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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenous administration of ethchlorvynol (Placidyl) is known to produce noncardiogenic pulmonary edema in animals and humans. Since intrapulmonary sequestration of leukocytes has been observed to occur following injection of ethchlorvynol, we evaluated the role of these elements of the blood in producing pulmonary edema. In vivo studies in dogs showed intrapulmonary trapping of leukocytes, as evidenced by increasing leukocyte differences between blood from the pulmonary artery and arterial blood. In both animals with normal leukocyte counts and those depleted of leukocytes (less than 500 cells per millimeter), pulmonary edema occurred, as evidenced by increased pulmonary water after injection of ethchlorvynol. Preparations of isolated lung perfused with either whole blood or leukocyte-poor plasma had similar gains in weight following injection of ethchlorvynol, in spite of marked differences in leukocyte counts. We conclude that intrapulmonary sequestered leukocytes do not play a role in ethchlorvynol-induced pulmonary edema.
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PMID:The role of leukocytes in ethchlorvynol-induced pulmonary edema. 62 May 61

Noncardiogenic pulmonary edema has been reported to follow the intravenous use of ethchlorvynol (Placidyl) in both human clinical and animal experimental situations. In a further attempt to define ethchlorvynol-pulmonary tissue inter-relations, we measured ethchlorvynol concentrations in venous and arterial blood and lung and liver tissue of dogs after intravenous injection of 15 to 25 mg of the drug per kg of body weight. In 10 dogs, the mean +/- SEM lung concentrations 1, 3, and 5 min after injection were 70 +/- 20, 50 +/- 13, and 24 +/- 9 mug per g of tissue, respectively. Simultaneous mean +/- SEM venous contrations were 75 +/- 40, 29+/-5, and 22 +/- 5 mug per ml of blood, respectively. During minutes 1 and 3, the liver concentrations were lower than those found in the lung. In an additional 3 dogs, injection of ethchlorvynol into the portal vein led to higher concentrations (at all sample times) in the liver when compared to the lung. In vitro lung slice studies using ethchlorvynol labeled with iodine-131 revealed no active energy-dependent uptake. Intravenously administered ethchlorvynol rapidly fluxes into and out of lung tissue, apparently following the laws of diffusion.
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PMID:Pulmonary tissue concentrations of ethchlorvynol after intravenous injection. 83 95

The ultrastructure of alveolar septae in dogs is investigated at times ranging from 30 seconds to 60 minutes after intravenous injection of ethchlorvynol (Placidyl). Pulmonary edematous fluid first appears in alveolar spaces 5 minutes after injection and becomes progressively more prominent with increasing time. Alveolar septae are initially somewhat fibrotic, and subsequently, most interstitial spaces become swollen and hydrated. Vesicles in endothelial cells increase with postinjectional time, and they seem to form channels or pores interconnecting capillaries and interstitial spaces. Similar vesicles in epithelial cells (Type 1) show an increase after 30 minutes, and they also seem to form channels or pores interconnecting interstitial spaces and the alveolus. Vesicles, whether in endothelial or epithelial cells, contain a flocculent filamentous material similar to plasma protein and the filamentous proteinaceous material in edematous fluid in alveolar spaces. Ethchlorvynol injection rapidly induces a non-hemodynamic form of pulmonary edema. Since cell junctions of both endothelial and epithelial cells remained intact, it is proposed that transalveolar transport of edematous proteinaceous fluid is mediated by means of endothelial and epithelial vesicles.
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PMID:The effect of ethchlorvynol on pulmonary ultrastructure in dogs. 86 12

