Delayed
captopril, started after the healing phase of
myocardial infarction, improves perfusion by reducing tissue weight without affecting the vascular capacity of the heart. Early
captopril, during the healing phase, prevents reactive
hypertrophy, but the effects on angiogenesis are unknown. Therefore, the effects of early
captopril (2 g/l
drinking water, from 1 day until 3 weeks after
myocardial infarction) on regional coronary flow related to tissue mass, were studied in isolated perfused hearts from rats, subjected to coronary artery
ligation. Regional maximal vascular capacity was measured during
nitroprusside-induced vasodilation, using radioactive
microspheres. Maximal vascular capacity was not changed by
captopril. Reactive
hypertrophy in infarcted hearts only reached statistical significance in the left ventricular free wall. Since
captopril prevented
hypertrophy but did not affect regional capacity, peak tissue perfusion was improved. Indicating effects on metabolism,
captopril restored the increased
lactate/
purine ratio in infarcted hearts. Thus, early
captopril treatment prevented post-
myocardial infarction hypertrophy but did not suppress angiogenesis, thus beneficially influencing the vascularization/tissue mass ratio, probably reflected by preservation of aerobic metabolism.