Effects of captopril on ischaemia-reperfusion-induced arrhythmias in an in vivo rat model

Abstract

The antiarrhythmic effects of captopril, an angiotensin converting enzyme (ACE) inhibitor, were investigated in an in vivo rat model of coronary artery ligation. Captopril (0.3-3 mg kg-1) or saline were administered by intravenously 10 min before coronary ischaemia. The left main coronary artery was then occluded for 7 min, followed by 7 min of reperfusion. Captopril caused a marked decrease in mean arterial blood pressure which was transient at 0.3 and 1 mg kg-1, and at doses of 1 and 3 mg kg-1, it produced marked bradycardia. The incidence of ventricular tachycardia (VT) on ischaemia was significantly reduced the captopril at a dose of 3 mg kg-1 only and on reperfusion at doses of 1 and 3 mg kg-1. At the same doses, captopril significantly reduced the mean duration of ventricular fibrillation (VF) on reperfusion. The incidence of mortality resulting from reperfusion-induced irreversible VF in the control group decreased from 42.9% to 14.3% (NS), 21.4% (NS) and 7.7% (P < 0.05) in captopril at 0.3, 1 and 3 mg kg-1, respectively. Our results indicate that captopril appears to limit the arrhythmias following reperfusion and this may be due in part to the antiischemic effect associated with bradycardia and vasodepression.