metabolites in both animal models and human disease have substantially increased our understanding of PAH in women. This review will focus on general knowledge of PAH, translational and basic science data regarding sex hormones in the pulmonary vasculature and on clinical issues that are particular to women with PAH. Future directions for study include the influence of sex hormones on right ventricular responses, improving the understanding of the influence of estrogen exposure in human disease and the study of dehydroepiandrosterone in basic science and human disease. PMID:20187732

  19. 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…

  20. Brain Edema After Ischaemic Stroke

    PubMed Central

    Dostovic, Zikrija; Dostovic, Ernestina; Smajlovic, Dzevdet; Ibrahimagic, Omer C.; Avdic, Leila

    2016-01-01

    Objectives: To determine the incidence of brain edema after ischaemic stroke and its impact on the outcome of patients in the acute phase of ischaemic stroke. Patients and Methods: We retrospectively analyzed 114 patients. Ischaemic stroke and brain edema are verified by computed tomography. The severity of stroke was determined by National Institutes of Health Stroke Scale. Laboratory findings were made during the first four days of hospitalization, and complications were verified by clinical examination and additional tests. Results: In 9 (7.9%) patients developed brain edema. Pneumonia was the most common complication (12.3%). Brain edema had a higher incidence in women, patients with hypertension and elevated serum creatinine values, and patients who are suffering from diabetes. There was no significant correlation between brain edema and survival in patients after acute ischaemic stroke. Patients with brain edema had a significantly higher degree of neurological deficit as at admission, and at discharge (p = 0.04, p = 0.004). Conclusion: The cerebral edema is common after acute ischaemic stroke and no effect on survival in the acute phase. The existence of brain edema in acute ischaemic stroke significantly influence the degree of neurological deficit. PMID:27994292

  1. Therapeutic implications of melatonin in cerebral edema.

    PubMed

    Rathnasamy, Gurugirijha; Ling, Eng-Ang; Kaur, Charanjit

    2014-12-01

    Cerebral edema/brain edema refers to the accumulation of fluid in the brain and is one of the fatal conditions that require immediate medical attention. Cerebral edema develops as a consequence of cerebral trauma, cerebral infarction, hemorrhages, abscess, tumor, hypoxia, and other toxic or metabolic factors. Based on the causative factors cerebral edema is differentiated into cytotoxic cerebral edema, vasogenic cerebral edema, osmotic and interstitial cerebral edema. Treatment of cerebral edema depends on timely diagnosis and medical assistance. Pragmatic treatment strategies such as antihypertensive medications, nonsteroidal anti-inflammatory drugs, barbiturates, steroids, glutamate and N-methyl-D-aspartate receptor antagonists and trometamol are used in clinical practice. Although the above mentioned treatment approaches are being used, owing to the complexity of the mechanisms involved in cerebral edema, a single therapeutic strategy which could ameliorate cerebral edema is yet to be identified. However, recent experimental studies have suggested that melatonin, a neurohormone produced by the pineal gland, could be an effective alternative for treating cerebral edema. In animal models of stroke, melatonin was not only shown to reduce cerebral edema but also preserved the blood brain barrier. Melatonin's beneficial effects were attributed to its properties, such as being a potent anti-oxidant, and its ability to cross the blood brain barrier within minutes after its administration. This review summarizes the beneficial effects of melatonin when used for treating cerebral edema.

  2. Reperfusion edema after thromboendarterectomy: radiographic patterns of disease.

    PubMed

    Miller, W T; Osiason, A W; Langlotz, C P; Palevsky, H I

    1998-07-01

    In patients with chronic pulmonary embolism, pulmonary thromboendarterectomy may result in a unique form of noncardiogenic pulmonary edema termed reperfusion edema. This report reviews the authors' experience after pulmonary thromboendarterectomy with particular emphasis on the radiographic manifestations of reperfusion edema. The clinical and radiographic record of 25 patients who underwent pulmonary thromboendarterectomy at the University of Pennsylvania from 1985 through 1995 were reviewed. The zonal distribution of radiographic opacity, time to maximal opacity, and the time to clearance of reperfusion edema were determined. The relationship of these radiographic manifestations to clinical severity of disease and clinical outcome was examined. Reperfusion edema, characterized by patchy bilateral perihilar alveolar opacities, occurred in all but one patient. There is a lower lung zone predominance of opacities, but in individual cases, striking unilateral or haphazard arrangements of opacities may be seen. In this small sample of patients, no association between preoperative pulmonary arterial pressures and radiographic appearance or clinical outcome was found. However, severity of radiographic opacities, as measured by the extent of involved lung, correlated with disease severity, as measured by time to extubation and time to discharge. Pneumonia, defined as a radiographic opacity that evolves discordantly with the reperfusion edema opacities, occurred in 20% of cases. Reperfusion edema is a common consequence of pulmonary thromboendarterectomy. The severity of radiographic manifestations and clinical severity of disease are related. This characteristically appears as perihilar alveolar opacities.

  3. Pulmonary hypertension and chronic cor pulmonale in COPD.

    PubMed

    Shujaat, Adil; Minkin, Ruth; Eden, Edward

    2007-01-01

    Hypoxia and endothelial dysfunction play a central role in the development of pulmonary hypertension. Cor pulmonale is a maladaptive response to pulmonary hypertension. The presence of peripheral edema in cor pulmonale is almost invariably associated with hypercapnia. Correction of abnormalities of gas exchange and ventilation can ameliorate pulmonary hypertension and improve survival. This review focuses on new information about the pathogenesis and treatment of pulmonary hypertension in COPD including information derived from lung volume reduction surgery, the role of brain natriuretic peptide, exhaled nitric oxide for diagnosis, and the treatment of cor pulmonale with recently available specific pulmonary vasodilators.

  4. Scintigraphy for Pulmonary Capillary Protein Leak

    DTIC Science & Technology

    1983-09-01

    det,,rmine the severity and duration of non- cardiogenic pulmonary edema (17). C. Approach to the Problem The anim-als were anesthetize,, intubated and...pulmonary lymphatics. If the leak exceeds the lymphatic capacity, which can increase flow by a factor of 20, pulmonary interstitial edema occurs. When...therefore, does not appear to cause permeability pulmonary edema in either the sheep or dog. The ARDS seen in patients following sclerotherapy of esophageal

  5. Pulmonary function in children with development coordination disorder.

    PubMed

    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. Two hundred and fifty participants (90 children with DCD and 160 TD children) aged 9-10 years old completed this study. Using the KoKo spirometry, forced vital capacity (FVC) and forced expiratory volume in 1s (FEV(1.0)) were used to measure pulmonary function. The 800-m run was also conducted to assess cardiopulmonary fitness of children in the field. There was a significant difference in pulmonary function between TD children and those with DCD. The values of FVC and FEV(1.0) in TD children were significantly higher than in children with DCD. A significant, but low correlation (r = -0.220, p < .001) was found between total score on the MABC and FVC; similarly, a positive but low correlation (r = 0.252, p < .001) was found between total score on the MABC and the completion time of 800-m run. However, no significant correlation between FVC and the time of 800-m run was found (p > .05). Significant correlations between total score on the MABC and the completion time of the 800-m run (r = 0.352, p < .05) and between FVC and the time of 800-m run (r = -0.285, p < .05) were observed in girls with DCD but not boys with this condition. Based on the results of this study, pulmonary function in children with DCD was significantly lower than that of TD children. The field test, 800-m run, may not be a good indicator to distinguish aerobic ability between children with DCD and those who are TD. It is possible that poor pulmonary function in children with DCD is due to reduced physical activity in this population.

  6. Amine oxidase activity regulates the development of pulmonary fibrosis.

    PubMed

    Marttila-Ichihara, Fumiko; Elima, Kati; Auvinen, Kaisa; Veres, Tibor Z; Rantakari, Pia; Weston, Christopher; Miyasaka, Masayuki; Adams, David; Jalkanen, Sirpa; Salmi, Marko

    2017-03-01

    In pulmonary fibrosis, an inflammatory reaction and differentiation of myofibroblasts culminate in pathologic deposition of collagen. Amine oxidase copper containing-3 (AOC3) is a cell-surface expressed oxidase that regulates leukocyte extravasation. Here we analyzed the potential role of AOC3 using gene-modified and inhibitor-treated mice in a bleomycin-induced pulmonary fibrosis model. Inflammation and fibrosis of lungs were assessed by histologic, flow cytometric, and quantitative PCR analysis. AOC3-deficient mice showed a 30-50% reduction in fibrosis, collagen synthesis, numbers of myofibroblasts, and accumulation of CD4(+) lymphocytes, NK T cells, macrophages, and type 2 innate lymphoid cells compared with wild-type control mice. AOC3 knock-in mice, which express a catalytically inactive form of AOC3, were also protected from lung fibrosis. In wild-type mice, a small-molecule AOC3 inhibitor treatment reduced leukocyte infiltration, myofibroblast differentiation, and fibrotic injury both in prophylactic and early therapeutic settings by about 50% but was unable to reverse the established fibrosis. AOC3 was also induced in myofibroblasts in human idiopathic pulmonary fibrosis. Thus, the oxidase activity of AOC3 contributes to the development of lung fibrosis mainly by regulating the accumulation of pathogenic leukocyte subtypes, which drive the fibrotic response.-Marttila-Ichihara, F., Elima, K., Auvinen, K., Veres, T. Z., Rantakari, P., Weston, C., Miyasaka, M., Adams, D., Jalkanen, S., Salmi, M. Amine oxidase activity regulates the development of pulmonary fibrosis.

  7. The Pulmonary Mesenchyme Directs Lung Development

    PubMed Central

    McCulley, David; Wienhold, Mark; Sun, Xin

    2016-01-01

    Each of the steps of respiratory system development relies on intricate interactions and coordinated development of the lung epithelium and mesenchyme. In the past, more attention has been paid to the epithelium than the mesenchyme. The mesenchyme is a source of specification and morphogenetic signals as well as a host of surprisingly complex cell lineages that are critical for normal lung development and function. This review highlights recent research focusing on the mesenchyme that has revealed genetic and epigenetic mechanisms of its development in the context of other cell layers during respiratory lineage specification, branching morphogenesis, epithelial differentiation, lineage distinction, vascular development, and alveolar maturation. PMID:25796078

  8. The development of a pseudo-chamber after balloon pulmonary angioplasty: long-term complications of balloon pulmonary angioplasty.

    PubMed

    Sugiyama, Hisashi; Kise, Hiroaki; Toda, Takako; Hoshiai, Minako

    2016-11-01

    We experienced a rare complication where extravasation developed a pseudo-chamber long after the balloon pulmonary angioplasty for supravalvular pulmonary stenosis. A 3-month-old girl was diagnosed with an anomalous origin of the left coronary artery from the pulmonary artery. She underwent the Takeuchi procedure at 10 months of age. During the follow-up, the supravalvular pulmonary stenosis deteriorated, and was treated by balloon pulmonary angioplasty with the double balloon technique catheter at 6 years of age. Angiography at the main pulmonary artery showed a small amount of extravasation contrast medium after the procedure. Follow-up echocardiography showed a diminished extravasation hemorrhage. Twelve years later, right ventricular enlargement due to pulmonary regurgitation had been observed on echocardiography. In addition, abnormal echo free space was detected at the left posterior of the left atrium. Enhanced computed tomography clearly demonstrated there was an orifice and extent of the pseudo-chamber. Surgical findings revealed a large tear just distal to the coronary tunnel. We speculated that extravasation blood was limited in the perivascular area early after the procedure but eventually reached the non-adhesive oblique pericardial sinus with age. Consequently, pulmonary to oblique pericardial sinus communication was established and looked like a pseudo-chamber long after the procedure. In conclusion, even if extravasation seems to be limited immediately after the balloon pulmonary angioplasty, it could expand for non-adhesive space and could develop a huge blood space like chamber. Long-term careful observation should be necessary for extravasation of pulmonary artery even with surgical adhesion.

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

    PubMed

    Rossi, Janet L; Todd, Tracey; Daniels, Zachary; Bazan, Nicolas G; Belayev, Ludmila

    2015-07-15

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

  10. Pathogenesis of Brain Edema and Investigation into Anti-Edema Drugs

    PubMed Central

    Michinaga, Shotaro; Koyama, Yutaka

    2015-01-01

    Brain edema is a potentially fatal pathological state that occurs after brain injuries such as stroke and head trauma. In the edematous brain, excess accumulation of extracellular fluid results in elevation of intracranial pressure, leading to impaired nerve function. Despite the seriousness of brain edema, only symptomatic treatments to remove edema fluid are currently available. Thus, the development of novel anti-edema drugs is required. The pathogenesis of brain edema is classified as vasogenic or cytotoxic edema. Vasogenic edema is defined as extracellular accumulation of fluid resulting from disruption of the blood-brain barrier (BBB) and extravasations of serum proteins, while cytotoxic edema is characterized by cell swelling caused by intracellular accumulation of fluid. Various experimental animal models are often used to investigate mechanisms underlying brain edema. Many soluble factors and functional molecules have been confirmed to induce BBB disruption or cell swelling and drugs targeted to these factors are expected to have anti-edema effects. In this review, we discuss the mechanisms and involvement of factors that induce brain edema formation, and the possibility of anti-edema drugs targeting them. PMID:25941935

  11. 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

  12. Histochemical analyses and quantum dot imaging of microvascular blood flow with pulmonary edema in living mouse lungs by "in vivo cryotechnique".

    PubMed

    Saitoh, Yurika; Terada, Nobuo; Saitoh, Sei; Ohno, Nobuhiko; Jin, Takashi; Ohno, Shinichi

    2012-02-01

    Light microscopic imaging of blood vessels and distribution of serum proteins is essential to analyze hemodynamics in living animal lungs under normal respiration or respiratory diseases. In this study, to demonstrate dynamically changing morphology and immunohistochemical images of their living states, "in vivo cryotechnique" (IVCT) combined with freeze-substitution fixation was applied to anesthetized mouse lungs. By hematoxylin-eosin staining, morphological features, such as shapes of alveolar septum and sizes of alveolar lumen, reflected their respiratory conditions in vivo, and alveolar capillaries were filled with variously shaped erythrocytes. Albumin was usually immunolocalized in the capillaries, which was confirmed by double-immunostaining for aquaporin-1 of endothelium. To capture accurate time-courses of blood flow in peripheral pulmonary alveoli, glutathione-coated quantum dots (QDs) were injected into right ventricles, and then IVCT was performed at different time-points after the QD injection. QDs were localized in most arterioles and some alveolar capillaries at 1 s, and later in venules at 2 s, reflecting a typical blood flow direction in vivo. Three-dimensional QD images of microvascular networks were reconstructed by confocal laser scanning microscopy. It was also applied to lungs of acute pulmonary hypertension mouse model. Erythrocytes were crammed in blood vessels, and some serum components leaked into alveolar lumens, as confirmed by mouse albumin immunostaining. Some separated collagen fibers and connecting elastic fibers were still detected in edematous tunica adventitia near terminal bronchioles. Thus, IVCT combined with histochemical approaches enabled us to capture native images of dynamically changing structures and microvascular hemodynamics of living mouse lungs.

  13. Polymeric nanoparticles in development for treatment of pulmonary infectious diseases.

    PubMed

    Lim, Young H; Tiemann, Kristin M; Hunstad, David A; Elsabahy, Mahmoud; Wooley, Karen L

    2016-11-01

    Serious lung infections, such as pneumonia, tuberculosis, and chronic obstructive cystic fibrosis-related bacterial diseases, are increasingly difficult to treat and can be life-threatening. Over the last decades, an array of therapeutics and/or diagnostics have been exploited for management of pulmonary infections, but the advent of drug-resistant bacteria and the adverse conditions experienced upon reaching the lung environment urge the development of more effective delivery vehicles. Nanotechnology is revolutionizing the approach to circumventing these barriers, enabling better management of pulmonary infectious diseases. In particular, polymeric nanoparticle-based therapeutics have emerged as promising candidates, allowing for programmed design of multi-functional nanodevices and, subsequently, improved pharmacokinetics and therapeutic efficiency, as compared to conventional routes of delivery. Direct delivery to the lungs of such nanoparticles, loaded with appropriate antimicrobials and equipped with 'smart' features to overcome various mucosal and cellular barriers, is a promising approach to localize and concentrate therapeutics at the site of infection while minimizing systemic exposure to the therapeutic agents. The present review focuses on recent progress (2005-2015) important for the rational design of nanostructures, particularly polymeric nanoparticles, for the treatment of pulmonary infections with highlights on the influences of size, shape, composition, and surface characteristics of antimicrobial-bearing polymeric nanoparticles on their biodistribution, therapeutic efficacy, and toxicity. WIREs Nanomed Nanobiotechnol 2016, 8:842-871. doi: 10.1002/wnan.1401 For further resources related to this article, please visit the WIREs website.

  14. Scintigraphy for Pulmonary Capillary Protein Leak.

    DTIC Science & Technology

    1986-06-01

    duration of non- cardiogenic pulmonary edema (17). C. Approach to the Problem The animals were anesthetized, intubated and placed beneath a Pho-ajiui: I...capacity, which can increase flow 1w a K factor of 20, pulmonary interstitial edema occurs. ien the interstitial Compartment reaches a critical volume and...of sheep is the accepted model for the study of pulmonary permeability edema (18). It is, therefore, necessary to compare our scintigraphic technique

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

    PubMed

    Hadinnapola, Charaka; Pepke-Zaba, Joanna

    2015-10-01

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

  16. 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.

  17. [Chronic administration of estradiol to ovariectomized female Wistar rats causes development of hypoxic pulmonary hypertension].

    PubMed

    Kovaleva, Iu O; Artem'eva, M M; Medvedev, O S; Medvedeva, N A

    2013-01-01

    We have studied the role of female sex hormone estradiol in the development of hypoxic pulmonary arterial hypertension. Previously, it was shown that the development of pulmonary hypertension in Wistar female rats is accompanied by a twofold increase in the estradiol level. Ovariectomy reduces the degree of pulmonary hypertension in these animals. In this work, the effect of various chronic doses of exogenous estradiol (5 and 15 microg/kg per day) on the development of hypoxic pulmonary hypertension in Wistar female rats has been studied. Pulmonary hypertension was induced by exposure to hypobaric hypoxia (10 h a day for 2 weeks) at simulated altitude of 5000 m (O2 concentration reduced to 10%). The administration of estradiol in different doses (5 and 15 microg/kg per day) for 21 day initiated the development of pulmonary hypertension in ovariectomized Wistar female rats.

  18. Uveitic Macular Edema: Treatment Update

    PubMed Central

    Goldhardt, Raquel; Rosen, Bradley Simon

    2016-01-01

    The aim of this review is to summarize recent developments in the treatment of uveitic macular edema (ME). ME represent a major cause of visual loss in uveitis and adequate management is crucial for the maintenance of useful vision in patients with chronic uveitis. PMID:27347446

  19. [Pulmonary function testing in Japan: present status and new developments].

    PubMed

    Tojo, Naoko

    2012-09-01

    In 2004, the Japanese Respiratory Society issued an initial set of recommendations on the standardized measurement of the most frequently used tests for pulmonary function, i.e., tests to assess slow vital capacity, forced vital capacity, and single-breath carbon monoxide diffusing capacity. This statement has not been updated, and the prediction equations for pulmonary function testing are not fully established. Thus, the guidelines will need to be periodically updated in accordance with new developments in this rapidly evolving field. Nitric oxide (NO) is now recognized as a biological mediator in animals and humans. The human lung produces NO and exhales it in breath. The fractional nitric oxide (NO) concentration in exhaled breath (FE(NO)) can be quantitatively measured by a simple, safe, and noninvasive procedure as a complementary tool for assessing airway inflammation in airway diseases such as asthma. While the measurement of exhaled NO is standardized for clinical use, FE(NO) measurement is not approved or covered under the public health insurance system in Japan.

  20. Wntless is required for peripheral lung differentiation and pulmonary vascular development.

    PubMed

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

    2013-07-01

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

  1. LUNG EDEMA FOLLOWING BILATERAL VAGOTOMY

    PubMed Central

    Lorber, Victor

    1939-01-01

    1. Small animals (rat and guinea pig) vagotomized in the neck die within a period of hours, the lungs showing extensive congestion and edema. 2. Tracheotomy permits appreciably longer survival with minimal lung changes approximating those seen in the control animals. 3. Intrathoracic vagotomy (sparing the recurrent laryngeal nerve) on one side, and cervical vagotomy on the other, permits almost indefinite survival (guinea pig and rabbit), unless laryngeal paralysis from the unilateral denervation produces respiratory obstruction (rat, guinea pig, and rabbit). 4. Pulmonary edema following bilateral vagotomy probably results primarily from respiratory obstruction. It is suggested that circulatory failure may also be a factor of some importance. The rôle of vagotomy itself is considered in relationship to these two phenomena. 5. The reaction of smaller animals to bilateral vagotomy, with regard to lung changes, apparently differs in no way from that of the larger animals, but is less readily demonstrated because of the smaller diameters of the air passages. PMID:19870894

  2. Handbook of pulmonary emergencies

    SciTech Connect

    Spaquolo, S.V.; Medinger, A

    1986-01-01

    This book presents information on the following topics: clinical assessment of the patient with pulmonary disease; interpretation of arterial blood gases in the emergency patient; life-threatening pneumonia; extrapulmonic ventilatory failure; acute inhalation lung disease; pulmonary edema; near drowning; chest trauma; upper airway emergencies; chronic lung disease with acute respiratory decompensation; acute respiratory failure in the patient with chronic airflow obstruction; asthma; hemoptysis; embolic pulmonary disease; superior vena cava syndrome; catastrophic pleural disease; ventilatory assistance and its complications; and ventilator emergencies.

  3. Pulmonary and tricuspid valvuloplasty in carcinoid heart disease.

    PubMed

    Karimi, Ashkan; Pourafshar, Negiin; Fudge, James C

    2016-12-28

    A 26-year-old female with carcinoid heart disease consisting of severe pulmonary and tricuspid valve stenosis was admitted with line associated sepsis. She recovered from sepsis with antibiotics and aggressive fluid resuscitation but became grossly volume overloaded with evidence of tense ascites and lower extremity edema. She developed worsening renal and hepatic function due to congestive nephropathy and hepatopathy, which did not respond to intravenous diuretics, and she was deemed too sick for surgical pulmonary and tricuspid valve replacement. Pulmonary and tricuspid valvuloplasty was performed as a rescue measure to alleviate her congestive symptoms and improve her candidacy for valve replacement. © 2016 Wiley Periodicals, Inc.

  4. Normal and abnormal development of pulmonary veins: state of the art and correlation with clinical entities.

    PubMed

    Douglas, Yvonne L; Jongbloed, Monique R M; Deruiter, Marco C; Gittenberger-de Groot, Adriana C

    2011-02-17

    Interest for the pulmonary veins has increased in the past decade after the potential arrhythmogenicity of the myocardial sleeve surrounding these structures has been recognized. Furthermore, there are several clinical entities, such as anomalous connection pattern and pulmonary vein stenosis, that are related to abnormal pulmonary vein development. In this review, we will describe current literature and aim to elucidate and reorganize current opinions on normal and abnormal pulmonary vein development in relation to clinical (management of) diseases. Several unresolved questions will be addressed, as well as current conceptual controversies. First, a general overview of development of structures at the venous pole of the heart, including normal development of the pulmonary vein from a primitive Anlage, will be provided. Recent insights indicate an important contributory role of the mesoderm behind the heart, the so-called second heart field, to this area. Subsequently, the formation of a myocardial and smooth muscle vascular wall of the pulmonary veins and the left atrium is described, as well as current insights in the mechanisms involved in the differentiation of these different cell types in this area. Next, developmental concepts of normal pulmonary venous drainage patterns are reviewed, and an overview is provided of clinical entities related to abnormal development at several anatomical levels. Lastly, attention is paid to arrhythmogenesis in relation to pulmonary vein development, as well the consequences for clinical management.

  5. 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

  6. Scintigraphy for Pulmonary Capillary Protein Leak

    DTIC Science & Technology

    1982-09-01

    adrministration (16). The method is noninvasive and has been used clinically to determine the severity and duration of non- cardiogenic pulmonary edema ...If the leak exceeds the 1.iiiphatic capacity, which can increase flow by a factor of 20, pulmcnary interstitial edema occurs. T•hen the interstitial...of shoee is the accepted !::odel for the scudv of pulmonary permehbility - edema (18). It is, therefore, necessary to comnpare our scintigraphic

  7. 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...

