Improvement of endocardial and vascular endothelial function on myocardialperformance by captopril treatment in postinfarct rat hearts

Background-Endocardial (EE) and myocardial capillary vascular endothelial ( myocap VE) cells have been shown to modulate the contractile characteristic s of myocardium in a calcium-dependent manner. We evaluated the endothelial -myocardial interaction in the rat postinfarction myocardial infarction (MI ) model and the effects of captopril. Methods and Results-Wistar rats were divided into 4 groups treated for 4 we eks: (1) control; (2) infarcted controls (left anterior coronary artery lig ation); (3) infarcted+captopril 2 g/L in drinking water; and (4) infarct+ca ptopril+triton intracoronary injection. Coronary VE function was evaluated by infusion of serotonin in Langendorff preparations (n=31), and the myocar dial contractile characteristics were investigated by use of isolated papil lary muscles (n=44). Cardiac mRNA for endothelial constitutive nitric oxide synthase (ecNOS) was measured, and its cellular location was evaluated by immunohistochemistry. Serotonin-induced increase in coronary flow was decre ased in infarct controls compared with controls (4.6% versus 53.4%, P<0.01) but not in the 2 infarct+captopril groups. Intracoronary triton injection decreased serotonin-induced coronary flow in the infarct+captopril+triton g roup. All MI groups had decreased total tension in isolated papillary muscl es. EE removal by triton immersion decreased total tension in all groups ex cept for infarct controls (3.3 versus 3.2 g/mm(2)). Cardiac ecNOS mRNA decr eased in the control infarct group but remained normal in the infarct+capto pril group. Conclusions-Chronic postinfarction endothelium-induced coronary vasodilatat ion is impaired, and both EE and myocap VE dysfunction contribute to myocar dial depression. Captopril use prevents these abnormalities and the reducti on of cardiac ecNOS mRNA.