Intravenous injection of ethchlorvynol (Placidyl) causes noncardiogenic pulmonary edema in humans and laboratory animals. We studied the effects of intravenous ethchlorvynol (15 to 25 mg per kg of body weight) on pulmonary alveolar membrane permeability to various endogenous and exogenous solutes in the in vivo saline-filled dog lung model. Baseline and postethchlorvynol times in minutes for 50 per cent equilibration between the blood and saline-filled alveoli were, respectively, for urea, 37.3 +/- 12.4 and 12 +/- 6.3; for albumin 8,160 +/- 4,400 and 267 +/- 93; for dextrans of molecular weight 10,400 daltons, 1,150 +/- 80 and 185 +/- 160; for dextrans of molecular weight 250,000 daltons, 24,000 +/- 800 and 1,120 +/- 900; for dextrans of molecular weight 500,000 daltons, 24,500 +/- 150 and 1,020 +/- 590. All of these pairs of values were significantly different (P less than 0.01). In addition, lung liquid histamine (but not blood histamine) concentrations increased significantly (P less than 0.001) after ethchlorvynol injection. Intravenous ethchlorvynol causes marked increases in alveolar membrane permeability.
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PMID:The effects of ethchlorvynol on pulmonary alveolar membrane permeability. 92 Oct 65

Two patients experienced severe nonhemodynamic pulmonary edema following the intravenous injection of 25 and 40 mg/kg of body weight of ethchlorvynol (Placidyl). The pulmonary edema cleared rapidly. Injection of Placidyl (12 to 80 mg/kg of body weight) intravenously into dogs caused acute, severe, nonhemodynamic pulmonary edema (as evidenced by markedly elevated lung weights and microscopic evidence of intra-alveolar edema), hypotension with a relative bradycardia, and a decreased cardiac output. Injection of polyethylene glycol, the vehicle in which ethchlorvynol is diluted, did not reproduce the syndrome.
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PMID:Ethchlorvynol (Placidyl)-induced pulmonary edema. 94 81

Traditional thinking suggests that pleural fluid develops on the basis of systemic venous hypertension or a primary pleural process. Recent investigations, however, indicate that both acute lung injury and pulmonary venous hypertension can be important in the pathogenesis of pleural effusions. To evaluate the role of acute lung injury in the formation of pleural effusions, we developed a model of acute, reversible lung injury in NZW rabbits. Intravenous ethchlorvynol (ECV), known to produce permeability edema in humans, was used to produce permeability pulmonary edema in rabbits. The injury was examined over 14 days with bronchoalveolar lavage, pleural fluid analysis, and morphologic analysis. Ethchlorvynol injection (40 mg/kg) produced a PMN-predominant, exudative alveolitis (2 h), alveolar hemorrhage (6 to 10 h), and pleural effusions by 2 h (peak, 10 h). Pathologic findings included a patchy, subpleural, hemorrhagic PMN inflammatory response, which peaked by 24 h, and an acute PMN vasculitis of small arterioles and capillaries; these changes resolved in 5 to 7 days. No parietal pleural abnormalities were observed. We conclude that ECV induces an acute, reversible parenchymal lung injury resulting in a capillary leak and that fluid moves from the interstitium of the lung into the pleural space along a pressure gradient through a relatively permeable mesothelium. The data support the concept that diffuse or localized lung injury can result in pleural effusions.
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PMID:Pleural effusions associated with ethchlorvynol lung injury result from visceral pleural leak. 278 46

A 71-year-old man with a long-standing history of rheumatoid arthritis required methotrexate treatment since 1986, with a total dose of 210 mg. In April 1987, before arthroplastic surgery, methotrexate was discontinued. Four weeks later a syndrome of fever, dry cough, shortness of breath, and diffuse air-space consolidations on the chest radiograph evolved. An antibiotic therapy had no beneficial effect, and a bronchoscopy yielded no pathogens. An open lung biopsy led to the diagnosis of methotrexate-induced pneumonitis. This is the first report of a case where methotrexate-induced pneumonitis developed several weeks after cessation of the treatment. Methotrexate can cause four types of pulmonary adverse reactions: pneumonitis, pulmonary edema, pulmonary fibrosis, and pleuritis. Possible pathogenetic mechanisms, symptoms, treatment, and prognosis are discussed.
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PMID:Methotrexate-induced pneumonitis: appearance four weeks after discontinuation of treatment. 280 69