  8. Development of Pulmonary Artery Aneurysms Due to Behçet's Disease and Resolution after Treatment

    PubMed Central

    Kage, Hidenori; Goto, Yasushi; Amano, Yosuke; Makita, Kosuke; Isago, Hideaki; Kobayashi, Kouichi; Narumoto, Osamu; Okudaira, Reiko; Tanaka, Goh; Takami, Kazutaka; Ohishi, Nobuya; Nagase, Takahide

    2016-01-01

    We herein describe a patient with Behçet's disease in whom we followed the development and resolution of pulmonary artery aneurysms. He presented with intermittent hemoptysis, pulmonary thromboembolism was initially diagnosed, and anticoagulant therapy was started. Over the next several months, the expansion of pulmonary arteries was noted. Five months after his initial admission, he was readmitted for massive hemoptysis, and further examinations revealed that he had Behçet's disease. Corticosteroids and intravenous cyclophosphamide were started. Over the next five months, the pulmonary artery aneurysms and thrombosis resolved. The development of pulmonary artery aneurysms led to the diagnosis of Behçet's disease, and they resolved after immunosuppressive therapy. PMID:27853079

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

    PubMed Central

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

    2016-01-01

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

  10. Diabetic macular edema.

    PubMed

    Stefánsson, Einar

    2009-07-01

    A variety of treatment options are available for the treatment of diabetic macular edema. They include laser photocoagulation, anti-VEGF drugs, intravitreal steroids, and vitrectomy with or without release of vitreoretinal traction. A full understanding of the physiological mechanisms of these treatment modalities allows sensible combination of treatment options. Retinal photocoagulation has repeatedly been shown to improve retinal oxygenation, as does vitrectomy. Oxygen naturally reduces VEGF production and thereby decreases leakage of plasma proteins from capillaries into the tissue. In addition, vitrectomy allows faster clearance of cytokines, such as VEGF, from the retina into the vitreous cavity. The VEGF-lowering effect of photocoagulation and vitrectomy can be augmented with anti-VEGF drugs and corticosteroids reduce the effect of VEGF on capillary permeability. Starling's law explains vasogenic edema, which is controlled by osmotic and hydrostatic gradients between vessel and tissue. It explains how VEGF-induced vascular permeability causes plasma protein to leak into the tissue interstitial space, thus decreasing the osmotic pressure gradient between vessel and tissue, resulting in water accumulation, i.e. edema. This is reversed by reducing VEGF production, which is achieved with laser treatment; or by removing VEGF with antibodies or vitrectomy; or by reducing the permeability effect with steroids. At the same time, Starling's law takes into account hemodynamic changes that affect the hydrostatic gradient. High arterial blood pressure and hypoxic vasodilatation increase the hydrostatic pressure in the microcirculation, which increases water flux from vessel to tissue and induce edema. Treatment of arterial hypertension or reversal of retinal hypoxia with laser reverses this pathophysiology and reduces edema. Newton's third law explains, that vitreoretinal traction decreases hydrostatic tissue pressure in the retina, increases the pressure gradient

  11. 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.

  12. Novel treatment targets for cerebral edema.

    PubMed

    Walcott, Brian P; Kahle, Kristopher T; Simard, J Marc

    2012-01-01

    Cerebral edema is a common finding in a variety of neurological conditions, including ischemic stroke, traumatic brain injury, ruptured cerebral aneurysm, and neoplasia. With the possible exception of neoplasia, most pathological processes leading to edema seem to share similar molecular mechanisms of edema formation. Challenges to brain-cell volume homeostasis can have dramatic consequences, given the fixed volume of the rigid skull and the effect of swelling on secondary neuronal injury. With even small changes in cellular and extracellular volume, cerebral edema can compromise regional or global cerebral blood flow and metabolism or result in compression of vital brain structures. Osmotherapy has been the mainstay of pharmacologic therapy and is typically administered as part of an escalating medical treatment algorithm that can include corticosteroids, diuretics, and pharmacological cerebral metabolic suppression. Novel treatment targets for cerebral edema include the Na(+)-K(+)-2Cl(-) co-transporter (NKCC1) and the SUR1-regulated NC(Ca-ATP) (SUR1/TRPM4) channel. These two ion channels have been demonstrated to be critical mediators of edema formation in brain-injured states. Their specific inhibitors, bumetanide and glibenclamide, respectively, are well-characterized Food and Drug Administration-approved drugs with excellent safety profiles. Directed inhibition of these ion transporters has the potential to reduce the development of cerebral edema and is currently being investigated in human clinical trials. Another class of treatment agents for cerebral edema is vasopressin receptor antagonists. Euvolemic hyponatremia is present in a myriad of neurological conditions resulting in cerebral edema. A specific antagonist of the vasopressin V1A- and V2-receptor, conivaptan, promotes water excretion while sparing electrolytes through a process known as aquaresis.

  13. 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.

  14. [Limb edema and lymphoscintigraphy].

    PubMed

    Bourgeois, P; Munck, D; Belgrado, J P; Leduc, O; Leduc, A

    2003-02-01

    Lymphoscintigraphic investigations represent techniques of nuclear medicine very contributive for the management and treatment of the limb edemas, either primary or secundary. Their principle is presented and methodologies proposed in the literature are reviewed. Their diagnostic contributions are detailed. The sensitivities and specificities of several protocols of investigation are reported. Some limitations of these examinations are analyzed and discussed. Clinical indications for their use are proposed and their interest with regard to the various treatments that can be applied to these limb edemas is discussed.

  15. Selexipag in the treatment of pulmonary arterial hypertension: design, development, and therapy

    PubMed Central

    Hardin, Elizabeth Ashley; Chin, Kelly M

    2016-01-01

    Pulmonary arterial hypertension is characterized by abnormalities in the small pulmonary arteries including increased vasoconstriction, vascular remodeling, proliferation of smooth muscle cells, and in situ thrombosis. Selexipag, a novel, oral prostacyclin receptor agonist, has been shown to improve hemodynamics in a phase II clinical trial and reduce clinical worsening in a large phase III clinical trial involving patients with pulmonary arterial hypertension. In this paper, we describe the prostacyclin signaling pathway, currently available oral prostanoid medications, and the development and clinical use of selexipag. PMID:27895464

  16. Selexipag in the treatment of pulmonary arterial hypertension: design, development, and therapy.

    PubMed

    Hardin, Elizabeth Ashley; Chin, Kelly M

    2016-01-01

    Pulmonary arterial hypertension is characterized by abnormalities in the small pulmonary arteries including increased vasoconstriction, vascular remodeling, proliferation of smooth muscle cells, and in situ thrombosis. Selexipag, a novel, oral prostacyclin receptor agonist, has been shown to improve hemodynamics in a phase II clinical trial and reduce clinical worsening in a large phase III clinical trial involving patients with pulmonary arterial hypertension. In this paper, we describe the prostacyclin signaling pathway, currently available oral prostanoid medications, and the development and clinical use of selexipag.

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

    PubMed

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

    2015-03-01

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

  18. 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.

  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.

  20. Acute edema blisters in a hereditary angioedema cutaneous attack.

    PubMed

    Fernández Romero, D; Di Marco, P; Malbrán, A

    2008-01-01

    Hereditary angioedema is a rare autosomal dominant disease characterized by recurrent episodes of acute edema affecting the skin and the respiratory and digestive tracts. Acute edema blisters or hydro-static bullae develop after rapid accumulation of interstitial fluid usually associated to cardiac insufficiency. Lesions contain sterile fluid and break up easily resolving without scars. Blisters disappear when fluid accumulation resolves. We describe a patient developing recurrent acute edema blisters as a consequence of cutaneous hereditary angioedema attacks.

  1. Pulmonary hypertension

    MedlinePlus

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

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

    PubMed Central

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

    2016-01-01

    A 73-year-old man underwent left pneumonectomy for squamous cell lung carcinoma 3 years ago. The postoperative and follow-up periods were uneventful. A thrombus was detected in the left pulmonary artery stump during the last chest computed tomography (CT) scan. Anticoagulant treatment was applied: intravenous heparin for 3 days followed by oral warfarin. The follow-up chest CT examination revealed regression in the size of the thrombus. PMID:27785144

  3. S-Nitrosylation and the Development of Pulmonary Hypertension

    DTIC Science & Technology

    2010-02-01

    in which N-acetyl cysteine (NAC) is used as a tracer to 1) monitor S-nitrosothiol ( SNO ) formation, transfer and metabolism in vivo, 2) address the...physiological and pathological consequences of SNO signaling in the pulmonary vasculature, and 3) identify SNO target proteins in this signaling...pathway. Differences in SNO formation, transfer and metabolism and the role this pathway plays in gender specific differences in the presentation of this

  4. Pulmonary manifestations of malaria : recognition and management.

    PubMed

    Taylor, Walter R J; Cañon, Viviam; White, Nicholas J

    2006-01-01

    Lung involvement in malaria has been recognized for more than 200 hundred years, yet our knowledge of its pathogenesis and management is limited. Pulmonary edema is the most severe form of lung involvement. Increased alveolar capillary permeability leading to intravascular fluid loss into the lungs is the main pathophysiologic mechanism. This defines malaria as another cause of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).Pulmonary edema has been described most often in non-immune individuals with Plasmodium falciparum infections as part of a severe systemic illness or as the main feature of acute malaria. P.vivax and P.ovale have also rarely caused pulmonary edema.Clinically, patients usually present with acute breathlessness that can rapidly progress to respiratory failure either at disease presentation or, interestingly, after treatment when clinical improvement is taking place and the parasitemia is falling. Pregnant women are particularly prone to developing pulmonary edema. Optimal management of malaria-induced ALI/ARDS includes early recognition and diagnosis. Malaria must always be suspected in a returning traveler or a visitor from a malaria-endemic country with an acute febrile illness. Slide microscopy and/or the use of rapid antigen tests are standard diagnostic tools. Malaria must be treated with effective drugs, but current choices are few: e.g. parenteral artemisinins, intravenous quinine or quinidine (in the US only). A recent trial in adults has shown that intravenous artesunate reduces severe malaria mortality by a third compared with adults treated with intravenous quinine. Respiratory compromise should be managed on its merits and may require mechanical ventilation.Patients should be managed in an intensive care unit and particular attention should be paid to the energetic management of other severe malaria complications, notably coma and acute renal failure. ALI/ARDS may also be related to a coincidental bacterial

  5. [Brain edema--historical aspects and contemporary suggestions].

    PubMed

    Meskheli, M K; Gereshidze, M M

    2007-01-01

    The aim of this article was to show the historical aspects of elaboration of the brain edema study. To draft the main stages of study development from naive medievals suggestions till the creation of modern technologies and the possibility of the brain edema neurovisualization. The possibility to watch and control these processes grants the real perspective to enhance the effectiveness of the brain edema therapy.

  6. Effects of gender and age on development of concurrent extrapulmonary tuberculosis in patients with pulmonary tuberculosis: a population based study.

    PubMed

    Lin, Chun-Yu; Chen, Tun-Chieh; Lu, Po-Liang; Lai, Chung-Chih; Yang, Yi-Hsin; Lin, Wei-Ru; Huang, Pei-Ming; Chen, Yen-Hsu

    2013-01-01

    Most cases of adult-onset tuberculosis (TB) result from reactivation of a pre-existing Mycobacterium tuberculosis infection. Mycobacterium tuberculosis usually invades the respiratory tract and most patients develop intrapulmonary TB; however, some patients develop concurrent pulmonary and extra-pulmonary TB. The purpose of the present study was to identify the demographic and clinical factors associated with an increased risk of concurrent extra-pulmonary diseases in patients with pulmonary TB. We compared patients who had isolated pulmonary TB with patients who had concurrent pulmonary and extra-pulmonary TB. We initially analyzed one-million randomly selected subjects from the population-based Taiwan National Health Insurance database. Based on analysis of 5414 pulmonary TB patients in this database, women were more likely than men to have concurrent extra-pulmonary TB (OR: 1.30, p = 0.013). A separate analysis of the Kaohsiung Medical University Hospital database, which relied on sputum culture-proven pulmonary TB, indicated that women were more likely than men to have concurrent extra-pulmonary TB (OR: 1.62, p = 0.039). There was no significant gender difference in extra-pulmonary TB for patients younger than 45 years in either database. However, for patients 45 years and older, women were more likely than men to have concurrent extra-pulmonary TB (insurance database: 9.0% vs. 6.8%, p = 0.016, OR: 1.36; hospital database: 27.3% vs. 16.0%, p = 0.008, OR = 1.98). Our results indicate that among patients who have pulmonary TB, older females have an increased risk for concurrent extra-pulmonary TB.

  7. 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.

  8. [The role of oxygen radicals in bleomycin-induced pulmonary fibrosis].

    PubMed

    Wang, X Z

    1992-06-01

    A model of pulmonary fibrosis in rat has been developed using intratracheal administration of bleomycin (BLM) A5 (5mg/kg). Histopathologic features and total lung collagen were studied. We found that type I pneumocytes detached, basement membrane denuded and endothelia edema were the earliest changes in BLM induced pulmonary fibrosis. Serum MDA (an index of lipid peroxidation) level in rats receiving intratracheal bleomycin were increased at earlier time after bleomycin administration. Meanwhile, MDA level in the lung homogenate was elevated too. Our results indicated that the injured type I pneumocytes and endothelia caused by oxygen radicles are the fundamental damages in bleomycin-induced pulmonary fibrosis.

  9. 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

    ...: Developing Drugs for Treatment; Availability AGENCY: Food and Drug Administration, HHS. ACTION: Notice... industry entitled ``Pulmonary Tuberculosis: Developing Drugs for Treatment.'' The purpose of the draft guidance is to assist sponsors in the development of antimycobacterial drugs for the treatment of...

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

    PubMed

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

    2016-02-15

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

  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. Leg edema from intrathecal opiate infusions.

    PubMed

    Aldrete, J A; Couto da Silva JM

    2000-01-01

    Despite the increasing popularity of intrathecal infusions to treat patients with long-term non-cancer-related pain, this therapy is not without serious side-effects. Five out of 23 patients who had intrathecal infusions of opiates for longer than 24 months developed leg and feet edema. As predisposing factors, cardiovascular disease, deep venous thrombosis, peripheral vascular disease, and venous stasis of the lower extremities were considered. Every patient who developed pedal and leg edema after the implantation of an infusion pump was also found to have leg edema and venous stasis prior to the time when the pump was inserted. This complication was severe enough to limit their physical activity, and to produce lymphedema, ulcerations and hyperpigmentation of the skin. Reduction of the edema occurred when the dose of the opiate was decreased, and in two cases in which the infusion was discontinued, there was almost complete resolution of the syndrome. It appears that the pre-existence of pedal edema and of venous stasis is a relative contraindication to the long-term intrathecal infusion of opiates in patients with chronic non-cancer pain.

  13. Pulmonary Hypertension in Scleroderma

    MedlinePlus

    PULMONARY HYPERTENSION IN SCLERODERMA PULMONARY HYPERTENSION Pulmonary hypertension (PH) is high blood pressure in the blood vessels ... with scleroderma are at increased risk for developing PH from several mechanisms. Frequently patients with scleroderma have ...

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

    PubMed

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

    2013-01-01

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

  15. Fulminant development of pulmonary arteriovenous fistulas in an infant after total cavopulmonary shunt.

    PubMed

    Bernstein, H S; Ursell, P C; Brook, M M; Hanley, F C; Silverman, N H; Bristow, J

    1996-01-01

    An infant with cyanotic congenital heart disease and polysplenia syndrome developed profound cyanosis within months of undergoing bilateral cavopulmonary anastomoses. Intrapulmonary shunting was diagnosed by contrast echocardiography with peripheral venous and selective pulmonary artery injection. Histopathology revealed abnormal, thin-walled vessels within the interstitium of the lung lobule. These vessels have not been reported previously and are likely to be the anatomic site of arteriovenous shunting. This case demonstrates that pulmonary arteriovenous fistulas (PAVFs) may develop rapidly after cavopulmonary anastomosis in young infants. It also illustrates the use of contrast echocardiography for following PAVF progression in these patients.

  16. Pitting type of pretibial edema in a patient with silent thyroiditis successfully treated by angiotensin ii receptor blockade

    PubMed Central

    Kazama, Itsuro; Mori, Yoko; Baba, Asuka; Nakajima, Toshiyuki

    2014-01-01

    Patient: Female, 56 Final Diagnosis: Thyroiditis – silent Symptoms: Palpitations • pretibial pitting edema • short of breath • sweating Medication: — Clinical Procedure: — Specialty: Endocrinology and Metabolic Objective: Unknown etiology Background: Hyper- or hypothyroidism sometimes causes pretibial myxedema characterized by non-pitting infiltration of a proteinaceous ground substance. However, in those patients, the “pitting” type of pretibial edema as a result of increased sodium and fluid retention or vascular hyper-permeability rarely occurs, except in cases complicated by heart failures due to severe cardiomyopathy or pulmonary hypertension. Case Report: A 56-year-old woman developed bilateral pretibial pitting edema, followed by occasional sweating, palpitations, and shortness of breath, which persisted for more than 2 months. The diagnosis of hyperthyroidism due to silent thyroiditis was supported by elevated levels of free thyroxine (T4) and triiodothyronine (T3), with a marked decrease in thyroid-stimulating hormone (TSH), and the negative results for TSH receptor antibodies with typical findings of destructive thyrotoxicosis. Despite her “pitting” type of pretibial edema, a chest radio-graph demonstrated the absence of cardiomyopathy or congestive heart failure. Oral administration of angiotensin II receptor blocker (ARB) was initiated for her systolic hypertension, with a relatively higher elevation of plasma renin activity compared to that of the aldosterone level. Although the symptoms characteristic to hyperthyroidism, such as increased sweating, palpitations and shortness of breath, slowly improved with a spontaneous resolution of the disease, ARB quickly resolved the pretibial pitting edema shortly after the administration.. Conclusions: In this case, increased activity of the renin-angiotensin-aldosterone system stimulated by thyroid hormone was likely responsible for the patient’s pitting type of edema. The pharmacological

  17. 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.

  18. 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.

  19. Steps forward in the treatment of pulmonary arterial hypertension: latest developments and clinical opportunities

    PubMed Central

    Badlam, Jessica B.; Bull, Todd M.

    2017-01-01

    Pulmonary arterial hypertension (PAH) is a chronic disease that results in narrowing of the small pre-capillary pulmonary arteries leading to elevation of pulmonary artery pressure and pulmonary vascular resistance, subsequent right ventricular failure, and if unchecked, death. Advances in the treatment of PAH over the last two decades have markedly improved survival. These improvements reflect a combination of changes in treatments, improved patient care strategies, and varying disease phenotypes in the PAH population. Currently approved therapies for PAH are directed at the recognized abnormalities within the pulmonary vasculature and include endothelin receptor antagonists, phosphodiesterase-5 inhibitors, soluble guanylate cyclase stimulators, and prostacyclin pathway agents. Most of these drugs have been approved on the basis of short-term trials that mainly demonstrated improvements in exercise capacity. More recently, long-term, event-driven trials of novel drugs have been performed, demonstrating new efficacy parameters. There have also been exciting advances in the understanding of right heart failure pathophysiology in PAH that have the potential to inspire the development of right ventricular targeted therapy and continued discoveries in the heterogeneity of disease and response to treatment has great potential for developing more ‘personalized’ therapeutic options. In this article, we review the current available data regarding the management of PAH, with an emphasis on the pharmacologic therapies and discussion of novel therapeutic directions for the treatment of this fatal disease. PMID:28348727

  20. 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

  1. Bilateral ankle edema with bilateral iritis.

    PubMed

    Kumar, Sunil

    2007-07-01

    I report two patient presented to me with bilateral symmetrical ankle edema and bilateral acute iritis. A 42-year-old female of Indian origin and 30-year-old female from Somalia both presented with bilateral acute iritis. In the first patient, bilateral ankle edema preceded the onset of bilateral acute iritis. Bilateral ankle edema developed during the course of disease after onset of ocular symptoms in the second patient. Both patients did not suffer any significant ocular problem in the past, and on systemic examination, all clinical parameters were within normal limit. Lacrimal gland and conjunctival nodule biopsy established the final diagnosis of sarcoidosis in both cases, although the chest x-rays were normal.

  2. 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.

  3. Pulmonary neuroendocrine cells (PNEC) and neuroepithelial bodies (NEB): chemoreceptors and regulators of lung development.

    PubMed

    Van Lommel, A

    2001-06-01

    The airway and alveolar epithelia contain pulmonary neuroendocrine cells whose structure indicates an endocrine function. They are also in contact with sensory nerve fibres. These cells often aggregate into distinct corpuscles-neuroepithelial bodies-and carry membrane receptors sensitive to a number of stimuli, including hypoxia and nicotine. They synthesise, store and release a number of bioactive substances such as serotonin, calcitonin gene-related peptide and the mitogen bombesin. When these are released they contribute to redistribution of pulmonary blood flow, regulation of bronchomotor tone, modulation of the immune response, stimulation of sensory nerve fibres and regulation of lung growth and development. Pulmonary neuroendocrine cells and neuroepithelial bodies seem to be most important in the fetal and neonatal lung as regulators of airway development and hypoxia-sensitive chemoreceptors. There is a link between these cells and specific types of lung cancer and their involvement in lung and paediatric pathology may be profound.

  4. 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

  5. Pulmonary circulation at exercise.

    PubMed

    Naeije, Robert; 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 in young adults, increasing to 2.5 mmHg/min/L over four to six 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 to 25 mmHg threshold associated with interstitial lung edema and altered ventilation/perfusion relationships. Pulmonary artery pressures of 40 to 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.

  6. 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

  7. 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.

  8. Medial defects of the small pulmonary arteries in fatal pulmonary hypertension in infants with trisomy 13 and trisomy 18.

    PubMed

    Tahara, Masahiro; Shimozono, Saiko; Nitta, Tetsuya; Yamaki, Shigeo

    2014-02-01

    Congestive heart failure is a major cause of early death in patients with trisomy 13 or 18 and congenital heart disease (CHD). Pulmonary artery banding for these patients early in life is preferred to protect the lungs from high pulmonary flow rates and improve survival. We performed open lung biopsies in 11 patients with trisomy 13 or 18 accompanied by CHD and severe pulmonary artery hypertension (PAH) between 2009 and 2011. Two (18.2%) of these 11 patients had medial defects of the small pulmonary arteries. One patient with trisomy 13 and an atrial septal defect developed lung hemorrhage and lung edema at the age of 9 months and died at the age of 13 months. The lumens of the small pulmonary arteries of the other patient with trisomy 18 and a ventricular septal defect became occluded due to the intimal proliferation of fibrous tissues at the age of 2 months. This patient died at the age of 27 months. The deaths of both patients were associated with heart-related factors. Patients with medial defects are vulnerable to intimal proliferation in the small pulmonary arteries. More patients with trisomy 13 or 18 and CHD might have similar pulmonary vascular changes. The small pulmonary arteries of patients with trisomy 13 and 18 should be further analyzed.

  9. 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.

  10. 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

  11. 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…

  12. Overview of diabetic macular edema.

    PubMed

    Holekamp, Nancy M

    2016-07-01

    Diabetes mellitus (DM) is a rapidly growing epidemic in the United States, and it is expected to affect 592 million individuals within the next 20 years. Diabetic retinopathy (DR) and diabetic macular edema (DME) are the 2 most common ophthalmic complications of DM. DR is the leading cause of blindness among working-age adults around the world, and development of DR is tied to DM disease duration. With the only identifier of early markers of DR being a complete ophthalmic exam, early signs of the disease are asymptomatic. Yearly, or at least every other year, ophthalmic exams are recommended for all patients with DM; but often, individuals with DM have not undergone screening exams and do not have regular eye exams until vision loss has occurred. With spending estimates of $490 million to treat the vision complications of DM, it is clear that DR and DME impose a substantial burden for patients, caregivers, and healthcare systems.

  13. 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

  14. Cardio-pulmonary interactions at high altitude. Pulmonary hypertension as a common denominator.

    PubMed

    Maggiorini, Marco

    2003-01-01

    The purpose of this review is to find the evidence that a disproportionate pulmonary vasoconstriction persisting for days, weeks and years during residence at high altitude is the common pathophysiologic mechanism of high altitude pulmonary edema (HAPE), subacute mountain sickness and chronic mountain sickness. A recent finding in early HAPE suggests that transmission of excessively elevated pulmonary artery pressure to the pulmonary capillaries leading to alveolar hemorrhage as the pathophysiologic mechanism of HAPE. The elevated incidence of HAPE in Indian soldiers led the Indian Army to extend the acclimatization period from a few days to 5 weeks. Using this protocol, HAPE was prevented, but after several weeks of residence at an altitude of 6000m dyspnea, anasarca and pleuro-pericardial effusion developed. Clinical examination revealed severe congestive right heart failure. This condition has been previously described in long-term high altitude residents of the Himalaya and the Andes. In rats, smooth muscle cells appear in normally non-muscular arterioles within days of simulated altitude. Rapid remodeling of the small precapillary arteries may prevent HAPE but increase pulmonary vascular resistance leading to pulmonary hypertension in long-term high altitude residents. Symptoms and signs of HAPE, subacute mountain sickness and chronic mountain sickness reverse completely after residents are transfered to low altitude. In conclusion, these findings strongly suggest that pulmonary hypertension at high altitude, which could be named "high altitude pulmonary hypertension", is the principal and common pathogenic factor of all three cardio-pulmonary manifestations of high altitude illness. Accordingly, subacute mountain sickness and chronic mountain sickness could be renamed in "acute-" and "chronic right heart failure of high altitude", respectively.

