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某些前列腺素对血管加压素诱导的离体灌注大鼠肾脏血管收缩的拮抗作用。

Opposition of the vasopressin-induced vasoconstriction in the isolated perfused rat kidney by some prostaglandins.

作者信息

Pace-Asciak C R, Rosenthal A

出版信息

Prostaglandins. 1981 Oct;22(4):567-74. doi: 10.1016/0090-6980(81)90066-6.

Abstract

PGE2 can vasoconstrict or vasodilate the isolated Krebs-perfused rat kidney depending on the tone of the renal vasculature. Thus, it is weakly constrictor (thres-hold 5-10 ng bolus dose) in the perfused kidney whose perfusion pressure is 47 +/- 2 SD mmHg (n = 6), but becomes a vasodilator (threshold approximately 10 pg) in the kidney whose perfusion pressure has been raised to 73 +/- 6 SD mmHg (n = 6) or 121 +/- 8 SD mmHg (n = 6) through constant infusion of Vasopressin (0.1 and 0.25 mU/ml respectively. PGE1 was equally effective as PGE2 while other PGs, I2, I1, and 6-keto E1, were less effective in opposing vasoconstriction. PGF2 alpha was inactive up to a dose of 10 ng.

摘要

根据肾血管的紧张度,前列腺素E2(PGE2)可使离体的用Krebs液灌注的大鼠肾脏血管收缩或舒张。因此,在灌注压为47±2标准差毫米汞柱(n = 6)的灌注肾脏中,它是弱收缩剂(推注剂量阈值为5 - 10纳克),但在通过持续输注血管加压素(分别为0.1和0.25毫单位/毫升)使灌注压升高到73±6标准差毫米汞柱(n = 6)或121±8标准差毫米汞柱(n = 6)的肾脏中,它则成为血管舒张剂(阈值约为10皮克)。前列腺素E1(PGE1)与PGE2的效果相同,而其他前列腺素,如前列环素(I2)、前列异环素(I1)和6 - 酮 - 前列腺素E1(6 - keto E1),在对抗血管收缩方面效果较差。前列腺素F2α(PGF2α)在剂量高达10纳克时无活性。

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