In vivo influence of prostaglandin I2 on systemic and renal circulation in the rat.
In vivo influence of prostaglandin I2 on systemic and renal circulation in the rat.
复制标题
前列腺素 I2 对大鼠全身和肾循环的体内影响。
DOI：
10.1161/01.hyp.7.6.867
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Ichikawa,I
中科院分区：
文献类型：
--
作者：
Yoshioka,T;Yared,A;Miyazawa,H;Ichikawa,I
在29只正常血容量的成年Sprague-Dawley大鼠中研究了前列腺素I2和另外两种血管扩张剂乙酰胆碱和硝普钠对体循环和肾循环的影响。主动脉内输注前列腺素I2（3.6 μ g/kg/hr; n = 6只大鼠）产生显著的血管舒张（p <0.05），如总外周血管阻力平均降低24.8 +/-2.0%所示，而肾血管阻力基本保持不变。在静脉注射saralasin（0.5 mg/kg/hr）预处理的单独一组6只大鼠中获得了基本相同的结果。相反，在另一组6只用saralasin预处理的大鼠中，主动脉内输注乙酰胆碱，（0.35 mg/kg/hr），导致总外周血管阻力降低（21.4 +/- 3.8%）与前列腺素I2诱导的相当，使肾血管阻力显著下降（平均27.7 +/- 5.0%），因此肾血流量增加（平均26.2 +/- 2.9%）。硝普钠（0.4mg/kg/hr i. v.）前列腺素I2和乙酰胆碱之间的中间：肾血管阻力和总外周血管阻力下降温和。这些结果表明，给予足以引起全身血管舒张的剂量的前列腺素I2，不能诱导任何可辨别的肾血管舒张反应，并且体内前列腺素I2引起的肾血管舒张的这种缺乏不是由于如先前所假设的肾内血管紧张素II释放的高效抵消影响。
The effect of prostaglandin I2 and two other vasodilator agents, acetylcholine and sodium nitroprusside, on systemic and renal circulation was studied in 29 adult euvolemic Sprague-Dawley rats. Intra-aortic infusion of prostaglandin I2 (3.6 micrograms/kg/hr; n = 6 rats) produced significant vasodilation (p less than 0.05), as indicated by an average reduction in total peripheral vascular resistance of 24.8 +/- 2.0%, while renal vascular resistance remained essentially unchanged. Essentially identical findings were obtained in a separate group of six rats pretreated with intravenous administration of saralasin (0.5 mg/kg/hr). In contrast, in another group of six rats pretreated with saralasin, intraaortic infusion of acetylcholine (0.35 mg/kg/hr), which caused a reduction in total peripheral vascular resistance (21.4 +/- 3.8%) comparable to that induced by prostaglandin I2, produced a significant fall in renal vascular resistance (average, 27.7 +/- 5.0%) and, hence, an increase in renal blood flow (average, 26.2 +/- 2.9%). The effect of sodium nitroprusside (0.4 mg/kg/hr i.v.) was intermediate between those of prostaglandin I2 and acetylcholine: both renal vascular resistance and total peripheral vascular resistance fell mildly. These results indicate that prostaglandin I2, given in a dose sufficient to cause systemic vasodilation, fails to induce any discernible renal vasodilative response and that this absence of renal vasodilation by prostaglandin I2 in vivo is not due, as previously postulated, to the highly efficient offsetting influence of intrarenal angiotensin II release.