  15. Sustained CTL activation by murine pulmonary epithelial cells promotes the development of COPD-like disease

    PubMed Central

    Borchers, Michael T.; Wesselkamper, Scott C.; Curull, Victor; Ramirez-Sarmiento, Alba; Sánchez-Font, Albert; Garcia-Aymerich, Judith; Coronell, Carlos; Lloreta, Josep; Agusti, Alvar G.; Gea, Joaquim; Howington, John A.; Reed, Michael F.; Starnes, Sandra L.; Harris, Nathaniel L.; Vitucci, Mark; Eppert, Bryan L.; Motz, Gregory T.; Fogel, Kevin; McGraw, Dennis W.; Tichelaar, Jay W.; Orozco-Levi, Mauricio

    2009-01-01

    Chronic obstructive pulmonary disease (COPD) is a lethal progressive lung disease culminating in permanent airway obstruction and alveolar enlargement. Previous studies suggest CTL involvement in COPD progression; however, their precise role remains unknown. Here, we investigated whether the CTL activation receptor NK cell group 2D (NKG2D) contributes to the development of COPD. Using primary murine lung epithelium isolated from mice chronically exposed to cigarette smoke and cultured epithelial cells exposed to cigarette smoke extract in vitro, we demonstrated induced expression of the NKG2D ligand retinoic acid early transcript 1 (RAET1) as well as NKG2D-mediated cytotoxicity. Furthermore, a genetic model of inducible RAET1 expression on mouse pulmonary epithelial cells yielded a severe emphysematous phenotype characterized by epithelial apoptosis and increased CTL activation, which was reversed by blocking NKG2D activation. We also assessed whether NKG2D ligand expression corresponded with pulmonary disease in human patients by staining airway and peripheral lung tissues from never smokers, smokers with normal lung function, and current and former smokers with COPD. NKG2D ligand expression was independent of NKG2D receptor expression in COPD patients, demonstrating that ligand expression is the limiting factor in CTL activation. These results demonstrate that aberrant, persistent NKG2D ligand expression in the pulmonary epithelium contributes to the development of COPD pathologies. PMID:19197141

  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.

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

    PubMed

    Wu, L J

    2016-03-24

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

  18. Ippolito Albertini and Michael Albertus: disparate old and innovative theories on dropsy and edema.

    PubMed

    Timio, Mario; Capodicasa, Enrico

    2002-07-01

    The concept of edema and dropsy as a part of heart and renal failure developed in the 17th and 18th centuries with the observations of Albertini, who realized that two clinical entities were derived from the blood rather than the tissues. Albertus, who lived in the same period, was the last physician to interpret fluid accumulation according to the old, scholastic and dogmatic procedures of medicine. The fundamental concepts of Albertus held little in addition to the classification and categories of the physicians of the Middle Ages. Bloody congestions were distinguished from stagnation: the former have the purpose of reducing superfluites of blood and occurred in plethoric patients. Plethora in turn is caused by the ancient villain, inculpated since Hippocrates and Galen: suppressed hemorrhoids, suppressed menstrual evacuation and cutaneous eruption driven inward. Because of its suppression, transfer of blood occurs toward the chest, which impedes thoracic expansion and contraction, then asthma and dyspnea occur. On the contrary, Albertini with his clinical and autoptic observations and pronouncements filled in the anatomical and clinical picture of fluid accumulation and created the rudiments of diagnostic criteria. Edema, dropsy, asthma, dyspnea were, according to Albertini, the signs and symptoms of heart and renal failure. Albertini was the first to point out that dyspnea is apt to arise with special rapidity when a lesion occurs in the left atrial chamber and ventricle and by implication the mitral valve. In modern physiopathological terms, he discovered the picture of pulmonary edema. To this important discovery, he added a number of extremely important comments: changes in the respiratory organs are secondary to changes in the cardiovascular system; edema that is accompanied by dyspnea also affects the viscera, most especially the lungs, and finally dropsy of the lungs must be differentiated anatomically and clinically from dropsy of the chest (hydrothorax

  19. 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

  20. 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

    2013-07-06

    , 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.

  1. Cardiovascular and blood coagulative effects of pulmonary zinc exposure

    SciTech Connect

    Gilmour, Peter S.; Nyska, Abraham; Schladweiler, Mette C.; McGee, John K.; Wallenborn, J. Grace; Richards, Judy H.; Kodavanti, Urmila P. . E-mail: kodavanti.urmila@epa.gov

    2006-02-15

    Cardiovascular damage induced by pulmonary exposure to environmental chemicals can result from direct action or, secondarily from pulmonary injury. We have developed a rat model of pulmonary exposure to zinc to demonstrate cardiac, coagulative, and fibrinolytic alterations. Male Wistar Kyoto rats were instilled intratracheally with saline or zinc sulfate, 131 {mu}g/kg (2 {mu}mol/kg); the alterations were determined at 1, 4, 24, and 48 h postexposure. High-dose zinc enabled us to show changes in circulating levels of zinc above normal and induce significant pulmonary inflammation/injury such that cardiac impairments were likely. At 1-24 h postexposure, plasma levels of zinc increased to nearly 20% above the base line. Significant pulmonary inflammation and injury were determined by analysis of bronchoalveolar lavage fluid and histopathology in zinc-exposed rats at all time points. Starting at 4 h postexposure, pulmonary damage was accompanied by persistently increased gene expressions of tissue factor (TF) and plasminogen activator-inhibitor-1 (PAI-1), but not thrombomodulin (TM). Cardiac tissues demonstrated similar temporal increases in expressions of TF, PAI-1, and TM mRNA following pulmonary instillation of zinc. In contrast to extensive pulmonary edema and inflammation, only mild, and focal acute, myocardial lesions developed in a few zinc-exposed rats; no histological evidence showed increased deposition of fibrin or disappearance of troponin. At 24 and 48 h postexposure to zinc, increases occurred in levels of systemic fibrinogen and the activated partial thromboplastin time. These data suggest that cardiovascular blood coagulation impairments are likely following pulmonary zinc exposure and associated pulmonary injury and inflammation.

  2. 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.

  3. 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.

  4. 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 ...

  5. Successful treatment of pseudophakic cystoid macular edema with intravitreal bevacizumab.

    PubMed

    Barone, Antonio; Prascina, Francesco; Russo, Vincenzo; Iaculli, Cristiana; Primavera, Vito; Querques, Giuseppe; Stella, Andrea; Delle Noci, Nicola

    2008-07-01

    A 67-year-old woman developed refractory pseudophakic cystoid macular edema (CME) after uneventful phacoemulsification. Three months after an intravitreal injection of bevacizumab (1.25 mg), the CME was completely resolved, with resultant improvement in visual acuity.

  6. The role of MIF, cyclinD1 and ERK in the development of pulmonary hypertension in broilers.

    PubMed

    Li, Haoyun; Wang, Yanmei; Chen, Lingli; Han, Lijuan; Li, Lifang; He, Han; Li, Yuan; Huang, Nan; Ren, Hao; Pei, Fangying; Li, Guilan; Cheng, Jia; Wang, Wenkui

    2017-04-01

    Pulmonary hypertension (PH) is a major disease in the broiler breeding industry. During PH, the pulmonary artery undergoes remodelling, which is caused by pulmonary vascular smooth muscle cell proliferation. CyclinD1 regulates cell proliferation. This study investigated the role of cyclinD1 in the development of PH in broilers, and which bioactivators and signalling pathway are involved in the pathological process. The PH group contained 3-4-week-old broilers with clinical PH, and the healthy group broilers from the same flock without PH. Histopathology indicated pulmonary arterial walls were thicker in the PH group compared with the healthy group. Target gene expressions of macrophage migration inhibitory factor (MIF), extracellular signal-regulated kinase (ERK), and cyclinD1 detected by quantitative real-time PCR were upregulated in the PH group compared with the healthy group. Immunohistochemistry showed MIF, phosphorylated ERK (p-ERK) and cyclinD1 were present on pulmonary vascular walls; MIF was present in the cytoplasm of arterial endothelial cells and smooth muscle cells; p-ERK and cyclinD1 were present in smooth muscle cell cytoplasm. Western blotting demonstrated that MIF, p-ERKand cyclinD1 levels were significantly higher (P < 0.01) in the PH group compared with the healthy group. In summary, increased MIF in PH broiler pulmonary arteries upregulated cyclinD1 via the ERK signalling pathway to induce pulmonary vascular smooth muscle cell proliferation, causing pulmonary artery remodelling and hypertension.

  7. Molecular physiopathogenetic mechanisms and development of new potential therapeutic strategies in persistent pulmonary hypertension of the newborn.

    PubMed

    Distefano, Giuseppe; Sciacca, Pietro

    2015-02-08

    Persistent pulmonary hypertension of the newborn (PPHN) is a cyanogenic plurifactorial disorder characterized by failed postnatal drop of pulmonary vascular resistance and maintenance of right-to-left shunt across ductus arteriosus and foramen ovale typical of intrauterine life. The pathogenesis of PPHN is very complex and can result from functional (vasoconstriction) or structural (arteriolar remodeling, reduced pulmonary vessels density) anomalies of pulmonary circulation. Etiopathogenetic factors heterogeneity can strongly condition therapeutical results and prognosis of PPHN that is particularly severe in organic forms that are usually refractory to selective pulmonary vasodilator therapy with inhaled nitric oxide. This paper reports the more recent acquisitions on molecular physiopathogenetic mechanisms underlying functional and structural forms of PPHN and illustrates the bases for adoption of new potential treatment strategies for organic PPHN. These strategies aim to reverse pulmonary vascular remodeling in PPHN with arteriolar smooth muscle hypertrophy and stimulate pulmonary vascular and alveolar growth in PPHN associated with lung hypoplasia.In order to restore lung growth in this severe form of PPHN, attention is focused on the results of studies of mesenchymal stem cells and their therapeutical paracrine effects on bronchopulmonry dysplasia, a chronic neonatal lung disease characterized by arrested vascular and alveolar growth and development of pulmonary hypertension.

  8. Diuretics in cardiac edema--1969.

    PubMed

    Shanoff, H M

    1969-10-04

    New and powerful diuretics have made it possible for the physician to control cardiac edema in most patients. At the same time their potentially dangerous side effects make it mandatory for the physician to be knowledgeable and judicious in their use. The appreciation of a few simplified facts about cardiac edema and renal reabsorption of sodium makes the clinical pharmacology of the diuretics much easier to understand, remember and apply.

  9. S-Nitrosylation and the Development of Pulmonary Hypertension

    DTIC Science & Technology

    2011-02-01

    SNOs to recipient target proteins on the surface of the endothelium as a function of oxygen saturation . In this context, erythrocytes can act as a...molecular switch, monitoring changes in oxygen saturation to deliver SNOs to the vascular endothelium. We have developed a model in which N- acetyl...in part, dependent on oxyhemoglobin saturation and thiols can accelerate the desaturation-induced loss of red blood SNO content. Task 2

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

    PubMed Central

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

    2015-01-01

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

  11. Pulmonary embolism caused by intimal sarcoma of the pulmonary artery.

    PubMed

    Yamamoto, Kei; Nozue, Tsuyoshi; Tsuchida, Masayuki; Iwaki, Taku; Nagamine, Hiroshi; Yasuda, Tamotsu; Kawase, Hiroshi; Matsushita, Kazuhiko; Michishita, Ichiro

    2012-01-01

    We herein report the case of a 39-year-old woman with a pulmonary embolism caused by intimal sarcoma of the pulmonary artery. She presented with shortness of breath and leg edema. Computed tomography showed a low density area that extended from the main pulmonary artery to the bilateral pulmonary arteries. We diagnosed her to have a pulmonary thromboembolism. The thrombosis did not decrease after the administration of anti-coagulant therapy, and she underwent resection of the thrombotic tissue. Histopathologically, the surgical specimen was not found to be thrombotic tissue but rather an intimal sarcoma of the pulmonary artery. After undergoing surgery, she received radiation therapy and chemotherapy; however, she died 31 months after being diagnosed.

  12. Intraoperative pulmonary hypertension occurred in an asymptomatic patient with pre-existent liver cirrhotic and portal hypertension

    PubMed Central

    Lu, Ling; Zhang, Feng; Li, Xiang-Cheng; Li, Guo-Qiang; Zhang, Chuan-Yong; Wang, Xue-Hao

    2008-01-01

    Portopulmonary hypertension (PPH) is clinically defined as the development of pulmonary arterial hypertension complicated by portal hypertension, with or without advanced hepatic disease. Physical signs may be absent in mild to moderate PPH and only appear in a hyperdynamic circulatory state. Similar signs of advanced liver disease can be observed in severe PPH, with ascites and lower extremity edema. Pulmonary hypertension is usually diagnosed after anesthetic induction during liver transplantation (LT). We present intraoperative pulmonary hypertension in a 41-year-old male patient with hepatic cirrhosis. Since this patient had no preoperation laboratory data supporting the diagnosises of pulmonary hypertension and was asymptomatic for a number of years, it was necessary to send him to the intensive care unit after operation. Further study should be focued on the diagnosis and treatment of pulmonary arterial hypertension in order to reduce its mortality. PMID:19084945

  13. [Pulmonary hypertension in pediatric heart surgery].

    PubMed

    Falcone, N

    2001-12-01

    Congenital heart disease can increase or decrease pulmonary blood flow, pulmonary vascular resistance (PVR) or pulmonary artery pressure (PAP). PAP is the product of PVR and pulmonary minute volume (Qp), such that pulmonary hypertension (PHT) may develop as a result of an increase in either PVR or Qp or both. Given that the pulmonary vascular bed is a low pressure system with high flow, any increase in resistance would generate PHT. The normal value of PVR is 2 Woods units (mm Hg/l/min). Increased PAP is due to hypoxic lesions of the endothelium, which release proteolytic enzymes that alter the balance of metabolites of arachidonic acid, regulators of pulmonary vasomotor tone. Hypoxia and acidosis cause intense pulmonary vasoconstriction (hypoxic vasoconstrictor reflex). An increase of PVR is due to a combination of vasoconstrictive processes and remodeling, with hypertrophy of the pulmonary artery. Structural lesions are related to hypertrophy of the endothelium, the transformation of fibroblasts to myocytes and the decrease of the alveolar/arteriolar ratio with the formation of new vessels.PHT may be primary or secondary to another disease. Primary PHT is a rare genetic disease. The most common secondary forms of PHT in pediatrics are due to persistence of neonatal anatomy (neonatal PHT), to heart diseases with left-right shunt (CIV, DAP, etc.), to diseases of the pulmonary parenchyma (interstitial viral infection, mucoviscidosis), and complications of heart surgery. All congenital heart diseases can lead to PHT if not treated promptly. Clinical signs of PHT are highly non-specific: dyspnea, fatigue, syncopes, exercise intolerance, precordialgia, cyanosis and edema. The best approaches to diagnosis and prognosis are echocardiography and cardiac catheterization with vasodilators. Anesthetics that do not alter PVR should be used in such patients, who are sensitive to changes in pulmonary ventilation, to changes in cardiac output and to anesthetics. The treatment of

  14. Progressive development of pulmonary hypertension leading to right ventricular hypertrophy assessed by echocardiography in rats.

    PubMed

    Kato, Yosuke; Iwase, Mitsunori; Kanazawa, Hiroaki; Kawata, Natsuki; Yoshimori, Yukie; Hashimoto, Katsunori; Yokoi, Toyoharu; Noda, Akiko; Takagi, Kenzo; Koike, Yasuo; Nishizawa, Takao; Nishimura, Masahiko; Yokota, Mitsuhiro

    2003-07-01

    The present study aimed to evaluate the development of pulmonary hypertension by serial echocardiography, including measurements of pulmonary artery (PA) flow velocities, and correlate echocardiographic indices with pathological findings in rats administered monocrotaline (MCT). MCT (60 mg/kg body weight) or physiologic saline was administered to a total of 9 male Wistar rats at the age of 4 weeks (MCT group: n = 4, control group: n = 5, respectively). Echocardiography was performed serially until the age of 8 weeks. The ratio of right ventricular (RV) outflow tract dimensions to aortic dimensions increased progressively in the MCT group and became significantly greater than that of the control group after the age of 6 weeks. Peak PA velocity (Peak V) in the MCT group was significantly less than that of the control group at the ages of 7 and 8 weeks. The ratio of acceleration time to ejection time (AT/ET) in PA flow waveforms declined progressively and was significantly less than that of the control group after the age of 6 weeks. The ratio of RV weight to body weight (RVW/BW) in the MCT group was significantly greater than that of the control group. Both AT/ET ratio and Peak V were significantly inversely correlated with RVW/BW ratio. Furthermore, these echocardiographic findings were also significantly inversely correlated with the mean cross-sectional RV myocyte area. In conclusion, the progressive development of pulmonary hypertension leading to RV hypertrophy can be evaluated appropriately by echocardiography including PA flow Doppler indices in rats.

  15. Development of a non-infectious rat model of acute exacerbation of idiopathic pulmonary fibrosis

    PubMed Central

    Chen, Shan-Shan; Yin, Zhao-Fang; Chen, Tao; Qiu, Hui; Wei, Ya-Ru; Du, Shan-Shan; Jin, Yue-Ping; Zhao, Meng-Meng; Wu, Qin

    2017-01-01

    Background Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease with severe pulmonary fibrosis. The main cause of IPF-associated death is acute exacerbation of IPF (AE-IPF). This study aims to develop a rat model of AE-IPF by two intratracheal perfusions with bleomycin (BLM). Methods Ninety male Sprague Dawley (SD) rats were randomized into three groups: an AE-IPF model group (BLM + BLM group), an IPF model group (BLM group), and a normal control group. Rats in the BLM + BLM group underwent a second perfusion with BLM on day 28 after the first perfusion with BLM. Rats in the other two groups received saline as the second perfusion. Six rats in each group were sacrificed on day 31, day 35, and day 42 after the first perfusion, respectively. Additional 18 rats in each group were observed for survival. Results Rats in the BLM + BLM group had significantly worse pulmonary alveolar inflammation and fibrosis than rats in the BLM group. Rats in the BLM + BLM group also developed large amounts of hyaline membrane, showed high levels of albumin (ALB) and various inflammatory factors in the bronchoalveolar lavage fluid (BALF), and had markedly increased lung water content. Furthermore, rat survival was reduced in the BLM + BLM group. The pathophysiological characteristics of rats in the BLM + BLM group resemble those of patients with AE-IPF. Conclusions A second perfusion with BLM appears to induce acute exacerbation of pulmonary fibrosis and may be used to model AE-IPF in rats. PMID:28203411

  16. 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.

  17. Left ventricular failure produces profound lung remodeling and pulmonary hypertension in mice: heart failure causes severe lung disease.

    PubMed

    Chen, Yingjie; Guo, Haipeng; Xu, Dachun; Xu, Xin; Wang, Huan; Hu, Xinli; Lu, Zhongbing; Kwak, Dongmin; Xu, Yawei; Gunther, Roland; Huo, Yuqing; Weir, E Kenneth

    2012-06-01

    Chronic left ventricular failure causes pulmonary congestion with increased lung weight and type 2 pulmonary hypertension. Understanding the molecular mechanisms for type 2 pulmonary hypertension and the development of novel treatments for this condition requires a robust experimental animal model and a good understanding of the nature of the resultant pulmonary remodeling. Here we demonstrate that chronic transverse aortic constriction causes massive pulmonary fibrosis and remodeling, as well as type 2 pulmonary hypertension, in mice. Thus, aortic constriction-induced left ventricular dysfunction and increased left ventricular end-diastolic pressure are associated with a ≤5.3-fold increase in lung wet weight and dry weight, pulmonary hypertension, and right ventricular hypertrophy. Interestingly, the aortic constriction-induced increase in lung weight was not associated with pulmonary edema but resulted from profound pulmonary remodeling with a dramatic increase in the percentage of fully muscularized lung vessels, marked vascular and lung fibrosis, myofibroblast proliferation, and leukocyte infiltration. The aortic constriction-induced left ventricular dysfunction was also associated with right ventricular hypertrophy, increased right ventricular end-diastolic pressure, and right atrial hypertrophy. The massive lung fibrosis, leukocyte infiltration, and pulmonary hypertension in mice after transverse aortic constriction clearly indicate that congestive heart failure also causes severe lung disease. The lung fibrosis and leukocyte infiltration may be important mechanisms in the poor clinical outcome in patients with end-stage heart failure. Thus, the effective treatment of left ventricular failure may require additional efforts to reduce lung fibrosis and the inflammatory response.

  18. Effectiveness of CT for clinical stratification of occupational lung edema.

    PubMed

    Masaki, Yoshinori; Sugiyama, Keisaku; Tanaka, Hiroyuki; Uwabe, Yasuhide; Takayama, Masanori; Sakai, Masao; Hayashi, Takuya; Otsuka, Masayuki; Suzuki, Shinya

    2007-01-01

    We treated two occupational lung diseases in different situations during military training. The purpose of this study is to investigate the availability of CT scanning for the evaluation of inhalation pulmonary edema. Two soldiers suffered severe lung edema after using a spray for the daily maintenance of their firearms. Four soldiers suffered severe dyspnea after undertaking drills in a narrow zone where numerous smoke bombs had been used. We evaluated these patients from several aspects. CT scans of the chest of spray-induced patients revealed bilateral infiltration predominantly in the upper lung fields. The patients received steroid pulse treatment and gradually recovered. CT scans of the chest of smoke-induced patients revealed bilateral ground-glass attenuation with peripheral lung sparing. The patients gradually recovered with steroid therapy. In accordance with previous studies, CT scans of the chest in our patients demonstrated that the periphery of the lungs remained normal, except in cases of serious injury. When differential diagnosis is required, we consider that CT scans of the chest are particularly useful; CT findings are useful in determining the severity of lung injury as well as the diagnosis of inhalation pulmonary edema.

  19. Bosentan for pulmonary hypertension secondary to idiopathic pulmonary fibrosis.

    PubMed

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

    2015-01-01

    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.

  20. 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

  1. Acute Hemorrhagic Edema of Infancy.

    PubMed

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

    2016-01-01

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

  2. 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

  3. Edema: a silent but important factor.

    PubMed

    Villeco, June P

    2012-01-01

    Edema is a normal response to injury. Even the smallest injury is associated with some inflammation, and initial edema is part of the normal inflammatory process. However, edema becomes a concern when it persists beyond the inflammatory phase. Once we have progressed into the rebuilding, or fibroplastic phase of healing, edema will delay healing and contribute to complications such as pain and stiffness. Early prevention and management to prevent this progression are therefore critical. This article discusses edema in relation to stages of healing and presents the research behind techniques available to the clinician to manage localized extracellular upper extremity edema in the patient with an intact lymphatic system.

  4. Calcium-Sensing Receptor Regulates Cytosolic [Ca2+] and Plays a Major Role in the Development of Pulmonary Hypertension

    PubMed Central

    Smith, Kimberly A.; Ayon, Ramon J.; Tang, Haiyang; Makino, Ayako; Yuan, Jason X.-J.

    2016-01-01

    Pulmonary arterial hypertension (PAH) is a progressive disease characterized by elevated pulmonary vascular resistance (PVR) leading to right heart failure and premature death. The increased PVR results in part from pulmonary vascular remodeling and sustained pulmonary vasoconstriction. Excessive pulmonary vascular remodeling stems from increased pulmonary arterial smooth muscle cell (PASMC) proliferation and decreased PASMC apoptosis. A rise in cytosolic free Ca2+ concentration ([Ca2+]cyt) in PASMC is a major trigger for pulmonary vasoconstriction and a key stimulus for PASMC proliferation and migration, both contributing to the development of pulmonary vascular remodeling. PASMC from patients with idiopathic PAH (IPAH) have increased resting [Ca2+]cyt and enhanced Ca2+ influx. Enhanced Ca2+ entry into PASMC due to upregulation of membrane receptors and/or Ca2+ channels may contribute to PASMC contraction and proliferation and to pulmonary vasoconstriction and pulmonary vascular remodeling. We have shown that the extracellular Ca2+-sensing receptor (CaSR), which is a member of G protein-coupled receptor (GPCR) subfamily C, is upregulated, and the extracellular Ca2+-induced increase in [Ca2+]cyt is enhanced in PASMC from patients with IPAH in comparison to PASMC from normal subjects. Pharmacologically blockade of CaSR significantly attenuate the development and progression of experimental pulmonary hypertension in animals. Additionally, we have demonstrated that dihydropyridine Ca2+ channel blockers (e.g., nifedipine), which are used to treat PAH patients but are only effective in 15–20% of patients, activate CaSR resulting in an increase in [Ca2+]cyt in IPAH-PASMC, but not normal PASMC. Our data indicate that CaSR functionally couples with transient receptor potential canonical (TRPC) channels to mediate extracellular Ca2+-induced Ca2+ influx and increase in [Ca2+]cyt in IPAH-PASMC. Upregulated CaSR is necessary for the enhanced extracellular Ca2+-induced

  5. Primary antiphospholipid syndrome presenting as chronic thromboembolic pulmonary hypertension. Treatment with thromboendarterectomy.

