Modulation of splanchnic vascular sensitivity to angiotensin II.
Modulation of splanchnic vascular sensitivity to angiotensin II.
复制标题
调节内脏血管对血管紧张素 II 的敏感性。
作者：
Yuping Wu;Li Ss;Campbell Ka;Sitzmann Jv
我们研究了门静脉高压症患者输注血管紧张素II后内脏血管反应性降低是否与前列环素（PGI 2）水平升高有关。应用多普勒血流探头测定正常家兔（NL）和门脉高压家兔（PHT）在血管紧张素II（Ang II）灌注过程中肠系膜上级动脉阻力（RSMA）和体循环阻力（RRR）的变化。在环氧化酶阻断（CO）后、CO后和持续输注300 ng/kg PGI 2期间，NL中血管紧张素II输注导致RSMA的增加不成比例地大于RSMA（p <0.01）。在PHT中，RSMA的血管紧张素II反应低于NL（p <0.05）。CO显著改善PHT动物对血管紧张素II的内脏反应，但没有显著改变NL的RSMA反应。NL、NL + CO和PHT + CO中的PGI 2定量地建立了PHT中所见的内脏血管对血管紧张素II的低反应性。我们的结论是，PGI 2将直接减少内脏反应血管紧张素II的NL，和CO将消融之间的NL和PHT内脏反应血管紧张素II的差异。这强烈地暗示，在PHT中观察到的血管紧张素II反应的降低大部分是由PGI 2介导的，并且NL和PHT血管反应之间的差异部分是循环血管舒张物质的结果。
We studied whether the diminished splanchnic vascular response to angiotensin II infusion in portal hypertension could be related to elevated levels of prostacyclin (PGI2). The changes in superior mesenteric artery resistance (RSMA) and systemic vascular resistance (RSYS) during angiotensin II infusion were measured by Doppler flow probe in normal rabbits (NL) and portal hypertensive rabbits (PHT), and in NL and PHT after cyclooxygenase blockade (CO) and after CO and during continuous PGI2 infusion at 300 ng/kg/min. Angiotensin II infusion in NL caused a disproportionately greater increase in RSMA than in RSYS (p less than 0.01). In PHT, angiotensin II response of RSMA was reduced from NL (p less than 0.05). CO dramatically improved the splanchnic response to angiotensin II in PHT animals, but did not significantly alter the RSMA response in NL. PGI2 in NL, NL + CO, and PHT + CO quantitatively established the splanchnic vascular hyporesponsiveness to angiotensin II seen in PHT. We conclude that PGI2 will directly diminish splanchnic response to angiotensin II in NL, and CO will ablate differences in splanchnic response between NL and PHT to angiotensin II. This strongly implies that much of the observed decrease in angiotensin II response in PHT is mediated by PGI2 and that the differences between NL and PHT vascular response is in part the result of circulating vasodilatory substances.