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前列腺素E1可抑制肺血管对缺氧及前列腺素F2α的升压反应。

Prostaglandin E1 inhibits the pulmonary vascular pressor response to hypoxia and prostaglandin F2alpha.

作者信息

Weir E K, Reeves J T, Grover R F

出版信息

Prostaglandins. 1975 Oct;10(4):623-31. doi: 10.1016/s0090-6980(75)80009-8.

Abstract

In the anesthetised dog an infusion of exogenous prostaglandin E1 (100muG/min) inhibits the pulmonary vascular pressor response to hypoxia. Both 25 and 100muG/min PGE1 can reduce the transient pulmonary hypertension caused by a bolus of prostaglandin F2alpha. This suggests that hypoxia and PGF2alpha may share a final common pathway in producing pulmonary vasoconstriction. These results may help to explain the mechanism by which endotoxin inhibits the pulmonary vascular response to hypoxia. This effect is probably achieved by stimulating the production of an endogenous dilator prostaglandin. Exogenous PGE1 can mimic this effect.

摘要

在麻醉犬中,输注外源性前列腺素E1(100μg/分钟)可抑制肺血管对缺氧的升压反应。25μg/分钟和100μg/分钟的前列腺素E1均可减轻前列腺素F2α推注引起的短暂性肺动脉高压。这表明缺氧和前列腺素F2α在产生肺血管收缩方面可能有共同的最终途径。这些结果可能有助于解释内毒素抑制肺血管对缺氧反应的机制。这种作用可能是通过刺激内源性舒张性前列腺素的产生来实现的。外源性前列腺素E1可模拟这种作用。

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