    PubMed

    Sandoval, J; Amigo, M C; Barragan, R; Izaguirre, R; Reyes, P A; Martinez-Guerra, M L; Palomar, A; Gomez, A; Garcia-Torres, R

    1996-04-01

    Pulmonary hypertension may occur in the antiphospholipid syndrome as a result of recurrent pulmonary embolism or microthrombosis of pulmonary vessels. We describe 3 cases of primary antiphospholipid syndrome (APS) and cor pulmonale that fulfilled the criteria for chronic major vessel thromboembolic pulmonary hypertension. Pulmonary thromboendarterectomy was performed in all 3 patients and it was successful in 2. One patient died in the immediate postoperative period from hemorrhagic pulmonary edema. Chronic thromboembolic pulmonary hypertension should be added to the list of pulmonary vascular complications of primary APS. Despite its risk, pulmonary thromboendarterectomy represents a treatment option for this otherwise lethal condition.

  6. 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

  7. 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.

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

    PubMed

    Muro, Shigeo

    2011-10-01

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

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

    NASA Astrophysics Data System (ADS)

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

    2015-03-01

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

  10. Pulmonary lesions induced by Pasteurella haemolytica in neutrophil sufficient and neutrophil deficient calves.

    PubMed Central

    Breider, M A; Walker, R D; Hopkins, F M; Schultz, T W; Bowersock, T L

    1988-01-01

    The role of neutrophils in the development of peracute lung lesions of bovine pneumonic pasteurellosis was investigated. Eight calves were divided into two groups of four calves each. Group I was treated with intravenous phosphate-buffered saline and served as the neutrophil sufficient calves. Group II was treated with intravenous hydroxyurea which produced a state of neutropenia. When peripheral blood neutrophil numbers dropped below 300 cells/microL in group II, all calves were challenged with an intrabronchial bolus of Pasteurella haemolytica in the log phase of growth. An acute inflammatory process occurred in both groups of calves indicated by a rise in body temperature. While pulmonary lesions occurred in both groups by six hours postinoculation, they varied in pathological characteristics. Pulmonary lesions in the neutrophil sufficient calves consisted of fibrinopurulent alveolitis-bronchiolitis with associated alveolar septal necrosis, interlobular edema, and intravascular thrombi. The neutrophil deficient calves had extensive intra-alveolar edema, interlobular edema, intraalveolar hemorrhage, atelectasis, and focal areas of alveolar septal necrosis. These results show that P. haemolytica can induce severe pulmonary tissue damage through both neutrophil dependent and neutrophil independent mechanisms. Images Fig. 1. Fig. 2. PMID:3370555

  11. Redispersible liposomal-N-acetylcysteine powder for pulmonary administration: development, in vitro characterization and antioxidant activity.

    PubMed

    Ourique, Aline Ferreira; Chaves, Paula Dos Santos; Souto, Gabriele Dadalt; Pohlmann, Adriana Raffin; Guterres, Silvia Stanisçuaski; Beck, Ruy Carlos Ruver

    2014-12-18

    Liposomal dry powders of N-acetylcysteine (SD-NAC-Lip) were developed for pulmonary administration. Liposomes were prepared by reverse phase evaporation and spray dried using lactose (10%, w/w) as drying adjuvant. The powders were characterized according to process yield, drug content, residual water content, particle size distribution, morphology and redispersion behavior. In vitro aerosol performance was evaluated using an eight-stage Andersen Cascade Impactor. Moreover, in vitro antioxidant activity was determined by measuring thiobarbituric acid reactive species (TBARS) present in the lungs of healthy Wistar rats after induction of oxidation by iron/EDTA. The spray-drying process had a high yield (71%±2), drug content (mg/g) according to the expected value, moisture content below 9%, geometric mean diameter under 3μm with span value lower than 1. Spherical particles were observed by scanning electron microscopy. Liposomal dry-powders were able to recover the nanometric size of the original dispersion after their redispersion in aqueous medium, as shown by laser diffraction and transmission electron microscopy. Furthermore, the powders presented aerodynamic diameter of about 7μm and respirable fraction above 30%, indicating suitable properties for pulmonary use. The encapsulation of N-acetylcysteine in liposomes was essential to maintain its in vitro antioxidant activity after the drying process. In addition, the powder containing the encapsulated drug had better in vitro antioxidant activity than the liquid and solid formulations containing the non-encapsulated drug, which makes it a good candidate for the treatment of pulmonary diseases associated with oxidative stress.

  12. When Pulmonary Function Test is Available, Should we Wait for the COPD Symptoms to Develop?

    PubMed

    Mehta, Varshil; Desai, Nimit; Patel, Smit

    2016-10-01

    Adolescent smokers are more likely to be addicted to nicotine and develop a chronic habit. Chronic smoking has a direct impact on quality of life and life expectancy. Repeated environmental exposure and smoke inhalation can be deleterious to health. In order to evaluate the core functioning of the lungs, Pulmonary Function Tests (PFTs) are conducted. This panel of tests should be advised for all patients complaining of shortness of breath. Since clinical features resulting from chronic smoking tend to appear late in the course of the disease, PFTs are immensely useful for early identification of abnormalities in asymptomatic adult smokers. Numerous studies have shown that normal PFT parameters begin to deteriorate immediately after smoking is initiated. However, most physicians prefer to wait for characteristic signs and symptoms of Chronic Obstructive Pulmonary Disease (COPD) to develop before proceeding with PFTs in the patients. This leads to inadvertent and often dangerous delay in reaching a definitive diagnosis and initiating treatment. Therefore, we undertook this review to determine whether conducting PFTs in asymptomatic adult smokers can facilitate the early detection and/or prevention of COPD. We reviewed and analyzed articles from PubMed, Google Scholar, Index Medicus, WHO Global Health Library and Scopus, which specifically demonstrated the presence of abnormal PFT changes in asymptomatic adult smokers. With PFTs, we now have the advantage of diagnosing early changes in the lung volumes. Hence, we conclude that PFTs should be performed early in smokers and cessation of smoking should be encouraged to check the increasing incidence of COPD.

  13. Regulation of pulmonary surfactant secretion in the developing lizard, Pogona vitticeps.

    PubMed

    Sullivan, Lucy C; Orgeig, Sandra; Daniels, Christopher B

    2002-11-01

    Pulmonary surfactant is a mixture of lipids and proteins that is secreted by alveolar type II cells in the lungs of all air-breathing vertebrates. Pulmonary surfactant functions to reduce the surface tension in the lungs and, therefore, reduce the work of breathing. In mammals, the embryonic maturation of the surfactant system is controlled by a host of factors, including glucocorticoids, thyroid hormones and autonomic neurotransmitters. We have used a co-culture system of embryonic type II cells and lung fibroblasts to investigate the ability of dexamethasone, tri-iodothyronine (T(3)), adrenaline and carbamylcholine (carbachol) to stimulate the cellular secretion of phosphatidylcholine in the bearded dragon (Pogona vitticeps) at day 55 (approx. 92%) of incubation and following hatching. Adrenaline stimulated surfactant secretion both before and after hatching, whereas carbachol stimulated secretion only at day 55. Glucocorticoids and triiodothyronine together stimulated secretion at day 55 but did not after hatching. Therefore, adrenaline, carbachol, dexamethasone and T(3), are all involved in the development of the surfactant system in the bearded dragon. However, the efficacy of the hormones is attenuated during the developmental process. These differences probably relate to the changes in the cellular environment during development and the specific biology of the bearded dragon.

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

    PubMed

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

    2011-10-31

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

  15. Pulmonary complications after abdominal surgery in patients with mild-to-moderate chronic obstructive pulmonary disease

    PubMed Central

    Kim, Tae Hoon; Lee, Jae Seung; Lee, Sei Won; Oh, Yeon-Mok

    2016-01-01

    Postoperative pulmonary complications (PPCs) are one of the most important causes of postoperative morbidity and mortality after abdominal surgery. Although chronic obstructive pulmonary disease (COPD) has been considered a risk factor for PPCs, it remains unclear whether mild-to-moderate COPD is a risk factor. This retrospective cohort study included 387 subjects who underwent abdominal surgery with general anesthesia in a tertiary referral hospital. PPCs included pneumonia, pulmonary edema, pulmonary thromboembolism, atelectasis, and acute exacerbation of COPD. Among the 387 subjects, PPCs developed in 14 (12.0%) of 117 patients with mild-to-moderate COPD and in 13 (15.1%) of 86 control patients. Multiple logistic regression analysis revealed that mild-to-moderate COPD was not a significant risk factor for PPCs (odds ratio [OR] =0.79; 95% confidence interval [CI] =0.31–2.03; P=0.628). However, previous hospitalization for respiratory problems (OR =4.20; 95% CI =1.52–11.59), emergency surgery (OR =3.93; 95% CI =1.75–8.82), increased amount of red blood cell (RBC) transfusion (OR =1.09; 95% CI =1.05–1.14 for one pack increase of RBC transfusion), and laparoscopic surgery (OR =0.41; 95% CI =0.18–0.93) were independent predictors of PPCs. These findings suggested that mild-to-moderate COPD may not be a significant risk factor for PPCs after abdominal surgery. PMID:27877032

  16. Pulmonary embolus

    MedlinePlus

    ... clot - lung; Embolus; Tumor embolus; Embolism - pulmonary; DVT-pulmonary embolism; Thrombosis - pulmonary embolism ... Main symptoms of a pulmonary embolism include chest pain that may be any of the following: Under the breastbone or on one side Sharp or stabbing ...

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

    PubMed Central

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

    2011-01-01

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

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

    PubMed

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

    2016-10-01

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

  19. Development of pulmonary fibrosis in mice during infection with Paracoccidioides brasiliensis conidia.

    PubMed

    Restrepo, S; Tobon, A; Trujillo, J; Restrepo, A

    1992-01-01

    Pulmonary fibrosis is a feared sequelae of paracoccidioidomycosis. We sought to determine if mice exposed to Paracoccidioides brasiliensis conidia would develop pulmonary fibrosis. BALB/c mice were infected intranasally with P. brasiliensis conidia and sacrificed at regular intervals. One lung was sectioned for histopathology and sections were stained with haematoxylin and eosin, trichromic and argentic stains; the other lung was homogenized and cultured to determine the viability of the fungus. One week post-challenge, only small peribronchial foci were apparent. After 4 weeks, reticular fibres appeared disorganized and disrupted. Six to 8 weeks later peribronchial infiltrates were larger and appeared surrounded by reticular fibres; thick collagen I fibres were noticed in the infiltrated areas at this time. On weeks 10-12, infiltrates were confluent and reticular fibres were concentrated around the inflammatory foci; collagenization was apparent. Observations up to 16 weeks revealed diffuse involvement of the lung parenchyma with extensive collagenization. Lung cultures were always positive. We suggest that inhalation of P. brasiliensis conidia induces adverse lung responses leading to changes in the proportion of collagen fibres I and III.

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

    PubMed

    Metting, Esther I; In 't Veen, Johannes C C M; Dekhuijzen, P N Richard; van Heijst, Ellen; Kocks, Janwillem W H; Muilwijk-Kroes, Jacqueline B; Chavannes, Niels H; van der Molen, Thys

    2016-01-01

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

  1. [The influence of smoking and occupational factors on the development of chronic obstructive pulmonary disease in oil industry workers].

    PubMed

    Abdullaev, A Iu

    2012-01-01

    The influence of smoking and occupational factors on the development of chronic obstructive pulmonary disease (COPD) in employees of a sea oil and gas company is considered. The primary role of smoking in pathogenesis of COPD is confirmed Direct and indirect influence of smoking is enhanced by occupational and climatic factors leading to the development of persistent disturbances of ventilation.

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

    NASA Astrophysics Data System (ADS)

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

    2011-06-01

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

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

    PubMed Central

    Scott, J Elliott

    2004-01-01

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

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

    PubMed Central

    Scott, J Elliott

    2004-01-01

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

  5. Serotonin transporter is not required for the development of severe pulmonary hypertension in the Sugen hypoxia rat model.

    PubMed

    de Raaf, Michiel Alexander; Kroeze, Yvet; Middelman, Anthonieke; de Man, Frances S; de Jong, Helma; Vonk-Noordegraaf, Anton; de Korte, Chris; Voelkel, Norbert F; Homberg, Judith; Bogaard, Harm Jan

    2015-11-15

    Increased serotonin serum levels have been proposed to play a key role in pulmonary arterial hypertension (PAH) by regulating vessel tone and vascular smooth muscle cell proliferation. An intact serotonin system, which critically depends on a normal function of the serotonin transporter (SERT), is required for the development of experimental pulmonary hypertension in rodents exposed to hypoxia or monocrotaline. While these animal models resemble human PAH only with respect to vascular media remodeling, we hypothesized that SERT is likewise required for the presence of lumen-obliterating intima remodeling, a hallmark of human PAH reproduced in the Sugen hypoxia (SuHx) rat model of severe angioproliferative pulmonary hypertension. Therefore, SERT wild-type (WT) and knockout (KO) rats were exposed to the SuHx protocol. SERT KO rats, while completely lacking SERT, were hemodynamically indistinguishable from WT rats. After exposure to SuHx, similar degrees of severe angioproliferative pulmonary hypertension and right ventricular hypertrophy developed in WT and KO rats (right ventricular systolic pressure 60 vs. 55 mmHg, intima thickness 38 vs. 30%, respectively). In conclusion, despite its implicated importance in PAH, SERT does not play an essential role in the pathogenesis of severe angioobliterative pulmonary hypertension in rats exposed to SuHx.

  6. Development of a Multicompartment Permeability-Limited Lung PBPK Model and Its Application in Predicting Pulmonary Pharmacokinetics of Antituberculosis Drugs

    PubMed Central

    Gaohua, L; Wedagedera, J; Small, BG; Almond, L; Romero, K; Hermann, D; Hanna, D; Jamei, M; Gardner, I

    2015-01-01

    Achieving sufficient concentrations of antituberculosis (TB) drugs in pulmonary tissue at the optimum time is still a challenge in developing therapeutic regimens for TB. A physiologically based pharmacokinetic model incorporating a multicompartment permeability-limited lung model was developed and used to simulate plasma and pulmonary concentrations of seven drugs. Passive permeability of drugs within the lung was predicted using an in vitro-in vivo extrapolation approach. Simulated epithelial lining fluid (ELF):plasma concentration ratios showed reasonable agreement with observed clinical data for rifampicin, isoniazid, ethambutol, and erythromycin. For clarithromycin, itraconazole and pyrazinamide the observed ELF:plasma ratios were significantly underpredicted. Sensitivity analyses showed that changing ELF pH or introducing efflux transporter activity between lung tissue and ELF can alter the ELF:plasma concentration ratios. The described model has shown utility in predicting the lung pharmacokinetics of anti-TB drugs and provides a framework for predicting pulmonary concentrations of novel anti-TB drugs. PMID:26535161

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

    SciTech Connect

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

    1980-01-01

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

  8. A case of insulin edema with inappropriate hyperaldosteronism.

    PubMed

    Kalambokis, G; Tsatsoulis, A; Economou, G; Tsianos, E V

    2004-11-01

    Edema of variable severity is an uncommon complication of insulin treatment. Increased sodium reabsorption, transient proteinuria and hypoalbuminemia are the most frequently reported laboratory disorders at the time of edema formation. This case report describes a 44-yr-old man with a 4-month history of anorexia, polyuria, polydipsia and weight loss of 25 kg who presented with diabetic ketoacidosis. On admission, there were no clinical or laboratory signs of volume depletion. Following insulin treatment he developed marked insulin edema and a cluster of abnormalities, including decreased sodium excretion, hypokalemia, hypouricemia, proteinuria, hypoalbuminemia and anemia. The diagnostic work-up showed the presence of high renin and aldosterone values despite the absence of evident hypovolemia and no evidence of gastrointestinal, cardiovascular, renal, thyroid, hepatic or other endocrine disorder. Complement values were normal; autonomic neuropathy and venoocclusive intraabdominal lesions were excluded and no other drugs except insulin were administered. Initiation of spironolactone was associated with prompt resolution of the edema and gradual correction of the laboratory abnormalities. Our findings show that hyperaldosteronism may occur in patients with insulin edema, even in the absence of volume depletion, contributing to the development of increased sodium reabsorption and of other laboratory disorders.

  9. The role of leptin in the development of pulmonary neutrophilia in infection and Acute Lung Injury

    PubMed Central

    Ubags, Niki D.; Vernooy, Juanita H.; Burg, Elianne; Hayes, Catherine; Bement, Jenna; Dilli, Estee; Zabeau, Lennart; Abraham, Edward; Poch, Katie R.; Nick, Jerry A.; Dienz, Oliver; Zuñiga, Joaquin; Wargo, Matthew J.; Mizgerd, Joseph P.; Tavernier, Jan; Rincón, Mercedes; Poynter, Matthew E.; Wouters, Emiel F.M.; Suratt, Benjamin T.

    2014-01-01

    Objective One of the hallmarks of severe pneumonia and associated Acute Lung Injury (ALI) is neutrophil recruitment to the lung. Leptin is thought to be up-regulated in the lung following injury and to exert diverse effects on leukocytes, influencing both chemotaxis and survival. We hypothesized that pulmonary leptin contributes directly to the development of pulmonary neutrophilia during pneumonia and ALI. Design Controlled human and murine in vivo and ex vivo experimental studies. Settings Research laboratory of a university hospital. Subjects Healthy human volunteers and subjects hospitalized with bacterial and H1N1 pneumonia. C57Bl/6 and db/db mice were also used. Interventions Lung samples from patients and mice with either bacterial or H1N1 pneumonia and associated ALI were immunostained for leptin. Human bronchoalveolar-lavage (BAL) samples obtained after lipopolysaccharide (LPS)-induced lung injury were assayed for leptin. C57Bl/6 mice were examined after oropharyngeal aspiration of recombinant leptin alone or in combination with E.coli- or K.pneumonia-induced pneumonia. Leptin-resistant (db/db) mice were also examined using the E.coli model. BAL neutrophilia and cytokine levels were measured. Leptin-induced chemotaxis was examined in human blood- and murine marrow-derived neutrophils in vitro. Measurements and Main Results Injured human and murine lung tissue showed leptin induction compared to normal lung, as did human BAL following LPS instillation. BAL neutrophilia in uninjured and infected mice was increased and lung bacterial-load decreased by airway leptin administration, whereas BAL neutrophilia in infected leptin-resistant mice was decreased. In sterile lung injury by LPS, leptin also appeared to decrease airspace neutrophil apoptosis. Both human and murine neutrophils migrated towards leptin in vitro, and this required intact signaling through the JAK2/PI3K pathway. Conclusion We demonstrate that pulmonary leptin is induced in injured human and

  10. Foxp transcription factors suppress a non-pulmonary gene expression program to permit proper lung development.

    PubMed

    Li, Shanru; Morley, Michael; Lu, MinMin; Zhou, Su; Stewart, Kathleen; French, Catherine A; Tucker, Haley O; Fisher, Simon E; Morrisey, Edward E

    2016-08-15

    The inhibitory mechanisms that prevent gene expression programs from one tissue to be expressed in another are poorly understood. Foxp1/2/4 are forkhead transcription factors that repress gene expression and are individually important for endoderm development. We show that combined loss of all three Foxp1/2/4 family members in the developing anterior foregut endoderm leads to a loss of lung endoderm lineage commitment and subsequent development. Foxp1/2/4 deficient lungs express high levels of transcriptional regulators not normally expressed in the developing lung, including Pax2, Pax8, Pax9 and the Hoxa9-13 cluster. Ectopic expression of these transcriptional regulators is accompanied by decreased expression of lung restricted transcription factors including Nkx2-1, Sox2, and Sox9. Foxp1 binds to conserved forkhead DNA binding sites within the Hoxa9-13 cluster, indicating a direct repression mechanism. Thus, Foxp1/2/4 are essential for promoting lung endoderm development by repressing expression of non-pulmonary transcription factors.

  11. Noncardiogenic Pulmonary Edema as a Result of Urosepsis

    DTIC Science & Technology

    2010-03-01

    cause could be aortic stenosis , which may require surgery to correct, or it could be coronary artery disease, which can be treated through a variety...systolic dysfunction. Left ventricular dysfunction can occur due to many processes such as aortic or mitral valve dysfunction, coronary artery disease

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

    PubMed

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

    2015-12-01

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

  13. Inhalation Exposure Systems for the Development of Rodent Models of Sulfur Mustard-Induced Pulmonary Injury

    PubMed Central

    Weber, Waylon M.; Kracko, Dean A.; Lehman, Mericka R.; Irvin, Clinton M.; Blair, Lee F.; White, Richard K.; Benson, Janet M.; Grotendorst, Gary R.; Cheng, Yung-Sung; McDonald, Jacob D.

    2011-01-01

    Sulfur mustard (SM) is a chemical threat agent for which its effects have no current treatment. Due to the ease of synthesis and dispersal of this material, the need to develop therapeutics is evident. The present manuscript details the techniques used to develop SM laboratory exposure systems for the development of animal models of pulmonary injury. These models are critical for evaluating SM injury and developing therapeutics against that injury. Iterative trials were conducted to optimize a lung injury model. The resulting pathology was used as a guide, with a goal of effecting homogeneous and diffuse lung injury comparable to that of human injury. Inhalation exposures were conducted by either nose-only inhalation or intubated inhalation. The exposures were conducted to either directly vaporized SM or SM that was nebulized from an ethanol solution. Inhalation of SM by nose-only inhalation resulted in severe nasal epithelial degeneration and minimal lung injury. The reactivity of SM did not permit it to transit past the upper airways to promote lower airway injury. Intratracheal inhalation of SM vapors at a concentration of 5400 mg · min/m3 resulted in homogeneous lung injury with no nasal degeneration. PMID:20025432

  14. Inhalation exposure systems for the development of rodent models of sulfur mustard-induced pulmonary injury.

    PubMed

    Weber, Waylon M; Kracko, Dean A; Lehman, Mericka R; Irvin, Clinton M; Blair, Lee F; White, Richard K; Benson, Janet M; Grotendorst, Gary R; Cheng, Yung-Sung; McDonald, Jacob D

    2010-01-01

    Sulfur mustard (SM) is a chemical threat agent for which its effects have no current treatment. Due to the ease of synthesis and dispersal of this material, the need to develop therapeutics is evident. The present manuscript details the techniques used to develop SM laboratory exposure systems for the development of animal models of pulmonary injury. These models are critical for evaluating SM injury and developing therapeutics against that injury. Iterative trials were conducted to optimize a lung injury model. The resulting pathology was used as a guide, with a goal of effecting homogeneous and diffuse lung injury comparable to that of human injury. Inhalation exposures were conducted by either nose-only inhalation or intubated inhalation. The exposures were conducted to either directly vaporized SM or SM that was nebulized from an ethanol solution. Inhalation of SM by nose-only inhalation resulted in severe nasal epithelial degeneration and minimal lung injury. The reactivity of SM did not permit it to transit past the upper airways to promote lower airway injury. Intratracheal inhalation of SM vapors at a concentration of 5400 mg x min/m(3) resulted in homogeneous lung injury with no nasal degeneration.

  15. Lower extremity edema in a child due to pectus excavatum.

    PubMed

    Iannucci, Glen J; Slesnick, Timothy C; Kogon, Brian; Samai, Cyrus

    2015-02-01

    A previously healthy 11-year-old girl was referred for pediatric cardiology evaluation because of the development of progressive bilateral lower extremity swelling over the course of 2 years. Her prior workup had included a negative result for proteinuria and a negative ultrasound for deep venous thrombosis. On physical examination, in addition to her edema, she was found to have a severe pectus excavatum deformity, which prompted cardiac magnetic resonance imaging. This study demonstrated compression of the inferior vena cava. She underwent uneventful pectus repair with use of a modified Ravitch procedure and experienced complete resolution of her lower extremity edema.

