Effect of captopril on postischemic myocardial expansion

The effects of captopril on systolic function and diastolic myocardial expansion were assessed in an open-chest multiple occlusion model of myocardial stunning. Captopril was given as a 0.25 mg/kg bolus followed by a continuous infusion at 0.25 mg/kg/h for the duration of the stunning protocol, which was initiated 30 min after the bolus dose was given. The coronary artery was occluded for 5 min and reperfused for 10 min. This procedure was performed 12 times. Regional systolic function and end-diastolic length (EDL) in both the stunned region and normal zone were measured by sonomicrometry. Heart rate (HR) and left ventricular diastolic blood pressure (LVDP) were not significantly different between untreated (n = 11) and captopril-treated (n = 10) groups. The mean aortic pressure (MAP) in the captopril-treated group was ∼10 mm Hg lower than in the untreated group, p < 0.05. Systolic function as determined by the percentage systolic shortening was significantly decreased to 20% of baseline (preocclusion) function in both untreated and captopril treated groups as a result of the stunning procedure, p < 0.001. However, there was an important treatment effect on diastolic expansion of stunned myocardium. In the untreated group, the stunned myocardium underwent a 5-7% relative increase in end-diastolic length (expansion), p < 0.05. In the captopril-treated group, this expansion process was abolished. We conclude that in a multiple occlusion model of myocardial stunning, captopril had no effects in preserving systolic function but had favorable attributes in dilation and expansion of postischemic myocardium.