麻醉犬吲哚美辛与缓激肽拮抗作用的研究。

H Tost, G Kövér, K Szemerédi
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引用次数: 0

摘要

在吲哚美辛抑制前列腺素合成的过程中,在左肾动脉内注入舒缓激肽(0.05微克/分钟/公斤体重),以测定其对前列腺素的依赖和独立作用。注射吲哚美辛0.1 mg/min/kg体重后,麻醉犬的排尿量和钠排泄量明显下降。肾血管阻力增加,肾血流量(RBFdir)下降30%。左肾动脉静脉注射消炎痛缓激肽时,左肾RBFdir、尿流量和钠排泄量均升高至控制值,右肾RBFdir、尿流量和钠排泄量均降低。结果表明,缓激肽增加肾血流量的作用不需要前列腺素的调解。静脉注射吲哚美辛时肾脏血流量的减少可能是尿流量和钠排泄减少的原因。消炎痛不能抑制缓激肽的利钠和利尿作用,这表明前列腺素并不是这些反应的重要决定因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Study of the indomethacin and bradykinin antagonism in anaesthetized dogs.

To determine the prostaglandin dependent and independent effects of bradykinin in the kidney, bradykinin (0.05 microgram/min/kg body weight) was infused into the left renal artery during inhibition of prostaglandin synthesis by indomethacin. Indomethacin, 0.1 mg/min/kg body weight i.v. produced a marked fall in urine output and sodium excretion in anaesthetized dogs. Renal vascular resistance increased and renal blood flow (RBFdir) decreased by 30%. When during the i.v. infusion of indomethacin bradykinin was infused into the left renal artery, RBFdir, urine flow and sodium excretion increased to the control values in the left kidney while remained lower in the right kidney. The results suggest that bradykinin increases renal blood flow by an action which does not require the mediation of prostaglandins. A decrease in renal blood flow, which was a constant feature during i.v. indomethacin infusion, is probably responsible for the decrease in urine flow and sodium excretion. The failure of indomethacin to inhibit the natriuretic and diuretic effects of bradykinin suggests that the prostaglandins are not important determinants of these responses.

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