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

    PubMed

    Brănişteanu, Daniel; Moraru, Andreea

    2014-01-01

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

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

    SciTech Connect

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

    1998-10-14

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

  18. Hantavirus pulmonary syndrome.

    PubMed

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

    2011-12-01

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

  19. Early life influences on the development of chronic obstructive pulmonary disease.

    PubMed

    Stocks, Janet; Sonnappa, Samatha

    2013-06-01

    There is increasing evidence that chronic obstructive pulmonary disease (COPD) is not simply a disease of old age that is largely restricted to heavy smokers, but may be associated with insults to the developing lung during foetal life and the first few years of postnatal life, when lung growth and development are rapid. A better understanding of the long-term effects of early life factors, such as intrauterine growth restriction, prenatal and postnatal exposure to tobacco smoke and other pollutants, preterm delivery and childhood respiratory illnesses, on the subsequent development of chronic respiratory disease is imperative if appropriate preventive and management strategies to reduce the burden of COPD are to be developed. The extent to which insults to the developing lung are associated with increased risk of COPD in later life depends on the underlying cause, timing and severity of such derangements. Suboptimal conditions in utero result in aberrations of lung development such that affected individuals are born with reduced lung function, which tends to remain diminished throughout life, thereby increasing the risk both of wheezing disorders during childhood and subsequent COPD in genetically susceptible individuals. If the current trend towards the ever-increasing incidence of COPD is to be reversed, it is essential to minimize risks to the developing lung by improvements in antenatal and neonatal care, and to reduce prenatal and postnatal exposures to environmental pollutants, including passive tobacco smoke. Furthermore, adult physicians need to recognize that lung disease is potentially associated with early life insults and provide better education regarding diet, exercise and avoidance of smoking to preserve precious reserves of lung function in susceptible adults. This review focuses on factors that adversely influence lung development in utero and during the first 5 years of life, thereby predisposing to subsequent COPD.

  20. Progress in Drug Treatment of Cerebral Edema.

    PubMed

    Deng, Y Y; Shen, F C; Xie, D; Han, Q P; Fang, M; Chen, C B; Zeng, H K

    2016-01-01

    Cerebral edema causes intracranial hypertension (ICH) which leads to severe outcome of patients in the clinical setting. Effective anti-edema therapy may significantly decrease the mortality in a variety of neurological conditions. At present drug treatment is a cornerstone in the management of cerebral edema. Osmotherapy has been the mainstay of pharmacologic therapy. Mannitol and hypertonic saline (HS) are the most commonly used osmotic agents. The relative safety and efficacy of HS and mannitol in the treatment of cerebral edema and reduction of enhanced ICP have been demonstrated in the past decades. Apart from its osmotic force, HS exerts anti-edema effects partly through inhibition of Na(+)-K(+)-2Cl(-) Cotransporter-1 (NKCC1) and aquaporin 4 (AQP4) expression in astrocytes. Melatonin may also reduce brain edema and exert neuroprotective effect on several central nervous system diseases through inhibition of inflammatory response. The inhibitors of Na/H exchanger, NKCC and AQP4 may attenuate brain edema formation through inhibition of excessive transportation of ion and water from blood into the cerebral tissue. In this review we survey some of the most recent findings in the drug treatment of brain edema focusing on the use of osmotherapy, melatonin and inhibitors of ion cotransporters and water channels. A better understanding of the molecular mechanism of these agents would help to improve in the clinical management of patients with brain edema.

  1. Delivery of imatinib-incorporated nanoparticles into lungs suppresses the development of monocrotaline-induced pulmonary arterial hypertension.

    PubMed

    Akagi, Satoshi; Nakamura, Kazufumi; Miura, Daiji; Saito, Yukihiro; Matsubara, Hiromi; Ogawa, Aiko; Matoba, Tetsuya; Egashira, Kensuke; Ito, Hiroshi

    2015-05-13

    Platelet-derived growth factor (PDGF) is implicated in the pathogenesis of pulmonary arterial hypertension (PAH). Imatinib, a PDGF-receptor tyrosine kinase inhibitor, improved hemodynamics, but serious side effects and drug discontinuation are common when treating PAH. A drug delivery system using nanoparticles (NPs) enables the reduction of side effects while maintaining the effects of the drug. We examined the efficacy of imatinib-incorporated NPs (Ima-NPs) in a rat model and in human PAH-pulmonary arterial smooth muscle cells (PASMCs). Rats received a single intratracheal administration of PBS, FITC-NPs, or Ima-NPs immediately after monocrotaline injection. Three weeks after monocrotaline injection, intratracheal administration of Ima-NPs suppressed the development of pulmonary hypertension, small pulmonary artery remodeling, and right ventricular hypertrophy in the rat model of monocrotaline-induced PAH. We also examined the effects of imatinib and Ima-NPs on PDGF-induced proliferation of human PAH-PASMCs by (3)H-thymidine incorporation. Imatinib and Ima-NPs significantly inhibited proliferation after 24 hours of treatment. Ima-NPs significantly inhibited proliferation compared with imatinib at 24 hours after removal of these drugs. Delivery of Ima-NPs into lungs suppressed the development of MCT-induced PAH by sustained antiproliferative effects on PAS-MCs.

  2. Mechanical stretch-induced serotonin release from pulmonary neuroendocrine cells: implications for lung development.

    PubMed

    Pan, Jie; Copland, Ian; Post, Martin; Yeger, Herman; Cutz, Ernest

    2006-01-01

    Pulmonary neuroendocrine cells (PNEC) produce amine (serotonin, 5-HT) and peptides (e.g., bombesin, calcitonin) with growth factor-like properties and are thought to play an important role in lung development. Because physical forces are essential for lung growth and development, we investigated the effects of mechanical strain on 5-HT release in PNEC freshly isolated from rabbit fetal lung and in the PNEC-related tumor H727 cell line. Cultures exposed to sinusoidal cyclic stretch showed a significant 5-HT release inhibitable with gadolinium chloride (10 nM), a blocker of mechanosensitive channels. In contrast to hypoxia (Po2 approximately 20 mmHg), stretch-induced 5-HT release was not affected by Ca2+-free medium or nifedipine (50 microM), excluding the exocytic pathway. In H727 cells, stretch failed to release calcitonin, a peptide stored within dense core vesicles (DCV), whereas hypoxia caused massive calcitonin release. 5-HT released by mechanical stretch is derived predominantly from the cytoplasmic pool, because it is rapid ( approximately 5 min) and is releasable from early (20 days of gestation) fetal PNEC containing few DCV. Both mechanical stretch and hypoxia upregulated expression of tryptophan hydroxylase, the rate-limiting enzyme of 5-HT synthesis. We conclude that mechanical strain is an important physiological stimulus for the release of 5-HT from PNEC via mechanosensitive channels with potential effects on lung development and resorption of lung fluid at the time of birth.

  3. Cloacal dysgenesis sequence with bilateral renal agenesis and normal pulmonary development in twin pregnancy.

    PubMed

    Jegadeesh, Sundram; Mahajan, Jai Kumar

    2016-01-20

    Cloacal dysgenesis sequence (CDS) is a rare congenital anomaly. It is characterised by a smooth perineum with absence of anal and genitourinary orifices, with reported incidence of 1:50,000-250,000 births. Association with bilateral renal agenesis is still rarer and resultant severe oligohydramnios is associated with pulmonary hypoplasia. Only a few cases of CDS with bilateral renal agenesis have been reported in the English language literature, with associated pulmonary hypoplasia as a default phenomenon. We report a case of CDS and bilateral renal agenesis without associated pulmonary hypoplasia in a twin pregnancy, which, to the best of our knowledge, is the second reported case of this amalgamation.

  4. Pulmonary angiography

    MedlinePlus

    ... Pulmonary arteriography; Pulmonary angiogram; Angiogram of the lungs Images Pulmonary arteries References Jackson JE, Meaney JFM. Angiography. ... urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows ...

  5. Pulmonary Rehabilitation

    MedlinePlus

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

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

    NASA Astrophysics Data System (ADS)

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

    2014-03-01

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

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

    PubMed

    Hayreh, Sohan Singh

    2016-01-01

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

  8. PATHOGENESIS OF OPTIC DISC EDEMA IN RAISED INTRACRANIAL PRESSURE

    PubMed Central

    Hayreh, Sohan Singh

    2015-01-01

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

  9. Innate immunity dictates cytokine polarization relevant to the development of pulmonary fibrosis

    PubMed Central

    Strieter, Robert M.; Keane, Michael P.

    2004-01-01

    New data support the importance of the innate immune response in the resolution or progression of pulmonary fibrosis. The presence of CXC chemokine receptor 3–expressing cells, specifically pulmonary NK cells, is necessary to produce IFN-γ. This is critical in the polarization of the immune response to injury toward a favorable Th1 response and resolution. In contrast, a Th2 response is associated with progressive fibrosis. PMID:15254582

  10. Primary pulmonary hypertension.

    PubMed

    Rashid, A; Lehrman, S; Romano, P; Frishman, W; Dobkin, J; Reichel, J

    2000-01-01

    Primary pulmonary hypertension (PPH) is a condition characterized by sustained elevation of pulmonary artery pressure (PAP) without demonstrable cause. The most common symptom at presentation is dyspnea. Other complaints include fatigue, chest pain, syncope, leg edema, and palpitations. Right heart catheterization is diagnostic, showing a mean PAP >25 mmHg at rest and >30 mmHg during exercise, with a normal pulmonary capillary wedge pressure. In the National Institutes of Health-PPH registry, the median survival period was 2.8 years. Treatment is aimed at lowering PAP, increasing cardiac output, and decreasing in situ thrombosis. Vasodilators have been used with some success in the treatment of PPH. They include prostacyclin, calcium-channel blockers, nitric oxide and adenosine. Anticoagulation has also been advised for the prevention of deep vein thrombosis, pulmonary embolism, and in situ thromboses of the lungs. New drug treatments under investigation include L-arginine, plasma endothelin-I, and bosentan. Use of oxygen, digoxin, and diuretics for symptomatic relief have also been recommended. Patients with severe PPH refractory to medical management should be considered for surgery.

  11. Macular edema: definition and basic concepts.

    PubMed

    Coscas, Gabriel; Cunha-Vaz, José; Soubrane, Gisèle

    2010-01-01

    Macular edema is the result of an accumulation of fluid in the retinal layers around the fovea. It contributes to vision loss by altering the functional cell relationship in the retina and promoting an inflammatory reparative response. Macular edema may be intracellular or extracellular. Intracellular accumulation of fluid, also called cytotoxic edema, is an alteration of the cellular ionic distribution. Extracellular accumulation of fluid, which is more frequent and clinically more relevant, is directly associated with an alteration of the blood-retinal barrier (BRB). The following parameters are relevant for clinical evaluation of macular edema: extent of the macular edema (i.e., the area that shows increased retinal thickness); distribution of the edema in the macular area (i.e., focal versus diffuse macular edema); central foveal involvement (central area 500 microm); fluorescein leakage (evidence of alteration of the BRB or 'open barrier') and intraretinal cysts; signs of ischemia (broken perifoveolar capillary arcade and/or areas of capillary closure); presence or absence of vitreous traction; increase in retinal thickness and cysts in the retina (inner or outer), and chronicity of the edema (i.e., time elapsed since initial diagnosis and response to therapy). It is essential to establish associations and correlations of all the different images obtained, regardless of whether the same or different modalities are used.

  12. Conservative management of acute scrotal edema.

    PubMed

    Benjamin, Karen D

    2014-01-01

    Scrotal edema is a prevalent issue. It is difficult to treat and has a myriad of causes. Historical treatments for scrotal edema have lacked efficacy. If treated before fibrosis occurs, surgery can be avoided. A method for conservative management is outlined.

  13. Development of pulmonary neuroendocrine cells of fetal hamster in explant culture.

    PubMed

    Ito, T; Nogawa, H; Udaka, N; Kitamura, H; Kanisawa, M

    1997-11-01

    Fetal hamster lung explant was cultured in serum-free medium on gestational Day 11-2 days before the appearance of pulmonary neuroendocrine cells (PNEC)--and the development and differentiation of PNEC from immature fetal lung epithelium was examined through immunostaining for neural cell adhesion molecule (NCAM) to establish an in vitro system to study the mechanisms involved. PNEC were present in the main bronchus after 2 days of culture. Thereafter, NCAM-positive clusters of PNEC increased and were distributed from the large bronchus to the terminal bronchiole with a proximal-to-distal wave. To elucidate the role of NCAM in the fetal development of PNEC, whole fetal lung was cultured on gestational Day 11 with an anti-NCAM antibody. This antibody slightly inhibited the growth and branching morphogenesis of the lung and disturbed the formation of PNEC clusters. NCAM may function to form clusters of PNEC known as neuroepithelial bodies. We cultured fetal lung epithelial explant at gestational Day 11 after removing mesenchyme, including nerve tissue, with dispase digestion. Immunohistochemical staining for NCAM revealed that PNEC were induced in cultured fetal epithelium without mesenchymal tissue, but basement membrane Matrigel was necessary to maintain cultured epithelium. In conclusion, PNEC derive from immature airway epithelial cells. This organ culture system, therefore, is a useful experimental model and should facilitate further investigations of the development and differentiation of PNEC. Mesenchymal and neural tissues are not always necessary for the development of PNEC, but matrix substance and/or growth factors may be required to induce or maintain PNEC.

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

    PubMed Central

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

    2013-01-01

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

  15. Control of the development of the pulmonary surfactant system in the saltwater crocodile, Crocodylus porosus.

    PubMed

    Sullivan, Lucy C; Orgeig, Sandra; Daniels, Christopher B

    2002-11-01

    Pulmonary surfactant is a mixture of lipids and proteins that controls the surface tension of the fluid lining the inner lung. Its composition is conserved among the vertebrates. Here we hypothesize that the in ovo administration of glucocorticoids and thyroid hormones during late incubation will accelerate surfactant development in the saltwater crocodile, Crocodylus porosus. We also hypothesize that the increased maturation of the type II cells in response to hormone pretreatment will result in enhanced responsiveness of the cells to surfactant secretagogues. We sampled embryos at days 60, 68, and 75 of incubation and after hatching. We administered dexamethasone (Dex), 3,5,3'-triiodothyronine (T(3)), or a combination of both hormones (Dex + T(3)), 48 and 24 h before each prehatching time point. Lavage analysis indicated that the maturation of the phospholipids (PL) in the lungs of embryonic crocodiles occurs rapidly. Only T(3) and Dex + T(3) increased total PL in lavage at embryonic day 60, but Dex, T(3), and Dex + T(3) increased PL at day 75. The saturation of the PLs was increased by T(3) and Dex + T(3) at day 68. Swimming exercise did not increase the amount or alter the saturation of the surfactant PLs. Pretreatment of embryos with Dex, T(3), or Dex + T(3) changed the secretion profiles of the isolated type II cells. Dex + T(3) increased the response of the cells to agonists at days 60 and 68. Therefore, glucocorticoids and thyroid hormones regulate surfactant maturation in the crocodile.

  16. Cytotoxic edema: mechanisms of pathological cell swelling

    PubMed Central

    Liang, Danny; Bhatta, Sergei; Gerzanich, Volodymyr; Simard, J. Marc

    2009-01-01

    Cerebral edema is caused by a variety of pathological conditions that affect the brain. It is associated with two separate pathophysiological processes with distinct molecular and physiological antecedents: those related to cytotoxic (cellular) edema of neurons and astrocytes, and those related to transcapillary flux of Na+ and other ions, water, and serum macromolecules. In this review, the authors focus exclusively on the first of these two processes. Cytotoxic edema results from unchecked or uncompensated influx of cations, mainly Na+, through cation channels. The authors review the different cation channels that have been implicated in the formation of cytotoxic edema of astrocytes and neurons in different pathological states. A better understanding of these molecular mechanisms holds the promise of improved treatments of cerebral edema and of the secondary injury produced by this pathological process. PMID:17613233

  17. Cerebral Edema in Chronic Mountain Sickness: a New Finding

    PubMed Central

    Bao, Haihua; Wang, Duoyao; Zhao, Xipeng; Wu, Youshen; Yin, Guixiu; Meng, Li; Wang, Fangfang; Ma, Lan; Hackett, Peter; Ge, Ri-Li

    2017-01-01

    We observed patients with chronic mountain sickness (CMS) in our clinic who developed progressive neurological deterioration (encephalopathy) and we wished to investigate this. We studied nine such CMS patients, and compared them to 21 CMS patients without encephalopathy, and to 15 healthy control subjects without CMS. All 45 subjects lived permanently at 3200–4000 m. Measurements at 2260 m included CMS symptom score, multi-slice CT, perfusion CT, pulse oximetry (SpO2%), and hemoglobin concentration (Hb). One patient had MRI imaging but not CT; 5 had CSF pressure measurements. CMS subjects had lower SpO2, higher Hb, higher brain blood density, lower mean cerebral blood flow (CBF), and significant cerebral circulatory delay compared to controls. The nine CMS subjects with neurological deterioration showed diffuse cerebral edema on imaging and more deranged cerebral hemodynamics. CSF pressure was elevated in those with edema. We conclude that cerebral edema, a previously unrecognized complication, may develop in CMS patients and cause encephalopathy. Contributing factors appear to be exaggerated polycythemia and hypoxemia, and lower and sluggish CBF compared to CMS patients without cerebral edema; but what triggers this complication is unknown. Recognition and treatment of this serious complication will help reduce morbidity and mortality from CMS. PMID:28233815

  18. Polymorphisms in key pulmonary inflammatory pathways and the development of acute respiratory distress syndrome

    PubMed Central

    Brown, Samuel M.; Grissom, Colin K.; Rondina, Matthew T.; Hoidal, John R.; Scholand, Mary Beth; Wolff, Roger K.; Morris, Alan H.; Paine, Robert

    2015-01-01

    Purpose/Aim Acute Respiratory Distress Syndrome (ARDS) is an important clinical and public health problem. Why some at-risk individuals develop ARDS and others do not is unclear but may be related to differences in inflammatory and cell signaling systems. The Receptor for Advanced Glycation Endproducts (RAGE) and Granulocyte-Monocyte Stimulating Factor (GM-CSF) pathways have recently been implicated in pulmonary pathophysiology; whether genetic variation within these pathways contributes to ARDS risk or outcome is unknown. Materials and Methods We studied 842 patients from three centers in Utah and 14 non-Utah ARDS Network centers. We studied patients at risk for ARDS and patients with ARDS to determine whether Single Nucleotide Polymorphisms (SNPs) in the RAGE and GM-CSF pathways were associated with development of ARDS. We studied 29 SNPs in 5 genes within the two pathways and controlled for age, sepsis as ARDS risk factor, and severity of illness, while targeting a false discovery rate of ≤5%. In a secondary analysis we evaluated associations with mortality. Results Of 842 patients, 690 had ARDS, and 152 were at-risk. Sepsis was the risk factor for ARDS in 250 (30%) patients. When controlling for age, APACHE III score, sepsis as risk factor, and multiple comparisons, no SNPs were significantly associated with ARDS. In a secondary analysis, only rs743564 in CSF2 approached significance with regard to mortality (OR 2.17, unadjusted p = 0.005, adjusted p = 0.15). Conclusions Candidate SNPs within 5 genes in the RAGE and GM-CSF pathways were not significantly associated with development of ARDS in this multi-centric cohort. PMID:25513711

  19. Hantavirus Pulmonary Syndrome

    PubMed Central

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

    1995-01-01

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

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

    PubMed Central

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

    2015-01-01

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

  1. Pulmonary Vein Thrombosis: A Recent Systematic Review

    PubMed Central

    Vishnubhotla, Priya

    2017-01-01

    The pulmonary veins (PVs) are the most proximal source of arterial thromboembolism. Pulmonary vein thrombosis (PVT) is a rare but potentially lethal disease; its incidence is unclear, as most of the literature includes case reports. It most commonly occurs as a complica­tion of malignancy, post lung surgery, or atrial fibrillation and can be idiopathic in some cases. Most patients with PVT are commonly asymptomatic or have nonspecific symptoms such as cough, hemoptysis, and dyspnea from pulmonary edema or infarction. The thrombi are typically detected using a variety of imaging modalities including transesophageal echocardiogram (TEE), computed tomography (CT) scanning, magnetic resonance imaging (MRI), or pulmonary angiog­raphy. Treatment should be determined by the obstructing pathological finding and can include antibiotic therapy, anticoagulation, thrombectomy, and/or pulmonary resection. The delay in diagnosing this medical entity can lead to complications including pulmonary infarction, pulmonary edema, right ventricular failure, allograft failure, and peripheral embolism resulting in limb ischemia, stroke, and renal infarction (RI). PMID:28265529

  2. In Vitro and In Vivo Anti-Allergic and Anti-Inflammatory Effects of eBV, a Newly Developed Derivative of Bee Venom, through Modulation of IRF3 Signaling Pathway in a Carrageenan-Induced Edema Model

    PubMed Central

    Chung, Hwa-Jin; Lee, Jinho; Shin, Joon-Shik; Kim, Me-riong; Koh, Wonil; Kim, Min-Jeong; Lee, Jae-woong; Kim, Eun Jee; Lee, In-Hee; Kim, Won Kyung; Lee, Yoon Jae; Lee, Sang Kook

    2016-01-01

    Background Bee venom (BV), a type of toxin extracted from honeybees (Apis mellifera), has been empirically and widely used to treat inflammatory diseases throughout Asia. Essential BV (eBV) was developed by removing phospholipase A2 (PLA2) and histamine to lower occurrence of allergic reaction. This study investigated the anti-allergic and anti-inflammatory activities of eBV in vitro and in vivo and its underlying mechanism of action. Methods The anti-inflammatory potential of eBV was assessed in vivo using a carrageenan-induced paw edema model. To further investigate the mechanism by which eBV exerts anti-allergic and anti-inflammatory effects, compound 48/80-stimulated RBL-2H3 cells and lipopolysaccharide (LPS)-stimulated RAW 264.7 murine macrophage cells were studied in vitro. Results Release of β-hexosaminidase and histamine was increased by eBV in a dose-dependent manner, but these levels were lower in eBV compared to original BV at the same concentration. In addition, eBV suppressed compound 48/80-induced expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in RBL-2H3 cells. eBV was also shown to suppress nitric oxide (NO) production by down-regulating mRNA expression and subsequent protein expression of inflammatory mediators in LPS-induced RAW 264.7 cells. Phosphorylation of activators and signal transducers of transcription 1/interferon regulatory factor 3 (STAT1/IRF3) was attenuated by eBV treatment. eBV significantly inhibited carrageenan-induced acute edema in vivo. Serum levels of prostaglandin E2 (PGE2), TNF-α, and IL-1β were also down-regulated by eBV. Conclusions These results demonstrate that eBV inhibits allergic and inflammatory response by reducing inflammatory mediator production via regulation of the STAT1/IRF3 signaling pathway, suggesting that eBV is a feasible candidate for regulation of allergic-inflammatory response in complementary and alternative medicine. PMID:27930719

  3. EXUBERA: pharmaceutical development of a novel product for pulmonary delivery of insulin.

    PubMed

    White, Steven; Bennett, David B; Cheu, Scot; Conley, Patrick W; Guzek, Donald B; Gray, Steven; Howard, John; Malcolmson, Richard; Parker, Joann M; Roberts, Phil; Sadrzadeh, Negar; Schumacher, Jacqueline D; Seshadri, Sangita; Sluggett, Gregory W; Stevenson, Cynthia L; Harper, Nancy J

    2005-12-01

    Development of a product for pulmonary delivery of insulin presented significant technology challenges for this first-in-class pharmaceutical product. These included developing (a) a chemically stabilized protein, (b) a dry powder formulation exhibiting required aerosol physical characteristics, (c) low-dose powder filling and packaging technology, and (d) a mechanical device for powder dispersal and reliable dosing to the patient. The insulin drug is formulated using a novel excipient combination to create a powder with a high glass transition temperature (Tg). The high Tg minimizes insulin mobility (thus reactivity), enabling ambient storage conditions. The formulation composition results in minimal hygroscopicity, where customized packaging produced product ruggedness to humidity. The formulated insulin powder is manufactured by spray-drying. This technology was further engineered to produce the desired reproducible powder characteristics with tight control over particle size and moisture content. A solution step prior to drying assures homogeneity and minimizes dependence on the physical form of the components. Novel low-dose filling and packaging technology reproducibly meters milligram quantities of microfine powder to meet stringent quality requirements for dose control. The technology for accurate, uniform, high-throughput metering of drug powders allows for automation and is scaleable for commercial operations. Finally, the mechanical device design provides powder deagglomeration and dispersion processes in a reusable dry powder inhaler with unique characteristics. The device was designed to rely on patient-generated compressed air as the energy source. A sonic discharge of air through the novel TransJector reproducibly extracts, deagglomerates, and disperses the inhalation powder. A clear holding (spacer-type) chamber allows for patient feedback via dose visualization, and separates powder dispersal from the inspiratory effort. The EXUBERA [Pfizer (New

