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)

The Fischer rat is known for its susceptibility to develop liver necrosis when challenged with paraquat (Smith et al., J. Pharmacol. Exp. Ther. 235: 172-177, 1985). We postulated that other organs, specifically the lung, may also be more susceptible to injury and examined whether lungs from Fischer (F) rats were injured more easily when challenged with active oxygen species than Sprague-Dawley (SD) rat lungs. We aimed to investigate whether increased susceptibility to oxidant injury was related to differences in lung antioxidant defenses. Perfused lungs from both rat strains were challenged by addition of H2O2 to the perfusate or by short-term hyperoxic ventilation. To assess nonoxidant modes of lung injury, we examined lung responses after exposure to protamine sulfate or neutrophil elastase. Intravascular H2O2 or 3 h in vitro hyperoxia caused lung edema in F but not SD rats, and elastase injured F rat lungs more than the lungs from SD rats. Protamine, however, injured the lungs from both strains to a similar degree. Catalase, but not superoxide dismutase or allopurinol, protected F rat lungs against edema, resulting from 3 h in vitro hyperoxia. The lung homogenate levels for reduced glutathione or conjugated dienes and the activities of lung tissue catalase, glutathione peroxidase, and cytochrome P-450 were not different between the two strains. Lung tissue ATP levels, however, were lower in F than in SD rats. Although the F rat strain appears to have an altered oxidant-antioxidant defense balance, the exact cause of the greater susceptibility to oxidant stress of the F rat strain remains elusive.
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PMID:Lung injury in Fischer but not Sprague-Dawley rats after short-term hyperoxia. 226 Jun 76

Polycations, such as protamine sulfate and polylysine, have been implicated in the cause of pulmonary edema, but the mechanism is unknown. We studied the vascular effect of protamine in isolated rat lungs perfused with a cell- and plasma-free solution. Protamine (50-1,000 micrograms/ml) increased lung perfusion pressure and caused edema. Blocking the pulmonary vasoconstriction with papaverine (10(-4) M) did not prevent lung edema. In addition, lungs treated with protamine and papaverine showed increased extravascular leakage of 125I-albumin, indicating increased vascular permeability. Histological examination of these lungs showed marked endothelial injury. Functional endothelial damage was further demonstrated by the impairment of the acetylcholine-induced vascular relaxation in protamine-treated vascular rings. Antihistamines and indomethacin failed to block the pulmonary vasoconstriction and increased vascular permeability caused by protamine. In addition, we found that anionic substances, heparin and albumin, blocked the lung injury induced by protamine, whereas other polycations, polylysine and hexadimethrine bromide, caused pulmonary vasoconstriction and increased vascular permeability similar to protamine. We conclude that protamine causes pulmonary endothelial injury and lung edema and suggest that the injury may be charge mediated.
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PMID:Pulmonary vascular injury by polycations in perfused rat lungs. 288 3

Life threatening cardiopulmonary failure following protamine reversal of heparin after cardiopulmonary bypass (CPB) was reported to occur in adults but rarely in children. Atrial septal defect closure was performed in a 6-week-old infant erroneously suspected to suffer from right atrial thrombosis in addition. Protamine administration after CPB led to critical pulmonary hypertension and severe haemorrhagic pulmonary oedema resulting in severe hypoxia. Inhaled nitric oxide, together with high frequency oscillation ventilation supplemented by intravenous prostacycline, enabled complete recovery of cardiopulmonary and neurological function. Life threatening cardiovascular compromise after intravenous protamine can occur even in young infants which then require challenging paediatric critical care.
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PMID:Life threatening cardiopulmonary failure in an infant following protamine reversal of heparin after cardiopulmonary bypass. 1169 52