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)

Pulmonary edema after Escherichia coli (E. coli) endotoxin administration is characterized by marked pulmonary hypertension adn microvascular protein permeability. Conceivably, therapy directed at reducing pulmonary arterial hypertension should improve right ventricular mechanics and potentially may decrease the amount of edema formed. We studied the effect of nitroprusside (NP) on pulmonary hypertension, transvascular fluid filtration rate (reflected in lung lymph flow (QL)) and microvascular protein permeability after E. coli endotoxin lung injury. Using the unanesthetized sheep lung lymph preparation, we found the initial pulmonary hypertension after endotoxin infusion refractory to NP. One h after endotoxin, NP significantly reduced the pulmonary artery pressure (P PA) compared to the endotoxin control group. During NP infusion, cardiac output increased a P PA decreased. We found no difference in QL during NP infusion compared to the control group. After cessation of NP infusion, QL increased, whereas protein clearance (QL x lymph protein content) remained constant. We found no beneficial effect of nitroprusside on transvascular fluid flux and microvascular protein permeability after E coli endotoxin injury.
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PMID:Effect of nitroprusside on pulmonary hypertension and lung fluid balance after E. coli endotoxin. 704 81

CD47 modulates neutrophil transmigration toward the sites of infection or injury. Mice lacking CD47 are susceptible to Escherichia coli (E. coli) peritonitis. However, less is known concerning the role of CD47 in the development of acute lung inflammation and injury. In this study, we show that mice lacking CD47 are protected from LPS-induced acute lung injury and E. coli pneumonia with a significant reduction in pulmonary edema, lung vascular permeability, and bacteremia. Reconstitution of CD47(+/-) mice with CD47(-/-) neutrophils significantly reduced lung edema and neutrophil infiltration, thus demonstrating that CD47(+) neutrophils are required for the development of lung injury from E. coli pneumonia. Importantly, CD47-deficient mice with E. coli pneumonia had an improved survival rate. Taken together, deficiency of CD47 protects mice from LPS-induced acute lung injury and E. coli pneumonia. Targeting CD47 may be a novel pathway for treatment of acute lung injury.
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PMID:CD47 deficiency protects mice from lipopolysaccharide-induced acute lung injury and Escherichia coli pneumonia. 1845 16