Arroyo V, Bosch J, Mauri M, Ribera F, Navarro-López F, Rodés J
Eur J Clin Invest. 1981 Jun;11(3):221-9. doi: 10.1111/j.1365-2362.1981.tb01844.x.
We have studied the effect of angiotensin-II blockade with saralasin on the cardiovascular and hepatic hemodynamics and on the renin-angiotensin-aldosterone system in fourteen patients with cirrhosis and ascites. Control measurements showed that most of the patients had a low mean arterial pressure, high plasma volume, normal or high cardiac index, low peripheral resistance and high plasma renin activity and aldosterone concentration. The wedged hepatic venous pressure was increased in each patient and the estimated hepatic blood flow was normal in most of them. Overall, saralasin induced a significant reduction of the mean arterial pressure, cardiac index and peripheral resistance. The decrease of the peripheral resistance was greater than that of the cardiac index. Six of the patients developed a marked reduction of the mean arterial pressure with low doses of saralasin (1--2.5 microgram/kg/min), and they had significantly higher plasma renin activity and lower mean arterial pressure than the remaining eight patients who showed a slight or no hypotensive response in spite of infusing saralasin up to a dose of 10 micrograms/kg/min. Overall, the decrease of the mean arterial pressure correlated directly with the baseline values of plasma renin activity. Angiotensin-II blockade induced a significant reduction of the wedged hepatic venous pressure. The hepatic blood flow did not show any significant change. The decrease of the wedged hepatic venous pressure was directly related to the reduction of the mean arterial pressure and also to the control plasma renin activity. Our study indicates that in most patients with cirrhosis, ascites and high plasma renin activity, arterial pressure is maintained by the effect of endogenous angiotensin II on the peripheral vasculature, and we suggest that a pre-existing arterial hypotension secondary to an arteriolar vasodilatation is the cause of renin release in these patients. Our results also show that angiotensin-II blockade is accompanied by a reduction of the post-sinusoidal hepatic vascular resistance.
我们研究了用沙拉新进行血管紧张素 II 阻断对 14 例肝硬化腹水患者心血管和肝脏血流动力学以及肾素 - 血管紧张素 - 醛固酮系统的影响。对照测量显示，大多数患者平均动脉压较低、血浆容量较高、心脏指数正常或较高、外周阻力较低以及血浆肾素活性和醛固酮浓度较高。每位患者的肝静脉楔压均升高，大多数患者的估计肝血流量正常。总体而言，沙拉新使平均动脉压、心脏指数和外周阻力显著降低。外周阻力的降低大于心脏指数的降低。6 例患者使用低剂量沙拉新（1 - 2.5 微克/千克/分钟）后平均动脉压显著降低，他们的血浆肾素活性显著高于其余 8 例患者，而其余 8 例患者尽管输注高达 10 微克/千克/分钟的沙拉新，仍表现出轻微或无低血压反应，且平均动脉压较低。总体而言，平均动脉压的降低与血浆肾素活性的基线值直接相关。血管紧张素 II 阻断使肝静脉楔压显著降低。肝血流量未显示任何显著变化。肝静脉楔压的降低与平均动脉压的降低直接相关，也与对照血浆肾素活性相关。我们的研究表明，在大多数肝硬化、腹水且血浆肾素活性高的患者中，动脉压通过内源性血管紧张素 II 对外周血管系统的作用得以维持，并且我们认为这些患者中肾素释放的原因是继发于小动脉血管扩张的预先存在的动脉低血压。我们的结果还表明，血管紧张素 II 阻断伴随着肝窦后血管阻力的降低。
