Braillon A, Cailmail S, Gaudin C, Lebrec D
Unité de Recherches de Physiopathologie Hépatique (INSERM U-24), Hôpital Beaujon, Clichy, France.
J Hepatol. 1993 Jan;17(1):86-90. doi: 10.1016/s0168-8278(05)80526-4.
Decreased pressor reactivity to angiotensin II has been demonstrated in portal hypertension due to cirrhosis. The present study investigated the respective roles of portal hypertension and cirrhosis and the hemodynamic mechanisms of the depressor response in different models of portal hypertension in conscious rats. Dose-pressor curves were studied in sham-operated, portal vein stenosed (portal hypertension without cirrhosis) and biliary cirrhotic rats following angiotensin II administration. Decreased pressor response was observed in cirrhotic rats but not in portal vein stenosed rats. The hemodynamic effects of angiotensin II administration (11 ng.100 g-1 body wt.min-1, i.v.) were studied in conscious sham-operated and biliary cirrhotic rats (radioactive microsphere method). The percentage of change from basal values following angiotensin II administration were significantly more marked in sham-operated rats than in cirrhotic rats for mean arterial pressure (+34 vs. +6%), cardiac index (-36 vs. -22%), systemic vascular resistance (+117 vs. +40%). After angiotensin II, portal tributary and hepatic artery blood flows significantly decreased in sham-operated rats (-31 and -14%, respectively) but not in cirrhotic rats (+1 and +23%), whereas changes in renal blood flow were not significantly different between the two groups (-44 vs. -34%). In conclusion, in biliary cirrhotic rats, decreased pressor response to angiotensin II depends on the presence of liver disease rather than on portal hypertension or basal hemodynamic alterations. It also depends on the decreased vasoconstrictive effect which predominates in the splanchnic vascular bed.
肝硬化所致门静脉高压患者对血管紧张素II的升压反应降低。本研究在清醒大鼠不同门静脉高压模型中，探讨门静脉高压和肝硬化各自的作用以及降压反应的血流动力学机制。在假手术、门静脉狭窄（无肝硬化的门静脉高压）和胆汁性肝硬化大鼠中，给予血管紧张素II后研究剂量-升压曲线。肝硬化大鼠出现降压反应降低，而门静脉狭窄大鼠未出现。在清醒假手术和胆汁性肝硬化大鼠中（放射性微球法），研究了静脉注射血管紧张素II（11 ng·100 g-1体重·min-1）的血流动力学效应。血管紧张素II给药后，与肝硬化大鼠相比，假手术大鼠的平均动脉压（+34%对+6%）、心脏指数（-36%对-22%）、全身血管阻力（+117%对+40%）相对于基础值的变化百分比明显更显著。给予血管紧张素II后，假手术大鼠的门静脉分支和肝动脉血流显著减少（分别为-31%和-14%），而肝硬化大鼠未减少（+1%和+23%），而两组间肾血流变化无显著差异（-44%对-34%）。总之，在胆汁性肝硬化大鼠中，对血管紧张素II的降压反应降低取决于肝脏疾病的存在，而非门静脉高压或基础血流动力学改变。它还取决于内脏血管床中占主导的血管收缩作用降低。
