Author:
Chang S. W.,Westcott J. Y.,Henson J. E.,Voelkel N. F.
Abstract
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.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
86 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献