Hillon P, Lebrec D, Muńoz C, Jungers M, Goldfarb G, Benhamou J P
Hepatology. 1982 Sep-Oct;2(5):528-31. doi: 10.1002/hep.1840020503.
The effects on cardiac output and portal venous pressure of atenolol, a cardioselective beta-blocker, and propranolol, a nonselective beta-blocker, were compared in patients with portal hypertension due to cirrhosis. One hour after p.o. administration of 100 mg of atenolol, cardiac output decreased by 32%, and portal venous pressure by 16%; the decrease in cardiac output and the decrease in portal venous pressure were significantly correlated. One hour after p.o. administration of 40 mg of cardiac output and the decrease in portal venous pressure were not correlated. Whereas the decrease in cardiac output was similar after atenolol or propranolol, the decrease in portal venous pressure was significantly less marked after the former than after the latter beta-blocker. It is concluded that: (a) the decrease in portal venous pressure determined by atenolol results mainly from reduction in cardiac output; (b) the decrease in portal venous pressure determined by propranolol results not only from reduction in cardiac output, but also from extracardiac effects of this beta-blocker, and (c) atenolol might be less efficient in the prevention of recurrent gastrointestinal bleeding in cirrhosis, since the decrease in portal venous pressure is less marked than that which occurs with propranolol.
在肝硬化所致门静脉高压患者中，比较了心脏选择性β受体阻滞剂阿替洛尔和非选择性β受体阻滞剂普萘洛尔对心输出量和门静脉压力的影响。口服100mg阿替洛尔1小时后，心输出量下降32%，门静脉压力下降16%；心输出量的下降与门静脉压力的下降显著相关。口服40mg普萘洛尔1小时后，心输出量和门静脉压力的下降无相关性。虽然阿替洛尔或普萘洛尔后心输出量的下降相似，但前者后门静脉压力的下降明显小于后者β受体阻滞剂。得出以下结论：(a)阿替洛尔所致门静脉压力的下降主要源于心输出量的减少；(b)普萘洛尔所致门静脉压力的下降不仅源于心输出量的减少，还源于该β受体阻滞剂的心脏外效应；(c)阿替洛尔在预防肝硬化复发性胃肠道出血方面可能效果较差，因为门静脉压力的下降不如普萘洛尔明显。
