In rats with large myocardial infarctions, we compared the effects of captopril, a presumed arterial and venous vasodilator, with hydralazine, which is thought primarily to be an arterial vasodilator. To determine if the effects of captopril were dependent on the pathophysiological consequences of heart failure, we also studied a group of noninfarcted rats treated with captopril. In noninfarcted rats treated with captopril, left ventricular (LV) systolic and mean aortic pressures decreased from 132 ± 12 to 107 ± 15 mm Hg and 122 ± 1 to 100 ± 2, respectively (p < 0.01). In noninfarcted rats, captopril decreased LV weight, LV weight/body weight, and total heart weight/body weight but produced no effects on the peripheral venous circulation. Rats subjected to coronary artery ligation were selected by ECG criteria to have large myocardial infarctions and were treated for 4 weeks with captopril (n = 8), hydralazine (n = 5), or placebo (n = 9). In infarcted rats treated with captopril, LV systolic, mean aortic pressures and LV end-diastolic pressure (LVEDP) decreased (p < 0.01) from 115 ± 4 to 86 ± 3 mm Hg, 106 ± 4 to 74 ± 3 mm Hg, and 23 ± 2 to 11 ± 2 mm Hg, respectively. Mean circulatory filling pressure decreased (p < 0.05) from 11.2 ± 0.6 to 8.7 ± 0.8 mm Hg and venous compliance increased (p < 0.05) from 2.04 ± 0.07 to 2.70 ± 0.20 ml/mm Hg/kg. Blood volume decreased (p < 0.05) from 67.3 ± 0.9 to 58.2 ± 1.8 ml/kg. At LVEDP recorded during the hemodynamic study, LV end-diastolic volume ('operating' LV end-diastolic volume) decreased (p < 0.01) from 2.64 ± 0.15 to 1.88 ± 0.12 ml/kg. Hydralazine treatment decreased (p < 0.01) LV systolic (91 ± 3 mm Hg) and mean aortic (86 ± 2 mm Hg) pressures, increased (p < 0.05) LVEDP (27 ± 2 mm Hg) but did not change mean circulatory filling pressure, venous compliance, blood volume, or operating LV end-diastolic volume. We conclude that in rats with heart failure, captopril, in addition to being an arterial vasodilator, produced venodilatation and decreased blood volume. Operating LV end-diastolic volume and LVEDP were decreased. These changes appear to be caused by the decrease in blood volume and venodilatation in combination with afterload reduction because hydralazine which has no effect on the venous circulation did not alter LVEDP or operating LV end-diastolic volume.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine