Effects of captopril on pulmonary haemodynamics

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.