Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a prospective study, 22 patients with prolonged chest pain were monitored by serial serum tumour necrosis factor-alpha (TNF; cachectin) measurements. In five patients serum TNF markedly increased, peaking at greater than 145 ng l-1; all these patients had large infarcts complicated by hypotension, pulmonary oedema and/or arrhythmia. Two of these patients died. In contrast, TNF levels were either normal or only slightly raised in patients with small or uncomplicated infarcts and in patients with prolonged angina without evidence of infarction. The results show that extensive myocardial infarction induces the release of the monocyte/macrophage-derived polypeptide hormone TNF into circulation. This finding may be clinically relevant with respect to systemic metabolic consequences of myocardial infarction.
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PMID:Circulating tumour necrosis factor-alpha (cachectin) in myocardial infarction. 273 71

Even in the absence of inhalational injury, acute lung injury is a common cause of morbidity and mortality for patients sustaining severe burns. Other than general supportive measures, there are few therapeutic options for improving survival in these critically ill patients. Numerous clinical and laboratory studies have implicated tumor necrosis factor (TNF)-a and neutrophils as important participants in the pathogenesis of burn-induced lung injury. There is, however, little information regarding the mechanism by which these and other pro-inflammatory mediators affect the movement of fluid and protein across the microvascular barrier into the interstitium of the lung. In addition to reviewing the evidence implicating TNF-a and neutrophils in the pathophysiology of burn-induced lung injury, this report summarizes current theories regarding potential mechanisms by which these mediators may alter microvascular barrier function to lead ultimately to the development of pulmonary edema.
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PMID:Mechanisms of pulmonary microvascular dysfunction during severe burn injury. 1196 45