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

    PubMed Central

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

    2015-01-01

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

  5. Oropharyngeal aspiration of bleomycin: An alternative experimental model of pulmonary fibrosis developed in Swiss mice

    PubMed Central

    Bale, Swarna; Sunkoju, Manoj; Reddy, Shiva Shankar; Swamy, Veerabhadra; Godugu, Chandraiah

    2016-01-01

    Objective: Pulmonary fibrosis (PF) is a progressive and predominantly lethal form of several interstitial lung diseases with limited current therapeutics; it is, therefore, essential to develop a simple, homogeneous, and noninvasive disease model to investigate possible anti-fibrotic approaches. The present study is designed to develop oropharyngeal aspiration (OPA) model of bleomycin (BLM)-induced PF as a simple and alternative to intratracheal (IT) administration of BLM in Swiss mice strain. Materials and Methods: Mice were divided into two groups, BLM-treated and normal control. BLM via OPA (2 IU/kg) was used to induce PF. Water for injection was used as a vehicle in control animals. Body weights were measured once in a week, and the study was continued for 21 days. At the end of the study, animals were euthanized and bronchoalveolar lavage fluid was collected and subjected to lymphocytes count, estimation of albumin and protein levels. Lung tissues were collected, and various biochemical assays (malondialdehyde, glutathione, nitric oxide, hydroxyproline) and molecular techniques including ELISA and Western blot were performed to investigate the effect of OPA-BLM. Further, histopathology and Masson's trichrome staining techniques were performed in lung sections. Results: OPA administration of BLM in Swiss mice significantly induced PF, evident from lung index and morphology. Several oxidative stress parameters and hydroxyproline assay revealed the significant (P < 0.05) induction of PF. Further results obtained from histopathology, Masson's trichrome staining, ELISA, and Western blot confirmed the significant induction of PF via OPA-BLM. Conclusion: BLM administration by OPA route in Swiss mice can be used as a simple, homogeneous, and noninvasive model of inducing PF and to investigate the effect of various anti-fibrotic agents as an alternative to IT-BLM. PMID:28066100

  6. Flt1/VEGFR1 heterozygosity causes transient embryonic edema.

    PubMed

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

    2016-06-02

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

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

    PubMed

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

    2016-03-15

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

  8. Alveolar edema fluid clearance and acute lung injury.

    PubMed

    Berthiaume, Yves; Matthay, Michael A

    2007-12-15

    Although lung-protective ventilation strategies have substantially reduced mortality of acute lung injury patients there is still a need for new therapies that can further decrease mortality in patients with acute lung injury. Studies of epithelial ion and fluid transport across the distal pulmonary epithelia have provided important new concepts regarding potential new therapies for acute lung injury. Overall, there is convincing evidence that the alveolar epithelium is not only a tight epithelial barrier that resists the movement of edema fluid into the alveoli, but it is also actively involved in the transport of ions and solutes, a process that is essential for edema fluid clearance and the resolution of acute lung injury. The objective of this article is to consider some areas of recent progress in the field of alveolar fluid transport under normal and pathologic conditions. Vectorial ion transport across the alveolar and distal airway epithelia is the primary determinant of alveolar fluid clearance. The general paradigm is that active Na(+) and Cl(-) transport drives net alveolar fluid clearance, as demonstrated in several different species, including the human lung. Although these transport processes can be impaired in severe lung injury, multiple experimental studies suggest that upregulation of Na(+) and Cl(-) transport might be an effective therapy in acute lung injury. We will review mechanisms involved in pharmacological modulation of ion transport in lung injury with a special focus on the use of beta-adrenergic agonists which has generated considerable interest and is a promising therapy for clinical acute lung injury.

  9. Idiopathic pulmonary artery aneurysm.

    PubMed

    Kotwica, Tomasz; Szumarska, Joanna; Staniszewska-Marszalek, Edyta; Mazurek, Walentyna; Kosmala, Wojciech

    2009-05-01

    Pulmonary artery aneurysm (PAA) is an uncommon lesion, which may be associated with different etiologies including congenital cardiovascular diseases, systemic vasculitis, connective tissue diseases, infections, and trauma. Idiopathic PAA is sporadically diagnosed by exclusion of concomitant major pathology. We report a case of a 56-year-old female with an idiopathic pulmonary artery dilatation identified fortuitously by echocardiography and confirmed by contrast-enhanced computed tomography. Neither significant pulmonary valve dysfunction nor pulmonary hypertension and other cardiac abnormalities which might contribute to the PAA development were found. Here, we describe echocardiographic and computed tomography findings and review the literature on PAA management.

  10. The exacerbating roles of CCAAT/enhancer-binding protein homologous protein (CHOP) in the development of bleomycin-induced pulmonary fibrosis and the preventive effects of tauroursodeoxycholic acid (TUDCA) against pulmonary fibrosis in mice.

    PubMed

    Tanaka, Yuta; Ishitsuka, Yoichi; Hayasaka, Marina; Yamada, Yusei; Miyata, Keishi; Endo, Motoyoshi; Kondo, Yuki; Moriuchi, Hiroshi; Irikura, Mitsuru; Tanaka, Ken-ichiro; Mizushima, Tohru; Oike, Yuichi; Irie, Tetsumi

    2015-09-01

    The purpose of this study was to evaluate the role of CCAAT/enhancer-binding protein homologous protein (CHOP), an important transcription factor that regulates the inflammatory reaction during the endoplasmic reticulum (ER) stress response, in the development of pulmonary fibrosis induced by bleomycin (BLM) in mice. An intratracheal injection of BLM transiently increased the expression of CHOP mRNA and protein in an early phase (days 1 and 3) in mice lungs. BLM-induced pulmonary fibrosis was significantly attenuated in Chop gene deficient (Chop KO) mice, compared with wild-type (WT) mice. Furthermore, the inflammatory reactions evaluated by protein concentration, the total number of leucocytes and neutrophils in the bronchoalveolar lavage fluid (BALF), the mRNA expression of interleukin 1b and caspase 11, and the apoptotic cell death were suppressed in Chop KO mice compared with those in WT mice. In addition, administration of tauroursodeoxycholic acid (TUDCA), a pharmacological agent that can inhibit CHOP expression, inhibited the BLM-induced pulmonary fibrosis and inflammation, and the increase in Chop mRNA expression in WT mice in a dose-dependent manner. These results suggest that the ER stress-induced transcription factor, CHOP, at least in part, plays an important role in the development of BLM-induced pulmonary fibrosis in mice, and that the inhibition of CHOP expression by a pharmacological agent, such as TUDCA, may be a promising strategy for the prevention of pulmonary fibrosis.

  11. Functional characterization of pulmonary neuroendocrine cells in lung development, injury, and tumorigenesis

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Pulmonary neuroendocrine cells (PNECs) are proposed to be the first specialized cell type to appear in the lung, but their ontogeny remains obscure. Although studies of PNECs have suggested their involvement in a number of lung functions, neither their in vivo significance nor the molecular mechanis...

  12. emPHasis-10: development of a health-related quality of life measure in pulmonary hypertension

    PubMed Central

    Yorke, Janelle; Corris, Paul; Gaine, Sean; Gibbs, J. Simon R.; Kiely, David G.; Harries, Carl; Pollock, Val; Armstrong, Iain

    2014-01-01

    The aim of this study was to develop a measure of the impact of pulmonary hypertension (PH) on health-related quality of life (HRQoL) as there is a need for a short, validated instrument that can be used in routine clinical practice. Interviews were conducted with 30 PH patients to derive 32 statements, which were presented as a semantic differential six-point scale (0–5), with contrasting adjectives at each end. This item list was completed by patients attending PH clinics across the UK and Ireland. Rasch analysis was applied to identify items fitting a uni-dimensional model. 226 patients (mean age 55.6±14 years; 70% female) with PH (82% had pulmonary arterial hypertension) completed the study questionnaires. 10 of the 32 items demonstrated fit to the Rasch model (Chi-squared 16; p>0.05) and generated the emPHasis-10 questionnaire. Test–retest (intraclass correlation coefficient 0.95, n=33) and internal consistency (Chronbach’s α=0.9) were strong. emPHasis-10 scores correlated consistently with other relevant measures and discriminated subgroups of patients stratified by World Health Organization functional class (ANOVA F=1.73; p<0.001). The emPHasis-10 is a short questionnaire for assessing HRQoL in pulmonary arterial hypertension. It has excellent measurement properties and is sensitive to differences in relevant clinical parameters. It is freely available for clinical and academic use. PMID:24232702

  13. Edema - Multiple Languages: MedlinePlus

    MedlinePlus

    ... gov/languages/edema.html Other topics A-Z A B C D E F G H I J K L M N O P Q R S T U V W XYZ List of All Topics All Edema - Multiple Languages To use the sharing features on this page, please enable JavaScript. French (français) Russian (Русский) Somali (af Soomaali) Spanish (español) ...

  14. Pulmonary artery sarcoma masquerading as saddle pulmonary embolism.

    PubMed

    Kanjanauthai, Somsupha; Kanluen, Tony; Ray, Cynthia

    2008-10-01

    Pulmonary artery sarcoma is a highly malignant tumour. Therefore, making the diagnosis is very important. We describe a case which presented with dyspnea on exertion and was initially diagnosed as saddle pulmonary embolism per CT thorax with contrast. Despite adequate anticoagulation, symptoms still progressed. Follow-up CT thorax showed an extension of the presumed filling defect or clots into the left main pulmonary artery with new lung nodules. This prompted suspicion that this may not be a pulmonary embolism. Biopsy of the lung nodule revealed high grade soft tissue sarcoma with primary source from the pulmonary artery. Our case highlights that pulmonary artery sarcoma should always be included in the differential diagnosis of pulmonary embolism especially, if symptoms still progress while on adequate anticoagulation, or any pulmonary nodules develop on follow-up exam.

  15. Pulmonary Hypertension

    PubMed Central

    Kim, John S.; McSweeney, Julia; Lee, Joanne; Ivy, Dunbar

    2015-01-01

    Objective Review the pharmacologic treatment options for pulmonary arterial hypertension (PAH) in the cardiac intensive care setting and summarize the most-recent literature supporting these therapies. Data Sources and Study Selection Literature search for prospective studies, retrospective analyses, and case reports evaluating the safety and efficacy of PAH therapies. Data Extraction Mechanisms of action and pharmacokinetics, treatment recommendations, safety considerations, and outcomes for specific medical therapies. Data Synthesis Specific targeted therapies developed for the treatment of adult patients with PAH have been applied for the benefit of children with PAH. With the exception of inhaled nitric oxide, there are no PAH medications approved for children in the US by the FDA. Unfortunately, data on treatment strategies in children with PAH are limited by the small number of randomized controlled clinical trials evaluating the safety and efficacy of specific treatments. The treatment options for PAH in children focus on endothelial-based pathways. Calcium channel blockers are recommended for use in a very small, select group of children who are responsive to vasoreactivity testing at cardiac catheterization. Phosphodiesterase type 5 inhibitor therapy is the most-commonly recommended oral treatment option in children with PAH. Prostacyclins provide adjunctive therapy for the treatment of PAH as infusions (intravenous and subcutaneous) and inhalation agents. Inhaled nitric oxide is the first line vasodilator therapy in persistent pulmonary hypertension of the newborn, and is commonly used in the treatment of PAH in the Intensive Care Unit (ICU). Endothelin receptor antagonists have been shown to improve exercise tolerance and survival in adult patients with PAH. Soluble Guanylate Cyclase Stimulators are the first drug class to be FDA approved for the treatment of chronic thromboembolic pulmonary hypertension. Conclusions Literature and data supporting the

  16. Left pulmonary artery hypoplasia presenting with unilateral hyperluscent lung.

    PubMed

    Sunavala, A J; Thacker, H P; Khann, J N

    2011-03-01

    Agenesis or hypoplasia of the right or left pulmonary arteries are among the rarest pulmonary artery anomalies with left sided anomalies being reported even less frequently. Pulmonary artery agenesis should be suspected in asymptomatic patients if a plain chest X-ray shows asymmetric lung fields, lung hypoplasia, or hyperinflation of the contralateral lung. It must be considered as a rare cause of recurrent lower respiratory tract infections in childhood and in subjects with a low threshold for or recurrent "High Altitude Pulmonary Edema".

  17. Increasing recognition of dermatomyositis with subcutaneous edema - is this a poorer prognostic marker?

    PubMed

    Tu, Jenny; McLean-Tooke, Andrew; Junckerstorff, Reimar

    2014-01-15

    Subcutaneous edema as a presenting feature of dermatomyositis has infrequently been described and is thought to signify a more aggressive disease course. We report a case involving a 38-year-old man who presented with significant subcutaneous edema involving his neck and upper body; he later developed clinical features and biopsy results consistent with dermatomyositis. Only sixteen previous cases of dermatomyositis with subcutaneous edema involving adults have been published in the literature and we aim to review disease progression, prognosis, and optimal treatment of the condition.

  18. Isosmotic media prevent edema in amphibian larvae without cardiac function.

    PubMed

    Smith, S C

    2000-03-01

    The absence of cardiac and circulatory function causes severe edema in amphibian embryos. Analyzing the roles of embryonic and larval circulation in respiration may thus be confounded by the increased diffusion distance and decreased surface area/volume ratio caused by edema. Similarly, detailed morphological analyses of embryos/larvae with defective circulatory or renal function is difficult or impossible due to the gross morphological anomalies engendered by edematous swelling. To circumvent these problems, two media have been developed which are isosmotic with the plasma of a common experimental amphibian species (Ambystoma mexicanun). These media are remarkably effective in preventing fluid accumulation in embryos and larvae lacking heart function and, when used in slightly lower concentrations, cause no apparent harm to embryos and larvae with normal circulation for periods up to 3 weeks. These media should prove useful for a variety of studies on the developmental physiology of the circulatory system and possibly also when examining the development of renal function and ionoregulation.

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

    SciTech Connect

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

    2006-03-15

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

  20. Complement component C5 deficiency reduces edema formation in murine ligation-induced acute pancreatitis.

    PubMed

    Merriam, L T; Webster, C; Joehl, R J

    1997-01-01

    The complement cascade is activated in humans and animals with acute pancreatitis. Activation of complement component C5 liberates C5a, C5a-desarg, and terminal complement complexes (TCCs) that increase capillary permeability, edema, and leukocyte chemotaxis at injured sites. Complement activation plays a major role in pathogenesis of capillary leak and edema formation in severe acute pancreatitis; however, the contribution of C5 (C5a/C5a-desarg, TCCs) has not been defined. Using He gene mutant mice lacking circulating C5, the role of C5 in ligation-induced acute pancreatitis was evaluated. We performed the following experiments: C5-sufficient (Hc1/Hc1) and C5-deficient (Hc0/Hc0) mice had bile and pancreatic ducts ligated. Sham-operated mice had ducts dissected but not ligated. Mice were killed at 4, 8, and 24 hr after bilepancreatic duct ligation. Serologic and morphologic evidences of acute pancreatitis were evaluated. Pancreatic edema was assessed using analysis of pancreatic water content, histologic edema score, and determination of wet weight ratio. After 4, 8, and 24 hr of bile-pancreatic duct ligation, hyperamylasemia and histologic changes of acute pancreatitis were observed in both C5-deficient and C5-sufficient mice. Edema developed in all mice with acute pancreatitis. However, when compared to C5-sufficient mice, mice deficient in C5 developed significantly less pancreatic edema at both 8 and 24 hr of bile-pancreatic duct ligation. This difference was not observed 4 hr after induction of acute pancreatitis. We conclude that C5 contributes to edema formation in murine ligation-induced acute pancreatitis. The presence of an early C5-independent phase, in conjunction with the observation of significant edema in mice deficient in C5, suggests there are other mediators of edema formation in this acute pancreatitis model.

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

    PubMed Central

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

    2008-01-01

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

  2. Interferon gamma +874T/A polymorphism is associated with susceptibility to active pulmonary tuberculosis development in Tunisian patients.

    PubMed

    Ben Selma, Walid; Harizi, Hedi; Bougmiza, Iheb; Hannachi, Naila; Ben Kahla, Imen; Zaieni, Radhia; Boukadida, Jalel

    2011-06-01

    Interferon gamma (IFN-γ) is a key cytokine involved mainly in the defense against intracellular pathogens such as Mycobacterium tuberculosis. Given its key role in the control of tuberculosis (TB), in the present article we have investigated a possible association between IFN-γ gene single-nucleotide polymorphism linked to high and low producer phenotypes (IFN-γ [+874T(high) → A(low)]) (rs2430561) and risk development of active TB in Tunisian patients. Genomic DNA samples were obtained from 223 patients with active TB (168 pulmonary and 55 extrapulmonary cases) and 150 healthy blood donors. Genotypes were analyzed using polymerase chain reaction-restriction fragment length polymorphism method. The +874 AA genotype (low IFN-γ producer) was significantly associated with increased risk of developing of active pulmonary TB (odds ratio [OR] = 2.18; 95% confidence intervals [CI], 1.33-3.57; P corrected for the number of genotypes [Pc] = 0.003). By contrast, the AT genotype was found to be significantly associated with resistance to pulmonary TB (OR = 0.46; 95% CI, 0.28-0.74; Pc = 0.0018) and extrapulmonary TB development (OR = 0.46; 95% CI, 0.23-0.91; Pc = 0.045). Collectively, our data showed that the IFN-γ +874T/A polymorphism is a determinant in the resistance or susceptibility to the development of active TB in the studied population.

  3. [Pulmonary strongyloidiasis].

    PubMed

    Lozada, Heiler; Daza, Jorge E

    2016-10-01

    Strongyloidiasis is an infection caused by the parasite Strongyloides stercoralis, which can be asymptomatic and means a high morbidity and mortality in immunocompromised hosts, severe malnutrition and coinfection with HTLV-1 virus. The parasite has the potential to produce and multiply internal autoinfection in humans, thus an hyperinfection can be developed. A case of pulmonary infection by this parasite is presented in this study, infection which advanced into a respiratory failure and required mechanical ventilation and hemodynamic support in an intensive care unit. The standard treatment combined with ivermectin and albendazole was provided, achieving an appropriate response.

  4. Pulmonary Hypertension and Pulmonary Vasodilators.

    PubMed

    Keller, Roberta L

    2016-03-01

    Pulmonary hypertension in the perinatal period can present acutely (persistent pulmonary hypertension of the newborn) or chronically. Clinical and echocardiographic diagnosis of acute pulmonary hypertension is well accepted but there are no broadly validated criteria for echocardiographic diagnosis of pulmonary hypertension later in the clinical course, although there are significant populations of infants with lung disease at risk for this diagnosis. Contributing cardiovascular comorbidities are common in infants with pulmonary hypertension and lung disease. It is not clear who should be treated without confirmation of pulmonary vascular disease by cardiac catheterization, with concurrent evaluation of any contributing cardiovascular comorbidities.

  5. Prediction of final infarct volume on subacute MRI by quantifying cerebral edema in ischemic stroke.

    PubMed

    Tipirneni-Sajja, Aaryani; Christensen, Soren; Straka, Matus; Inoue, Manabu; Lansberg, Maarten G; Mlynash, Michael; Bammer, Roland; Parsons, Mark W; Donnan, Geoffrey A; Davis, Stephen M; Albers, Gregory W

    2016-01-01

    Final infarct volume in stroke trials is assessed on images obtained between 30 and 90 days after stroke onset. Imaging at such delayed timepoints is problematic because patients may be lost to follow-up or die before the scan. Obtaining an early assessment of infarct volume on subacute scans avoids these limitations; however, it overestimates true infarct volume because of edema. The aim of this study was to develop a novel approach to quantify edema so that final infarct volumes can be approximated on subacute scans. We analyzed data from 20 stroke patients (median age, 75 years) who had baseline, subacute (fu5d) and late (fu90d) MRI scans. Edema displaces CSF from sulci and ventricles; therefore, edema volume was estimated as change in CSF volume between baseline and spatially coregistered fu5d ADC maps. The median (interquartile range, IQR) estimated edema volume was 13.3 (7.5-37.7) mL. The fu5d lesion volumes correlated well with fu90d infarct volumes with slope: 1.24. With edema correction, fu5d infarct volumes are in close agreement, slope: 0.97 and strongly correlated with actual fu90d volumes. The median (IQR) difference between actual and predicted infarct volumes was 0.1 (-3.0-5.7) mL. In summary, this novel technique for estimation of edema allows final infarct volume to be predicted from subacute MRI.

  6. Pulmonary Rehabilitation

    MedlinePlus

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

  7. Pulmonary Fibrosis

    MedlinePlus

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

  8. Pulmonary Embolism

    MedlinePlus

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

  9. [Pulmonary Metastasis from a Phyllodes Tumor of the Breast Developing Sixteen Years after Initial Surgery].

    PubMed

    Chang, Sung-Soo; Nakano, Takayuki; Okamoto, Taku; Takabatake, Daisuke

    2015-11-01

    We report a case of solitary pulmonary metastasis from a phyllodes tumor of the breast appearing 16 years after initial surgery. The patient was a 56-year-old woman who had undergone surgical extirpation of a left breast tumor diagnosed as phyllodes tumor (borderline malignancy) in 1998, and a right breast tumor diagnosed as fibromatosis in 2000. Sixteen years after the initial operation, she consulted our hospital because of a chest X-ray abnormality detected at a screening examination. Chest computed tomography revealed a well defined nodular shadow in the left upper lobe of the lung. Surgery was done since primary lung cancer was suspected. However, pathological diagnosis was a pulmonary metastasis from the phyllodes tumor of the left breast. Right breast tumor was also diagnosed as a metastasis from the left breast tumor by histopathological re-evaluation.

  10. Diabetic Macular Edema Pathophysiology: Vasogenic versus Inflammatory

    PubMed Central

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

    2016-01-01

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

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

    PubMed

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

    2013-01-01

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

  12. Pulmonary Hypertension

    MedlinePlus

    ... on Twitter. What Is Pulmonary Hypertension? Pulmonary hypertension (PULL-mun-ary HI-per-TEN-shun), or PH, is increased pressure in the pulmonary arteries. These arteries carry blood from your heart to your lungs to pick up oxygen. PH causes symptoms such as shortness of ...

  13. Onset of alveolar recirculation in the developing lungs and its consequence on nanoparticle deposition in the pulmonary acinus

    PubMed Central

    Henry, Frank S.

    2015-01-01

    The structure of the gas exchange region of the human lung (the pulmonary acinus) undergoes profound change in the first few years of life. In this paper, we investigate numerically how the change in alveolar shape with time affects the rate of nanoparticle deposition deep in the lung during postnatal development. As human infant data is unavailable, we use a rat model of lung development. The process of postnatal lung development in the rat is remarkably similar to that of the human, and the structure of the rat acinus is indistinguishable from that of the human acinus. The current numerical predictions support our group's recent in vivo findings, which were also obtained by using growing rat lung models, that nanoparticle deposition in infants is strongly affected by the change in the structure of the pulmonary acinus. In humans, this major structural change occurs over the first 2 yr of life. Our current predictions would suggest that human infants at the age of ∼2 yr might be most at risk to the harmful effects of air pollution. Our results also suggest that dose estimates for inhalation therapies using nanoparticles, based on fully developed adult lungs with simple body weight scaling, are likely to overestimate deposition by up to 55% for newborns and underestimate deposition by up to 17% for 2-yr-old infants. PMID:26494453

  14. Role of vasopressin and aldosterone in pulmonary arterial hypertension: A pilot study.

    PubMed

    Bansal, Shweta; Badesch, David; Bull, Todd; Schrier, Robert W

    2009-09-01

    Much has been learned about the pathophysiological state that underlies the development of increased total body volume and edema in left ventricular failure. Very little, however, is known about the mechanism underlying systemic hypervolemia in patients with isolated right ventricular dysfunction. In this manuscript, we describe our randomized clinical trial to assess the relationship between severity of pulmonary arterial hypertension and neurohormonal activation, total plasma volume and renal function. We assess the role of aldosterone and vasopressin in volume retention in patients with pulmonary arterial hypertension with right ventricular failure. As understanding of the pathogenesis of left ventricular failure has been associated with improved therapies, the better understanding of the mechanisms of isolated right ventricular cardiac failure will also lead to improved patient care.

  15. Role of vasopressin and aldosterone in pulmonary arterial hypertension: A pilot study

    PubMed Central

    Bansal, Shweta; Badesch, David; Bull, Todd; Schrier, Robert W.