Ethchlorvynol injection in humans leads to a clinical picture consistent with increased permeability pulmonary edema, ie, the adult respiratory distress syndrome. There has been only one such case reported in which the pulmonary wedge pressure was measured. In an attempt to mimic the human disease, the authors established the awake, unanesthetized chronic sheep lung lymph fistula model and injected 15 mg/kg of ethchlorvynol intravenously after a baseline period. There were transient increases in pulmonary artery and systemic blood pressure with decreases in cardiac output. Lymph flow increased five-fold and remained elevated for 24 hr, returning to normal by 48 hr. All animals survived. Pulmonary morphologic changes consisted of alveolar and interstitial edema and some disruption of endothelial and epithelial cells. These findings resolved by 48 hr postinjection. The authors conclude that this model mimics the findings in humans who have injected ethchlorvynol intravenously.
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PMID:Ethchlorvynol-induced pulmonary edema: a chronically instrumented, awake sheep model mimicking human disease. 342 81

Ethchlorvynol (ECV), an agent which produces reversible pulmonary edema, was studied for its effects on cultured bovine pulmonary artery endothelial cell (BPAE) and human umbilical vein endothelial cell (HUVE) monolayers. Endothelial cell monolayers 6 days post-confluent were treated with 1 mg/ml ECV for time intervals of from 5 minutes to 15 hours. ECV treatment caused a mild endothelial cell retraction evident at 10 minutes which increased in severity with increasing duration of exposure to ECV. Retraction of endothelial cells resulted in the formation of irregularly delineated gaps between cells, which remained attached to one another by slender filamentous processes. Despite the severity of the endothelial cell lesion, no cell lysis or cell detachment from the substratum occurred. Furthermore, removal of ECV from cell cultures resulted in the reversal of the endothelial cell lesion. Cytochemical distribution of actin microfilaments in control monolayers localized to a dense peripheral band of actin filaments and to a set of interconnected central microfilaments oriented in general parallel to the long axis of the cell. Endothelial cells treated with ECV for as little as 10 minutes showed a loss of F-actin from the dense peripheral band of microfilaments progressing until the dense peripheral band was entirely lost after 4 hours' exposure to ECV. By 4 hours central microfilaments had reorganized into a prominent series of microfilament bundles aligned parallel to each other and to the long axis of the cell. For investigation of a possible loss of attachment sites of actin filaments as the basis for the lesion, the localization of vinculin was examined in control and ECV-treated BPAE monolayers. After 2 hours' exposure to ECV, vinculin localization within monolayers was affected little, if at all. No effects of ECV on intermediate filaments were observed either. It is proposed that the dense peripheral band of actin bundles is important in maintaining well-spread endothelial cells in monolayers and that ECV acts to destroy the integrity of this structure. It is further proposed that a reaction of endothelial cells to ECV in vivo analogous to that seen in tissue culture accounts for the production of pulmonary edema by creating gaps between cells.
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PMID:The effect of ethchlorvynol on cultured endothelial cells. A model for the study of the mechanism of increased vascular permeability. 401 37

A 71-year-old woman presented with acute non-cardiogenic pulmonary oedema. She proved to have a Pasteurella multocida pneumonia, with blood stream invasion by the organism, and required positive pressure ventilation for 53 days. Penicillin G., the drug of choice for this infection, failed to reverse the steady decline in her arterial oxygen-tension, and it was only after treatment with chloramphenicol and prednisolone that she began to improve. Serological tests strongly indicated the presence of a Staphylococcus aureus infection and the delay in giving antibiotics appropriate to this second pathogen may have been the reason for the patient's initial downhill course.
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PMID:Pasteurella multocida pneumonia complicated by Staphylococcus aureus. 670 48


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