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.
