Importance of venodilatation in prevention of left ventricular dilatation after chronic large myocardial infarction in rats: a comparison of captopril and hydralazine.

Abstract

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 less than 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 less than 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 less than 0.05) from 11.2 +/- 0.6 to 8.7 +/- 0.8 mm Hg and venous compliance increased (p less than 0.05) from 2.04 +/- 0.07 to 2.70 +/- 0.20 ml/mm Hg/kg. Blood volume decreased (p less than 0.05) from 67.3 +/- 0.9 to 58.2 +/- 1.8 ml/kg.(ABSTRACT TRUNCATED AT 250 WORDS)