Delayed captopril, started after the healing phase of myocardial infarction
, improves perfusion by reducing tissue weight without affecting the vascul
ar capacity of the heart. Early captopril, during the healing phase, preven
ts reactive hypertrophy, but the effects on angiogenesis are unknown. There
fore, the effects of early captopril (2 g/l drinking water, from 1 day unti
l 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 measur
ed during nitroprusside-induced vasodilation, using radioactive microsphere
s. Maximal vascular capacity was not changed by captopril. Reactive hypertr
ophy in infarcted hearts only reached statistical significance in the left
ventricular free wall. Since captopril prevented hypertrophy but did not af
fect regional capacity, peak tissue perfusion was improved. Indicating effe
cts on metabolism, captopril restored the increased lactate/purine ratio in
infarcted hearts. Thus, early captopril treatment prevented post-myocardia
l infarction hypertrophy but did not suppress angiogenesis, thus beneficial
ly influencing the vascularization/tissue mass ratio, probably reflected by
preservation of aerobic metabolism. (C) 1999 Elsevier Science B.V. All rig
hts reserved.