    2009-01-01

    Much has been learned about the pathophysiological state that underlies the development of increased total body volume and edema in left ventricular failure. Very little, however, is known about the mechanism underlying systemic hypervolemia in patients with isolated right ventricular dysfunction. In this manuscript, we describe our randomized clinical trial to assess the relationship between severity of pulmonary arterial hypertension and neurohormonal activation, total plasma volume and renal function. We assess the role of aldosterone and vasopressin in volume retention in patients with pulmonary arterial hypertension with right ventricular failure. As understanding of the pathogenesis of left ventricular failure has been associated with improved therapies, the better understanding of the mechanisms of isolated right ventricular cardiac failure will also lead to improved patient care. PMID:19375522

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

    PubMed Central

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

    2015-01-01

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

  17. Mechanisms of Astrocyte-Mediated Cerebral Edema

    PubMed Central

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

    2014-01-01

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

  18. Potential and development of inhaled RNAi therapeutics for the treatment of pulmonary tuberculosis.

    PubMed

    Man, Dede K W; Chow, Michael Y T; Casettari, Luca; Gonzalez-Juarrero, Mercedes; Lam, Jenny K W

    2016-07-01

    Tuberculosis (TB), caused by the infection of Mycobacterium tuberculosis (Mtb), continues to pose a serious threat to public health, and the situation is worsening with the rapid emergence of multidrug resistant (MDR) TB. Current TB regimens require long duration of treatment, and their toxic side effects often lead to poor adherence and low success rates. There is an urgent need for shorter and more effective treatment for TB. In recent years, RNA interference (RNAi) has become a powerful tool for studying gene function by silencing the target genes. The survival of Mtb in host macrophages involves the attenuation of the antimicrobial responses mounted by the host cells. RNAi technology has helped to improve our understanding of how these bacilli interferes with the bactericidal effect and host immunity during TB infection. It has been suggested that the host-directed intervention by modulation of host pathways can be employed as a novel and effective therapy against TB. This therapeutic approach could be achieved by RNAi, which holds enormous potential beyond a laboratory to the clinic. RNAi therapy targeting TB is being investigated for enhancing host antibacterial capacity or improving drug efficacy on drug resistance strains while minimizing the associated adverse effects. One of the key challenges of RNAi therapeutics arises from the delivery of the RNAi molecules into the target cells, and inhalation could serve as a direct administration route for the treatment of pulmonary TB in a non-invasive manner. However, there are still major obstacles that need to be overcome. This review focuses on the RNAi candidates that are currently explored for the treatment of TB and discusses the major barriers of pulmonary RNAi delivery. From this, we hope to stimulate further studies of local RNAi therapeutics for pulmonary TB treatment.

  19. Massive ovarian edema, due to adjacent appendicitis.

    PubMed

    Callen, Andrew L; Illangasekare, Tushani; Poder, Liina

    2017-04-01

    Massive ovarian edema is a benign clinical entity, the imaging findings of which can mimic an adnexal mass or ovarian torsion. In the setting of acute abdominal pain, identifying massive ovarian edema is a key in avoiding potential fertility-threatening surgery in young women. In addition, it is important to consider other contributing pathology when ovarian edema is secondary to another process. We present a case of a young woman presenting with subacute abdominal pain, whose initial workup revealed marked enlarged right ovary. Further imaging, diagnostic tests, and eventually diagnostic laparoscopy revealed that the ovarian enlargement was secondary to subacute appendicitis, rather than a primary adnexal process. We review the classic ultrasound and MRI imaging findings and pitfalls that relate to this diagnosis.

  20. External beam radiotherapy boosts to reduce the impact caused by edema in prostate permanent seed implants

    NASA Astrophysics Data System (ADS)

    Yue, Ning; Mori, Jonathan; Nath, Ravinder; Heron, Dwight E.; Saiful Huq, M.

    2006-05-01

    In prostate permanent seed implants, it has been shown that edema caused by the surgical procedure decreases dose coverage and hence may reduce treatment efficacy. This reduction in treatment efficacy has been characterized by an increase in tumour cell survival, and biomathematical models have been developed to calculate the tumour cell survival increases in seed implanted prostates of different edema magnitudes and durations. External beam boosts can be utilized to neutralize the negative impact of edema so that originally desired treatment efficacy can be achieved. In this study, a linear quadratic model is used to determine fractionation sizes of the external beam boosts for both 125I and 103Pd seed implants. Calculations were performed for prostates of different edema magnitudes and durations, and for tumour cells of different repair rates and repopulation rates.

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

    SciTech Connect

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

    2011-04-15

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

  2. Efficacy of moclobemide in a rat model of neurotoxicant-induced edema.

    PubMed

    Girard, Philippe; Verniers, Danielle; Pansart, Yannick; Gillardin, Jean-Marie

    2007-05-01

    The potent antidepressant effect of moclobemide, a selective and reversible type A monoamine oxidase (MAO) inhibitor, is clinically established. In view of the ongoing debate on the neuroprotective properties of MAO inhibitors, the present study was undertaken to further define the protective effect of moclobemide in a rat model of neurotoxicant-induced edema. In this model, daily oral triethyltin (TET) administration for 5 consecutive days strongly perturbed the rat behaviour and induced a cerebral edema at the 5th day. Oral coadministration of moclobemide (2 x 100 mg.kg-1.day-1) with TET blocked the development of brain edema and the increase in the cerebral chloride content induced by TET. Moreover, moclobemide reduced the increase in the cerebral sodium content and attenuated the neurological deficit. In conclusion, moclobemide possesses potent protective properties in this rat model of cerebral edema, suggesting potential clinical utility as a neuroprotectant.

  3. Edema, anemia, hypoproteinemia, and acrodermatitis enteropathica: an uncommon initial presentation of cystic fibrosis.

    PubMed

    Muñiz, Antonio E; Bartle, Sam; Foster, Robin

    2004-02-01

    Cystic fibrosis is a genetic disorder characterized by chronic obstructive pulmonary disease, pancreatic exocrine deficiency, and abnormally high sweat electrolyte concentrations. Less frequently, the presenting features in infants may include edema, anemia, hypoproteinemia, and acrodermatitis enteropathica. Liver involvement may produce hepatomegaly and mild elevation of transaminases. This clinical symptom usually presents within the first 6 months of life and is associated with a high morbidity and mortality. Early recognition and institution of appropriate nutritional supplementation and pancreatic enzymes is essential to improve outcome. Since the sweat test may be falsely negative, emergency physicians must maintain a high index of suspicion to make the diagnosis of cystic fibrosis in an infant who presents with edema, anemia, hypoproteinemia, and acrodermatitis enteropathica.

  4. Development and analysis of a finite element model to simulate pulmonary emphysema in CT imaging.

    PubMed

    Diciotti, Stefano; Nobis, Alessandro; Ciulli, Stefano; Landini, Nicholas; Mascalchi, Mario; Sverzellati, Nicola; Innocenti, Bernardo

    2015-01-01

    In CT imaging, pulmonary emphysema appears as lung regions with Low-Attenuation Areas (LAA). In this study we propose a finite element (FE) model of lung parenchyma, based on a 2-D grid of beam elements, which simulates pulmonary emphysema related to smoking in CT imaging. Simulated LAA images were generated through space sampling of the model output. We employed two measurements of emphysema extent: Relative Area (RA) and the exponent D of the cumulative distribution function of LAA clusters size. The model has been used to compare RA and D computed on the simulated LAA images with those computed on the models output. Different mesh element sizes and various model parameters, simulating different physiological/pathological conditions, have been considered and analyzed. A proper mesh element size has been determined as the best trade-off between reliable results and reasonable computational cost. Both RA and D computed on simulated LAA images were underestimated with respect to those calculated on the models output. Such underestimations were larger for RA (≈ -44 ÷ -26%) as compared to those for D (≈ -16 ÷ -2%). Our FE model could be useful to generate standard test images and to design realistic physical phantoms of LAA images for the assessment of the accuracy of descriptors for quantifying emphysema in CT imaging.

  5. Development of novel drug-eluting biodegradable nano-fiber for prevention of postoperative pulmonary venous obstruction.

    PubMed

    Mutsuga, Masato; Narita, Yuji; Yamawaki, Aika; Satake, Makoto; Kaneko, Hiroaki; Usui, Akihiko; Ueda, Yuichi

    2009-04-01

    Pulmonary venous obstruction (PVO) after correction of total anomalous pulmonary venous connection (TAPVC) frequently occurs due to intimal-hyperplasia and the required re-operation. We have developed a novel sustained-release drug delivery system, using Tacrolimus-eluting biodegradable nano-fiber (TEBN). It consists of nano-scale fiber composed of biodegradable polymer and Tacrolimus. This study evaluated the effects of TEBN for prevention of venous anastomotic stricture in a rat model to apply to PVO operation. Tacrolimus was incorporated into poly (L-lactide-co-glycolide). The venous stricture model was made by rat inferior vena cava anastomosis. The IVC anastomosis was covered with TEBN with 1.0 wt% Tacrolimus (n=12) or without TEBN as a control (n=12), and evaluated histologically at 1, 2, and 4 weeks after operation. The ratio of intimal area was significantly reduced in the TEBN group compared with the control group (ratio; 1 week: 0.43+/-0.26 vs. 0.07+/-0.04, P=0.04, 2 weeks: 0.39+/-0.19 vs. 0.05+/-0.02, P=0.01, 4 weeks: 0.31+/-0.15 vs. 0.09+/-0.04, P=0.03, control vs. TEBN, respectively). Histological findings showed endothelialization along the inner surface of the vein even in TEBN. The TEBN reduced intimal hyperplasia and preserved endothelialization even in a venous stricture. These results suggested that this strategy might be useful for prevention of recurrent PVO after TAPVC correction.

  6. Chronic thromboembolic pulmonary hypertension: time for research in pathophysiology to catch up with developments in treatment

    PubMed Central

    Toshner*, Mark

    2014-01-01

    The modern treatment era in chronic thromboembolic disease has seen significant advances in both surgical and medical treatment. One such treatment, the pulmonary endarterectomy (where established chronic organized thrombus is removed), has dramatically affected morbidity and mortality. These advances have outstripped basic research into the causes and pathophysiology of disease, which remain largely poorly understood. In this review, we will set out to explain some of the historical reasons for this, including the difficulties inherent in human studies and the lack of good animal models. We will review some of the recent advances in pathophysiology from registries and translational research, and we will summarize the treatment options, with some discussion of very recently published work, including medical and surgical treatments, both traditional and more experimental work in non-invasive techniques. PMID:24991415

  7. The effect of prostaglandin inhibition on the development of pulmonary pathology associated with dead Dirofilaria immitis.

    PubMed

    Tarish, J H; Atwell, R B

    1993-09-01

    Flunixin meglumine was used to examine the effect of prostaglandin inhibition on the pathogenesis of Dirofilaria immitis in the pulmonary arteries of dogs. Immunopathological reactions to dead filariae were monitored by light and transmission electron microscopy and serology. Lung lesions in prostaglandin-inhibited dogs exposed to dead filariae were enhanced compared to control dogs. This was associated with the persistence of parasitic antigen in lung tissue and in the blood. Serology demonstrated that after insertion of D. immitis in treated dogs, antibody levels did not change, while immune complex and antigen levels increased. These results indicate that prostaglandin may have a protective effect on the way the lung reacts to dead D. immitis, and that altered dynamics of the antigen processing may well contribute to the associated lung lesions.

  8. Dysphagia Caused by Chronic Laryngeal Edema.

    PubMed

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

    2015-10-01

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

  9. CARDIOVASCULAR AND BLOOD COAGULATION EFFECTS OF PULMONARY ZINC EXPOSURE

    EPA Science Inventory

    Cardiovascular damage induced by pulmonary exposure to environmental chemicals can result from direct action or, secondarily, from pulmonary injury. We have developed a rat model of pulmonary exposure to zinc to demonstrate cardiac, coagulative, and fibrinolytic alterations. Mal...

  10. Vascular Remodeling in Pulmonary Hypertension

    PubMed Central

    Shimoda, Larissa A; Laurie, Steven S.

    2013-01-01

    Pulmonary hypertension is a complex, progressive condition arising from a variety of genetic and pathogenic causes. Patients present with a spectrum of histologic and pathophysiological features, likely reflecting the diversity in underlying pathogenesis. It is widely recognized that structural alterations in the vascular wall contribute to all forms of pulmonary hypertension. Features characteristic of the remodeled vasculature in patients with pulmonary hypertension include increased stiffening of the elastic proximal pulmonary arteries, thickening of the intimal and/or medial layer of muscular arteries, development of vaso-occlusive lesions and the appearance of cells expressing smooth muscle specific markers in normally non-muscular small diameter vessels, resulting from proliferation and migration of pulmonary arterial smooth muscle cells and cellular trans-differentiation. The development of several animal models of pulmonary hypertension has provided the means to explore the mechanistic underpinnings of pulmonary vascular remodeling, although none of the experimental models currently used entirely replicates the pulmonary arterial hypertension observed in patients. Herein, we provide an overview of the histological abnormalities observed in humans with pulmonary hypertension and in preclinical models and discuss insights gained regarding several key signaling pathways contributing to the remodeling process. In particular, we will focus on the roles of ion homeostasis, endothelin-1, serotonin, bone morphogenetic proteins, Rho kinase and hypoxia-inducible factor 1 in pulmonary arterial smooth muscle and endothelial cells, highlighting areas of cross-talk between these pathways and potentials for therapeutic targeting. PMID:23334338

  11. Recent technological and application developments in computed tomography and magnetic resonance imaging for improved pulmonary nodule detection and lung cancer staging

    PubMed Central

    Sieren, Jessica C.; Ohno, Yoshiharu; Koyama, Hisanobu; Sugimura, Kazuro; McLennan, Geoffrey

    2010-01-01

    This review compares the emerging technologies and approaches in the application of magnetic resonance (MR) and computed tomography (CT) imaging for the assessment of pulmonary nodules and staging of malignant findings. Included in this review is a brief definition of pulmonary nodules and an introduction to the challenges faced. We have highlighted the current status of both MR and CT for the early detection of lung nodules. Developments are detailed in this review for the management of pulmonary nodules using advanced imaging, including; dynamic imaging studies, dual energy CT, computer aided detection and diagnosis, and imaging assisted nodule biopsy approaches which have improved lung nodule detection and diagnosis rates. Recent advancements linking in-vivo imaging to corresponding histological pathology are also highlighted. In-vivo imaging plays a pivotal role in the clinical staging of pulmonary nodules through TNM assessment. While CT and PET/CT are currently the most commonly clinically employed modalities for pulmonary nodule staging, studies are presented which highlight the augmentative potential of MR. PMID:21105140

  12. Massive edema of the ovary associated with androgenic manifestations.

    PubMed

    Siller, B S; Gelder, M S; Alvarez, R D; Partridge, E E

    1995-11-01

    Massive ovarian edema is a rare tumor-like condition of the ovary characterized by marked enlargement of one or both ovaries due to marked accumulation of edema fluid in the ovarian stroma. This paper reviews the literature on massive ovarian edema and presents a case associated with androgenic manifestations.

  13. Pulmonary Embolism

    MedlinePlus

    ... for the Public » Health Topics » Pulmonary Embolism Explore Pulmonary Embolism What Is... Other Names Causes Who Is at Risk Signs & Symptoms Diagnosis Treatments Prevention Living With Clinical Trials Links Related Topics Arrhythmia Deep Vein Thrombosis Lung VQ Scan Overweight and Obesity Send a ...

  14. The role of transforming growth factors beta1 and beta3 in pre- and post-natal pulmonary surfactant development.

    PubMed

    Qiu, Lin; Deng, Chun; Fu, Zhou; Guo, Chunbao

    2011-03-01

    The aim was to explore the pulmonary surfactant regulatory effect of TGF-β1 and TGF-β3 during pre- and post-natal porcine development. Pigs on embryonic day 99 (E94) (term = 114 days) and 1-h (D0) and 15-day (D20) neonates were killed to obtain whole lungs. DSPC (disaturated phosphatidylcholine) was separated from other phospholipids, and chemical methods were used to determine the amounts of DSPC, TPL (total phospholipids) and TP (total protein) in BALF (bronchoalveolar lavage fluid). TPL was elevated at E94. DSPC in TPL was significantly higher in the D20 group than in the E94 group. Reductions in TP correlated with developmental age. The levels of TGF-β1 and TGF-β3 mRNA were determined by RT (reverse transcription)-PCR and Northern blot. The expression of TGF-β1 mRNA was low at E94, increased at D0 and then decreased at D20. The expression of TGF-β3 was high at E94, reduced at D0, and then elevated at D20. We further examined the effect of exogenously administered TGF-1 on the expression of SPs (surfactant proteins) and cytidine triphosphorylate: CCT (phosphocholine cytidylyltransferase) activity in porcine fetal lung cells cultured for 5 days. The results indicated that TGF-β1 inhibited the expression of all three SPs (SP-A, SP-B and SP-C) and CCT activity, but did not alter the expression level of SP-D transcripts. We conclude that TGF-1 inhibits the expression of surfactant components. The alterations of TGF-β3 seem to partly explain the pulmonary surfactant changes observed in development, but this result needs further investigation.

  15. When a pulmonary embolism is not a pulmonary embolism: a rare case of primary pulmonary leiomyosarcoma

    PubMed Central

    Muganlinskaya, Nargiz; Guzman, Amanda; Dahagam, Chanukya; Selinger, Stephen R.

    2015-01-01

    Arterial leiomyosarcomas account for up to 21% of vascular leiomyosarcomas, with 56% of arterial leiomyosarcomas occurring in the pulmonary artery. While isolated cases of primary pulmonary artery leiomyosarcoma document survival up to 36 months after treatment, these uncommon, aggressive tumors are highly lethal, with 1-year survival estimated at 20% from the onset of symptoms. We discuss a rare case of a pulmonary artery leiomyosarcoma that was originally diagnosed as a pulmonary embolism (PE). A 72-year-old Caucasian female was initially diagnosed with ‘saddle pulmonary embolism’ based on computerized tomographic angiography of the chest 2 months prior to admission and placed on anticoagulation. Dyspnea escalated, and serial computed tomography scans showed cardiomegaly with pulmonary emboli involving the right and left main pulmonary arteries with extension into the right and left upper and lower lobe branches. An echocardiogram on admission showed severe pulmonary hypertension with a pulmonary artery pressure of 82.9 mm Hg, and a severely enlarged right ventricle. Respiratory distress and multiorgan failure developed and, unfortunately, the patient expired. Autopsy showed a lobulated, yellow mass throughout the main pulmonary arteries measuring 13 cm in diameter. The mass extended into the parenchyma of the right upper lobe. On microscopy, the mass was consistent with a high-grade primary pulmonary artery leiomyosarcoma. Median survival of patients with primary pulmonary artery leiomyosarcoma without surgery is one and a half months, and mortality is usually due to right-sided heart failure. Pulmonary artery leiomyosarcoma is a rare but highly lethal disease commonly mistaken for PE. Thus, we recommend clinicians to suspect this malignancy when anticoagulation fails to relieve initial symptoms. In conclusion, early detection and suspicion of pulmonary artery leiomyosarcoma should be considered in patients refractory to anticoagulation, prompting initiation

  16. Inflammatory cytokines in pulmonary hypertension

    PubMed Central

    2014-01-01

    Pulmonary hypertension is an “umbrella term” used for a spectrum of entities resulting in an elevation of the pulmonary arterial pressure. Clinical symptoms include dyspnea and fatigue which in the absence of adequate therapeutic intervention may lead to progressive right heart failure and death. The pathogenesis of pulmonary hypertension is characterized by three major processes including vasoconstriction, vascular remodeling and microthrombotic events. In addition accumulating evidence point to a cytokine driven inflammatory process as a major contributor to the development of pulmonary hypertension. This review summarizes the latest clinical and experimental developments in inflammation associated with pulmonary hypertension with special focus on Interleukin-6, and its role in vascular remodeling in pulmonary hypertension. PMID:24739042

  17. Pulmonary blastomycosis.

    PubMed

    Bariola, J Ryan; Vyas, Keyur S

    2011-12-01

    Blastomyces dermatitidis is acquired in almost all cases via inhalation, and pulmonary disease is the most frequent clinical manifestation of blastomycosis. Pulmonary disease can range from asymptomatic infection to rapidly severe and fatal disease. Most cases will present as pneumonia, either acute or chronic, or as a lung mass. In rare cases pulmonary blastomycosis is associated with the acute respiratory distress syndrome. Blastomycosis can present as isolated pulmonary disease or along with coexisting extrapulmonary disease that usually will involve the skin, bony structures, genitourinary tract, or central nervous system. Diagnosis is largely based on isolation of the organism via culture or visualization of the organism in clinical specimens. Detection of urinary Blastomyces antigen is a recent addition to diagnostic options. Itraconazole is the drug of choice for most forms of the disease; amphotericin B is reserved for the more severe forms. Newer azoles such as voriconazole and posaconazole have a limited role in the treatment of pulmonary blastomycosis.

  18. Design, development, and analysis of a surrogate for pulmonary injury prediction.

    PubMed

    Danelson, Kerry A; Gayzik, F Scott; Stern, Amber Rath; Hoth, J Jason; Stitzel, Joel D

    2011-10-01

    Current anthropomorphic test devices (ATDs) measure chest acceleration and deflection to assess risk of injury to the thorax. This study presents a lung surrogate prototype designed to expand the injury assessment capabilities of ATDs to include a risk measure for pulmonary contusion (PC). The surrogate augments these existing measures by providing pressure data specific to the lung and its lobes. The prototype was created from a rendering of a 50th percentile male lung inflated to normal inspiration, obtained from clinical CT data. Surrogate size, lobe volume, and airway cross sections were selected to match the morphology of the lung. Elastomeric urethane was molded via rapid prototyping to create a functional prototype. Pressure sensors in each of the five terminal airways independently monitored pressure traces in the lobes during impacts to the surrogate. Software was created to analyze the surrogate impact pressure data, determine the lobe with the greatest pressure rise for a particular impact, and estimate the initial speed of surface deformation. Calibration testing indicates an approximately linear relationship between peak lobe pressure and surface impact speed. No type I or II errors were demonstrated during lobe detection testing. During repeatability testing, the standard deviation was between 2 and 4% of the mean peak pressure. Ongoing research will focus on correlating surrogate data, pressure pulses, or surface deformation, to risk functions for PC.

  19. Corneal edema induced by cold in trigeminal nerve palsy

    SciTech Connect

    Thorgaard, G.L.; Holland, E.J.; Krachmer, J.H.

    1987-05-15

    We examined a 34-year-old man who complained of decreased visual acuity in the right eye when exposed to cold environmental temperatures. Although examination at room temperature was unremarkable, he developed prominent unilateral corneal edema of the right eye when placed in a cold room at 4 C. Corneal thickness increased from 525 to 789 microns in the affected eye. Further examination disclosed a right-sided trigeminal nerve palsy. He was eventually found to have a 3 X 2-cm tentorial ridge meningioma on the right.

  20. Pulmonary hypertension in congenital shunts.

    PubMed

    Beghetti, Maurice; Tissot, Cecile

    2010-10-01

    Pulmonary arterial hypertension frequently arises in patients with congenital heart disease. The vast majority present with congenital cardiac shunts. Initially these may manifest as left-to-right (i.e. systemic-to-pulmonary) shunts. The natural history of disease progression involves vascular remodeling and dysfunction that lead to increased pulmonary vascular resistance and, finally, to the development of Eisenmenger's syndrome, which is the most advanced form. The anatomical, pathological and structural abnormalities occurring in the pulmonary circulation of these patients are, to some extent, similar to those observed in other forms of pulmonary arterial hypertension. This understanding has recently led to significant changes in the management of Eisenmenger's syndrome, with the introduction of treatment specifically targeting pulmonary vascular disease. Early closure of the cardiac shunt remains the best way of preventing pulmonary vascular lesions. However, it is still not clear which preoperative parameters predict safe and successful repair, though hemodynamic evaluation is still routinely used for assessment. Postoperative pulmonary hypertension, both in the immediate period after surgical repair and during long-term follow-up, remains a real therapeutic challenge. The clinical situation of a single ventricle with Fontan circulation also presents difficulties when pulmonary vascular lesions are present. This article reviews pulmonary hypertension associated with congenital shunts and discusses a number of the specific problems encountered.

  1. Heme oxygenase-1-mediated autophagy protects against pulmonary endothelial cell death and development of emphysema in cadmium-treated mice.

