Richard C, Ricome J L, Rimailho A, Conrad M, Auzépy P
Eur J Clin Pharmacol. 1984;27(1):35-9.
The effects of oral captopril on pulmonary haemodynamics were studied in two groups of 6 patients, one of subjects with chronic respiratory failure (PaO2 52 +/- 5.1 mmHg, PaCO2 54 +/- 2.1 mmHg), and the others with chronic heart failure and high plasma renin activity. Two potential mechanisms of its actions were assessed, namely inhibition of hypoxic vasoconstriction and inhibition of the possible effects of angiotensin II on the pulmonary circulation. There were significant (p less than 0.05) decreases in mean arterial pressure, pulmonary wedge pressure and in systemic arterial resistance associated with improvement in cardiac index in both groups. In the chronic respiratory failure group there was no change in blood gases, mean pulmonary arterial pressure or pulmonary vascular resistance. An increase in driving pressure (p less than 0.05) indicated that captopril had had no effect on pulmonary haemodynamics. In chronic heart failure, mean pulmonary arterial pressure and pulmonary capillary wedge pressure were decreased by a similar extent, so that driving pressure and pulmonary vascular resistance were not changed. It is concluded that oral captopril did not inhibit hypoxic vasoconstriction, and that it modified pulmonary haemodynamics in chronic heart failure patients with high renin activity only as a consequence of reduction in systemic afterload.
对两组各6例患者研究了口服卡托普利对肺血流动力学的影响，一组为慢性呼吸衰竭患者（动脉血氧分压52±5.1mmHg，动脉血二氧化碳分压54±2.1mmHg），另一组为慢性心力衰竭且血浆肾素活性高的患者。评估了其作用的两种潜在机制，即抑制低氧性血管收缩以及抑制血管紧张素II对肺循环可能产生的影响。两组患者的平均动脉压、肺楔压和体循环动脉阻力均显著降低（p<0.05），同时心脏指数改善。在慢性呼吸衰竭组，血气、平均肺动脉压或肺血管阻力无变化。驱动压升高（p<0.05）表明卡托普利对肺血流动力学无影响。在慢性心力衰竭患者中，平均肺动脉压和肺毛细血管楔压下降程度相似，因此驱动压和肺血管阻力未改变。得出的结论是，口服卡托普利不抑制低氧性血管收缩，且仅通过降低体循环后负荷来改变高肾素活性慢性心力衰竭患者的肺血流动力学。
