The effect of hypoxia on angiotensin-stimulated release of PGI2 from the splanchnic bed.
The effect of hypoxia on angiotensin-stimulated release of PGI2 from the splanchnic bed.
复制标题
缺氧对血管紧张素刺激的内脏床 PGI2 释放的影响。
DOI：
10.1097/00005373-199008000-00008
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Myers,SI
中科院分区：
文献类型：
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作者：
Reed,M;Taylor,B;Myers,SI
本文观察了低氧对大鼠内脏血管紧张素Ⅱ（AII）刺激前列腺素（PG）释放的影响。将上级肠系膜动脉插管，并在pO 2为460或60 ℃的生理缓冲液中进行体外灌注。内脏血管被单独灌注（SV）或与小肠连续灌注（SV+ SI）。以推注方式输注AII（10-300 ng）。通过生物测定对SV+ SI流出物的定量分析表明，释放的主要PG是PGI 2。放射免疫定量分析证实PGI 2是刺激AII后SV和SV+ SI释放的主要PG。相对低氧显著降低AII刺激的SV释放PGI 2，而SV+ SI仅适度降低。这些数据表明，两个内脏来源的AII刺激血管扩张剂PG的合成，SV和SV+ SI，与SV更敏感的相对缺氧。内脏血管（SV）血管扩张剂PGI 2释放减少可能在缺氧和休克时AII介导的内脏血管收缩中起重要作用。
The effect of hypoxia on splanchnic angiotensin II (AII)-stimulated prostaglandin (PG) release was examined in male rats. The superior mesenteric artery was cannulated and perfused in vitro with physiologic buffer at a pO 2 of 460 or 60 torr. Splanchnic vessels were perfused isolated (SV) or in continuity with the small intestine (SV+ SI). AII (10–300 ng) was infused as bolus injections. Quantitative analysis of SV+ SI effluent by bioassay indicated the predominant PG released was PGI 2. Quantitative analysis by radioimmunoassay confirmed PGI 2 as the major PG released from the SV and SV+ SI following AII stimulation. Relative hypoxia significantly decreased AII-stimulated release of PGI 2 from the SV, and only modestly from the SV+ SI. These data demonstrate two splanchnic sources of AII-stimulated vasodilator PG synthesis, the SV and SV+ SI, with the SV more sensitive to relative hypoxia. Diminished release of splanchnic vascular (SV) vasodilator PGI 2 may be of importance in AII-mediated splanchnic vasoconstriction seen in hypoxia and shock.