    PubMed

    Surolia, Ranu; Karki, Suman; Kim, Hyunki; Yu, Zhihong; Kulkarni, Tejaswini; Mirov, Sergey B; Carter, A Brent; Rowe, Steven M; Matalon, Sadis; Thannickal, Victor J; Agarwal, Anupam; Antony, Veena B

    2015-08-01

    Pulmonary exposure to cadmium, a major component of cigarette smoke, has a dramatic impact on lung function and the development of emphysema. Cigarette smoke exposure induces heme oxygenase-1 (HO-1), a cytoprotective enzyme. In this study, we employed a truncated mouse model of emphysema by intratracheal instillation of cadmium (CdCl2) solution (0.025% per 1 mg/kg body wt) in HO-1(+/+), HO-1(-/-), and overexpressing humanized HO-1 bacterial artificial chromosome (hHO-1BAC) mice. We evaluated the role of HO-1 in cadmium-induced emphysema in mice by analyzing histopathology, micro-computed tomography scans, and lung function tests. CdCl2-exposed HO-1(-/-) mice exhibited more severe emphysema compared with HO-1(+/+) or hHO-1BAC mice. Loss of pulmonary endothelial cells (PECs) from the alveolar capillary membrane is recognized to be a target in emphysema. PECs from HO-1(+/+), HO-1(-/-), and hHO-1BAC were employed to define the underlying molecular mechanism for the protection from emphysema by HO-1. Electron microscopy, expression of autophagic markers (microtubule-associated protein 1B-light chain 3 II, autophagy protein 5, and Beclin1) and apoptotic marker (cleaved caspase 3) suggested induction of autophagy and apoptosis in PECs after CdCl2 treatment. CdCl2-treated HO-1(-/-) PECs exhibited downregulation of autophagic markers and significantly increased cleaved caspase 3 expression and activity (∼4-fold higher). Moreover, hHO-1BAC PECs demonstrated upregulated autophagy and absence of cleaved caspase 3 expression or activity. Pretreatment of HO-1(+/+) PECs with rapamycin induced autophagy and resulted in reduced cell death upon cadmium treatment. Induction of autophagy following CdCl2 treatment was found to be protective from apoptotic cell death. HO-1 induced protective autophagy in PECs and mitigated cadmium-induced emphysema.

  2. The LONFLIT4-VENORUTON study: a randomized trial prophylaxis of flight-edema in normal subjects.

    PubMed

    Belcaro, Gianni; Cesarone, Maria Rosaria; Nicolaides, Andrew N; Geroulakos, George; Acerbi, Giovanni; Candiani, Carlo; Griffin, Maura; Bavera, Peter; Dugall, Mark; Brandolini, Rossella; Di Renzo, Andrea; Ricci, Andrea; Ippolito, Edmondo; Winford, Michelle; Golden, Gerard

    2003-01-01

    This study evaluated the protective effects of Venoruton on the development of flight edema in normal subjects travelling in economy in long-haul flights (8-9 hours). Edema is a relevant aspect of long-haul flights affecting both venous patients and normal subjects. Edema and flight microangiopathy were studied in a group of 164 subjects randomized (after informed consent) into two groups to evaluate prophylaxis in 8- to 9-hour flights. The treatment group received Venoruton (hydroxyethyl rutosides) 1 g twice daily for 3 days (2 days before the flight and the day of the flight). The control group received comparable placebo. Edema was evaluated with a composite edema score based on the edema tester, on the measurements of ankle circumference, volume measurements, subjective swelling, and on a discomfort score. Items 1, 4, and 5 are based on an analogue scale line (1 to 10) directly defined by the subjects before and after the flights. Of the included subjects, 151 completed the study. Dropouts were due to poor compliance, travelling, or connection problems. Age and gender distribution were comparable in the two groups as were risk factor distributions. The level of edema at inclusion was comparable in the two groups of subjects. After the flight there was an average score of 6.7 (SD 1.7) in the control group, while in the Venoruton group the score was on average 3 (SD 1.1) (p < 0.05). In the control group 77% of the subjects had an evident increase in ankle circumference and volume, which was clearly visible at inspection and associated with discomfort. In the Venoruton group, edema was clearly present only in 8% of subjects (associated with discomfort rated between 3 and 6 on the analogue scale line) and it was mild, not associated with symptoms. Therefore the control of flight edema with Venoruton was clear both considering parametric data (circumference and volume) and non-parametric (analogue scale lines) measurements. The combined evaluation of the edema score

  3. Brain Abscesses Associated with Asymptomatic Pulmonary Arteriovenous Fistulas

    PubMed Central

    Nam, Taek-Kyun; Park, Yong-sook; Kwon, Jeong-taik

    2017-01-01

    Brain abscess commonly occurs secondary to an adjacent infection (mostly in the middle ear or paranasal sinuses) or due to hematogenous spread from a distant infection or trauma. Pulmonary arteriovenous fistulas (AVFs) are abnormal direct communications between the pulmonary artery and vein. We present two cases of brain abscess associated with asymptomatic pulmonary AVF. A 65-year-old woman was admitted with a headache and cognitive impairment that aggravated 10 days prior. An magnetic resonance (MR) imaging revealed a brain abscess with severe edema in the right frontal lobe. We performed a craniotomy and abscess removal. Bacteriological culture proved negative. Her chest computed tomography (CT) showed multiple AVFs. Therapeutic embolization of multiple pulmonary AVFs was performed and antibiotics were administered for 8 weeks. A 45-year-old woman presented with a 7-day history of progressive left hemiparesis. She had no remarkable past medical history or family history. On admission, blood examination showed a white blood cell count of 6290 cells/uL and a high sensitive C-reactive protein of 2.62 mg/L. CT and MR imaging with MR spectroscopy revealed an enhancing lesion involving the right motor and sensory cortex with marked perilesional edema that suggested a brain abscess. A chest CT revealed a pulmonary AVF in the right upper lung. The pulmonary AVF was obliterated with embolization. There needs to consider pulmonary AVF as an etiology of cerebral abscess when routine investigations fail to detect a source. PMID:28061502

  4. Smart respiratory monitoring: clinical development and validation of the IPI™ (Integrated Pulmonary Index) algorithm.

    PubMed

    Ronen, M; Weissbrod, R; Overdyk, F J; Ajizian, S

    2017-04-01

    Continuous electronic monitoring of patient respiratory status frequently includes PetCO2 (end tidal CO2), RR (respiration rate), SpO2 (arterial oxygen saturation), and PR (pulse rate). Interpreting and integrating these vital signs as numbers or waveforms is routinely done by anesthesiologists and intensivists but is challenging for clinicians in low acuity areas such as medical wards, where continuous electronic respiratory monitoring is becoming more common place. We describe a heuristic algorithm that simplifies the interpretation of these four parameters in assessing a patient's respiratory status, the Integrated Pulmonary Index (IPI). The IPI algorithm is a mathematical model combining SpO2, RR, PR, and PetCO2 into a single value between 1 and 10 that summarizes the adequacy of ventilation and oxygenation at that point in time. The algorithm was designed using a fuzzy logic inference model to incorporate expert clinical opinions. The algorithm was verified by comparison to experts' scoring of clinical scenarios. The validity of the index was tested in a retrospective analysis of continuous SpO2, RR, PR, and PetCO2 readings obtained from 523 patients in a variety of clinical settings. IPI correlated well with expert interpretation of the continuous respiratory data (R = 0.83, p < 0.001), with agreement of -0.5 ± 1.4. Receiver operating curves analysis resulted in high levels of sensitivity (ranging from 0.83 to 1.00), and corresponding specificity (ranging from 0.96 to 0.74), based on IPI thresholds 3-6. The IPI reliably interpreted the respiratory status of patients in multiple areas of care using off-line continuous respiratory data. Further prospective studies are required to evaluate IPI in real time in clinical settings.

  5. HEPES prevents edema in rat brain slices.

    PubMed

    MacGregor, D G; Chesler, M; Rice, M E

    2001-05-11

    Brain slices gain water when maintained in bicarbonate-buffered artificial cerebro-spinal fluid (ACSF) at 35 degrees C. We previously showed that this edema is linked to glutamate receptor activation and oxidative stress. An additional factor that may contribute to swelling is acidosis, which arises from high CO2 tension in brain slices. To examine the role of acidosis in slice edema, we added N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) to osmotically balanced ACSF (HEPES-ACSF), thereby increasing buffering capacity beyond that provided by bicarbonate/CO2. Water gain was markedly inhibited in HEPES-ACSF. After 3 h incubation in HEPES-ACSF at 35 degrees C, water gain was limited to that of fresh slices after 1 h recovery in ACSF at room temperature. The effect of HEPES in decreasing slice water gain was concentration dependent from 0.3 to 20 mM. The inhibition of water gain by HEPES suggests that tissue acidosis is a contributing factor in brain slice edema.

  6. Assessing local tissue edema in postmastectomy lymphedema.

    PubMed

    Mayrovitz, H N

    2007-06-01

    Overall limb lymphedema can be assessed by several methods but none are suitable to determine local edema. Quantifying local edema could provide important information not previously available. Our goal was to determine the suitability of using the tissue dielectric constant (TDC) as and index of local tissue water to detect and quantify edema in postmastectomy patients with unilateral arm lymphedema. Segmental arm volume and TDC were measured in both arms of 18 women with unilateral lymphedema, and in 15 premenopausal and 15 postmenopausal controls. TDC was measured at a frequency of 300 MHz using open-ended coaxial probes with effective measuring depths of 0.5, 1.5, 2.5 and 5.0 mm. For patients and controls, absolute TDC depended on measurement depth but for any depth the TDC of lymphedematous segments was significantly greater than for non-affected contralateral arms (p<0.001). At a depth of 2.5 mm, the TDC ratio between arms for patients was 1.64+/-0.30 vs.1.04+/-0.04 for both control groups (p<0.001). No patient's TDC ratio was as low as 1.2 and no control subject's TDC ratio was as great as 1.2. Results suggest that this method is a good quantitative discriminator of the presence of lymphedema in patients with unilateral limb lymphedema.

  7. Primary intimal sarcoma of pulmonary valve and trunk with osteogenic sarcomatous elements. Report of a case considered to be pulmonary embolus.

    PubMed

    Murthy, M S; Meckstroth, C V; Merkle, B H; Huston, J T; Cattaneo, S M

    1976-12-01

    A 49-year-old woman had a six-week history of increasing shortness of breath and fatigue. X-ray films and pulmonary scans showed multiple areas of emboli, especially in the right lung. Treatment with heparin was unsuccessful, and although a repeat scan showed only slight changes, the patient's condition deteriorated. Acute pulmonary edema and ventricular tachycardia preceded her death. Autopsy revealed a primary intimal sarcoma with osteogenic elements arising in the posterior leaflet of the pulmonary valve and obstructing the main pulmonary artery and its right branch.

  8. [Chronic thromboembolic pulmonary hypertension: diagnostic limitations].

    PubMed

    Dias, Bruno Arantes; Jardim, Carlos; Hovnanian, André; Fernandes, Caio Júlio César; Souza, Rogério

    2008-07-01

    Chronic thromboembolic pulmonary hypertension is the only potentially curable form of pulmonary hypertension, assuming that surgical treatment is possible. However, there are hindrances to making a definitive, noninvasive diagnosis. We present the case of a 40-year-old female patient with idiopathic pulmonary arterial hypertension, confirmed in 1994. This patient developed thrombi in pulmonary vessels (as an overlap syndrome) mimicking chronic thromboembolic pulmonary hypertension. The identification of these conditions, which present high intraoperative mortality and unsatisfactory surgical resolution, is quite difficult in clinical practice. We discuss the current approach to candidate selection for surgical treatment of chronic thromboembolic pulmonary hypertension and the possible repercussions of inappropriate selection.

  9. Endothelial HIF signaling regulates pulmonary fibrosis-associated pulmonary hypertension

    PubMed Central

    Carrick, Ryan P.; McConaha, Melinda E.; Jones, Brittany R.; Shay, Sheila D.; Moore, Christy S.; Blackwell, Thomas R.; Gladson, Santhi; Penner, Niki L.; Burman, Ankita; Tanjore, Harikrishna; Hemnes, Anna R.; Karwandyar, Ayub K.; Polosukhin, Vasiliy V.; Talati, Megha A.; Dong, Hui-Jia; Gleaves, Linda A.; Carrier, Erica J.; Gaskill, Christa; Scott, Edward W.; Majka, Susan M.; Fessel, Joshua P.; West, James D.; Blackwell, Timothy S.; Lawson, William E.

    2015-01-01

    Pulmonary hypertension (PH) complicating chronic parenchymal lung disease, such as idiopathic pulmonary fibrosis, results in significant morbidity and mortality. Since the hypoxia-inducible factor (HIF) signaling pathway is important for development of pulmonary hypertension in chronic hypoxia, we investigated whether HIF signaling in vascular endothelium regulates development of PH related to pulmonary fibrosis. We generated a transgenic model in which HIF is deleted within vascular endothelial cells and then exposed these mice to chronic intraperitoneal bleomycin to induce PH associated with lung fibrosis. Although no differences in the degree of fibrotic remodeling were observed, we found that endothelial HIF-deficient mice were protected against development of PH, including right ventricle and pulmonary vessel remodeling. Similarly, endothelial HIF-deficient mice were protected from PH after a 4-wk exposure to normobaric hypoxia. In vitro studies of pulmonary vascular endothelial cells isolated from the HIF-targeted mice and controls revealed that endothelial HIF signaling increases endothelial cell expression of connective tissue growth factor, enhances vascular permeability, and promotes pulmonary artery smooth muscle cell proliferation and wound healing ability, all of which have the potential to impact the development of PH in vivo. Taken together, these studies demonstrate that vascular endothelial cell HIF signaling is necessary for development of hypoxia and pulmonary fibrosis associated PH. As such, HIF and HIF-regulated targets represent a therapeutic target in these conditions. PMID:26637636

  10. Opioid receptor agonists reduce brain edema in stroke.

    PubMed

    Yang, Li; Wang, Hezhen; Shah, Kaushik; Karamyan, Vardan T; Abbruscato, Thomas J

    2011-04-06

    Cerebral edema is a leading cause of mortality in stroke patients. The purpose of this study was to assess a non-selective opioid receptor agonist, biphalin, in decreasing reducing brain edema formation using both in vitro and in vivo models of stroke. For the in situ model of ischemia, hippocampal slices were exposed to oxygen glucose deprivation (OGD) conditions and we observed that hippocampal water content was increased, compared to normoxia. Treatment with the mu agonist, Tyr-D-Ala', N-CH, -Phe4, Glyol-Enkephalin (DAMGO), delta opioid agonists, D-pen(2), D-phe(5) enkephalin (DPDPE), and kappa agonist, U50 488, all significantly decreased brain slice water gain. Interestingly, the non-selective agonist, biphalin, exhibited a statistically significant (P<0.01) greater effect in decreasing water content in OGD-exposed hippocampal slices, compared with mu, delta, and kappa selective opioid agonists. Moreover, biphalin exhibited anti-edematous effects in a dose responsive manner. The non-selective opioid antagonist, naloxone, returned the water content nearly back to original OGD values for all opioid agonist treatments, supporting that these effects were mediated by an opioid receptor pathway. Furthermore, biphalin significantly decreased edema (53%) and infarct (48%) ratios, and neuronal recovery from stroke, compared with the vehicle-treated groups in a 12h permanent middle cerebral artery occlusion (MCAO) model of focal ischemia. Biphalin also significantly decreased the cell volume increase in primary neuronal cells exposed to OGD condition. These data suggest that opioid receptor activation may provide neuroprotection during stroke and further investigations are needed in the development of novel opioid agonist as efficacious treatments for brain ischemia.

  11. Pulmonary α-1,3-Glucan-Specific IgA-Secreting B Cells Suppress the Development of Cockroach Allergy.

    PubMed

    Patel, Preeyam S; King, R Glenn; Kearney, John F

    2016-10-15

    There is a higher incidence of allergic conditions among children living in industrialized countries than those in developing regions. One explanation for this is reduced neonatal exposure to microbes and the consequent lack of immune stimulation. Sensitivity to cockroach allergen is highly correlated with the development of severe asthma. In this study, we determined that an Ab to microbial α-1,3-glucan binds an Enterobacter species and cockroach allergen. Neonatal, but not adult, mice immunized with this α-1,3-glucan-bearing Enterobacter (MK7) are protected against cockroach allergy. Following exposure to cockroach allergen, α-1,3-glucan-specific IgA-secreting cells are present in the lungs of mice immunized with MK7 as neonates but not in the lungs of those immunized as adults. Mice that are unable to generate anti-α-1,3-glucan IgA Abs were immunized with MK7 as neonates and were no longer protected against cockroach allergy. Thus, neonatal, but not adult, exposure to α-1,3-glucan results in suppressed development of cockroach allergy via pulmonary α-1,3-glucan-specific IgA-secreting cells.

  12. Pulmonary aspergilloma

    MedlinePlus

    ... Coccidioidomycosis Cystic fibrosis Histoplasmosis Lung abscess Lung cancer Sarcoidosis The most common species of fungus that causes ... fibrosis Histoplasmosis Lung cancer - small cell Pulmonary tuberculosis Sarcoidosis Review Date 7/31/2016 Updated by: Jatin ...

  13. Pulmonary atresia

    MedlinePlus

    ... blood flow from the right ventricle (right side pumping chamber) to the lungs. In pulmonary atresia, a ... Reconstructing the heart as a single ventricle (1 pumping chamber instead of 2) Heart transplant Outlook (Prognosis) ...

  14. Pulmonary artery aneurysm in Behcet's disease: a case report.

    PubMed

    Kasikcioglu, Erdem; Akhan, Hulya; Cuhadaroglu, Caglar; Erkan, Feyza

    2004-05-01

    The pulmonary artery is the second most common site of arterial involvement in Behcet's disease. A 32-year-old man presented with bilateral ankle edema, abdominal discomfort, and hemoptysis. He had a history of recurrent oral and genital aphthous ulcerations for 1 year. The diagnosis of Behcet's disease was made on the basis of the criteria published by the International Study Group for Behcet's Disease. His chest X-ray revealed left hilar enlargement. A helical computed tomography (CT) scan showed a pulmonary aneurysm with intramural thrombosis in the left pulmonary artery and enlarged hepatic veins. Treatment with colchicine and cyclophosphamide was given for 24 months, and helical thoracic CT was performed again. Helical CT showed that the pulmonary aneurysm was reduced by treatment. Helical CT could be used in Behcet's disease for the diagnosis and follow-up of pulmonary involvement.

  15. Pulmonary Agenesis.

    PubMed

    Chawla, Rakesh K; Madan, Arun; Chawla, Aditya; Arora, Harsh Nandini; Chawla, Kiran

    2015-01-01

    Unilateral opaque lung with ipsilateral mediastinal shift is an uncommon cause of respiratory distress in newborn which can be found on simple radiograph of the chest. Pulmonary agenesis is a rare cause of unilateral opaque lung in the newborn. Nearly 50% cases of pulmonary agenesis are associated with other congenital defects including cardiovascular, skeletal, gastrointestinal or genitourinary systems. We report an infant with agenesis of the right lung associated with other congenital anomalies.

  16. Aphakic cystoid macular edema and the operating microscope: is there a connection?

    PubMed Central

    Iliff, W J

    1985-01-01

    The literature documenting the phototoxic effect of relatively low intensity light on the retina and the suggestions by several authors that this might influence the development of cystoid macular edema in the aphakic and pseudophakic patient is reviewed. In particular, the possibility that the operating microscope may be a factor has been emphasized. A study is presented, designed to investigate the possibility that the operating microscope is a factor important in the development of cystoid macular edema. No correlation was found. The need for further investigation into other phototoxic effects from the light of the operating microscope is stressed. PMID:3832535

  17. Life-threatening upper airway edema caused by a distal rattlesnake bite.

    PubMed

    Hinze, J D; Barker, J A; Jones, T R; Winn, R E

    2001-07-01

    A 36-year-old man captured a timber rattlesnake and was accidentally envenomated in the thumb by the severed head. At a local emergency department, hypotension and confusion developed. Facial and glossal edema were also observed. Oxygen was delivered by face mask, and crystalloids and dopamine were administered. Respiratory distress developed with progressive hypoxemia. Intubation was unsuccessful because of massive glossal and epiglottic (laryngeal) edema, and an emergency cricothyrotomy was performed. High-dose antivenom therapy was administered, and mechanical ventilation was started. Recovery was rapid, and the patient was discharged from the hospital a week later. This is the first report of life-threatening upper airway edema caused by snake envenomation not in the vicinity of the head or neck.

  18. Modeling the impact of prostate edema on LDR brachytherapy: a Monte Carlo dosimetry study based on a 3D biphasic finite element biomechanical model

    NASA Astrophysics Data System (ADS)

    Mountris, K. A.; Bert, J.; Noailly, J.; Rodriguez Aguilera, A.; Valeri, A.; Pradier, O.; Schick, U.; Promayon, E.; Gonzalez Ballester, M. A.; Troccaz, J.; Visvikis, D.

    2017-03-01

    Prostate volume changes due to edema occurrence during transperineal permanent brachytherapy should be taken under consideration to ensure optimal dose delivery. Available edema models, based on prostate volume observations, face several limitations. Therefore, patient-specific models need to be developed to accurately account for the impact of edema. In this study we present a biomechanical model developed to reproduce edema resolution patterns documented in the literature. Using the biphasic mixture theory and finite element analysis, the proposed model takes into consideration the mechanical properties of the pubic area tissues in the evolution of prostate edema. The model’s computed deformations are incorporated in a Monte Carlo simulation to investigate their effect on post-operative dosimetry. The comparison of Day1 and Day30 dosimetry results demonstrates the capability of the proposed model for patient-specific dosimetry improvements, considering the edema dynamics. The proposed model shows excellent ability to reproduce previously described edema resolution patterns and was validated based on previous findings. According to our results, for a prostate volume increase of 10–20% the Day30 urethra D10 dose metric is higher by 4.2%–10.5% compared to the Day1 value. The introduction of the edema dynamics in Day30 dosimetry shows a significant global dose overestimation identified on the conventional static Day30 dosimetry. In conclusion, the proposed edema biomechanical model can improve the treatment planning of transperineal permanent brachytherapy accounting for post-implant dose alterations during the planning procedure.

  19. Proton nuclear magnetic resonance studies on brain edema

    SciTech Connect

    Naruse, S.; Horikawa, Y.; Tanaka, C.; Hirakawa, K.; Nishikawa, H.; Yoshizaki, K.

    1982-06-01

    The water in normal and edematous brain tissues of rats was studied by the pulse nuclear magnetic resonance (NMR) technique, measuring the longitudinal relaxation time (T1) and the transverse relaxation time (T2). In the normal brain, T1 and T2 were single components, both shorter than in pure water. Prolongation and separation of T2 into two components, one fast and one slow, were the characteristic findings in brain edema induced by both cold injury and triethyl tin (TET), although some differences between the two types of edema existed in the content of the lesion and in the degree of changes in T1 and T2 values. Quantitative analysis of T1 and T2 values in their time course relating to water content demonstrated that prolongation of T1 referred to the volume of increased water in tissues examined, and that two phases of T2 reflected the distribution and the content of the edema fluid. From the analysis of the slow component of T2 versus water content during edema formation, it was demonstrated that the increase in edema fluid was steady, and its content was constant during formation of TET-induced edema. On the contrary, during the formation of cold-injury edema, water-rich edema fluid increased during the initial few hours, and protein-rich edema fluid increased thereafter. It was concluded that proton NMR relaxation time measurements may provide new understanding in the field of brain edema research.

  20. Estimating the effect of air pollution from a coal-fired power station on the development of children's pulmonary function.

    PubMed

    Dubnov, Jonathan; Barchana, Micha; Rishpon, Shmuel; Leventhal, Alex; Segal, Isaac; Carel, Rafael; Portnov, Boris A

    2007-01-01

    Using geographical information systems (GIS) tools, the present study analyzed the association between children's lung function development and their long-term exposure to air pollution. The study covered the cohort of 1492 schoolchildren living in the vicinity of a major coal-fired power station in the Hadera sub-district of Israel. In 1996 and 1999, the children underwent subsequent pulmonary function tests (PFT) (forced vital capacity (FVC) and forced expiratory volume during the first second (FEV(1))), and the children's parents completed a detailed questionnaire on their health status and household characteristics. A negative association was found between changes in the results of PFT and the estimated individual levels of air pollution. A sensitivity test revealed a FEV(1) decline from -4.3% for the average pollution level to -10.2% for the high air pollution level. The results of a sensitivity test for FVC were found to be similar. Association with the reported health status was found to be insignificant. As we conclude, air pollution from a coal-fired power station, although not exceeding local pollution standards, had a negative effect on children's lung function development. As argued, previous studies carried out in the region failed to show the above association because they were based on zone approaches that assign average concentration levels of air pollutants to all individuals in each zone, leading to a misclassification bias of individual exposure.