VENTRICULAR-FUNCTION AND CONTRACTILE PROTEINS IN THE INFARCTED OVERLOADED RAT-HEART

Study objective - The aim was to determine whether surviving myocardium in the infarcted rat heart retains the ability to respond to sustained increases in afterload. Design - Cardiac mass, ventricular function, and actomyosin ATPase activity were compared in animals subjected to coronary artery ligation to produce infarction, superimposed renal artery constriction 4 weeks after infarction, and in sham operated animals. Experimental material - Female Wistar rats obtained at 10 weeks of age (200-225 g) were used for the studies. Measurements and main results - Four weeks after coronary artery ligation, infarcted hearts showed a 22% increase in heart weight and a significant reduction in peak systolic pressure and +/- dP/dt during acute volume infusion and aortic occlusion compared to sham operated hearts. Eight weeks after the initial surgical intervention, the infarct group showed significant impairment in ventricular performance compared to the sham operated group but no further decrement was observed between hearts with infarction and those with infarct and superimposed renal artery constriction for peak systolic pressure and +/- dP/dt during volume infusion and aortic occlusion. Actomyosin ATPase activity, however, was depressed and the shift to V3 myosin isoenzyme was greater in infarct and renal artery constriction compared to infarct alone. Conclusions - Left ventricular myocardium following infarction does not retain the ability to increase cardiac mass and shows depressed levels of actomyosin ATPase activity when exposed to a superimposed chronic afterload from renal artery constriction. However, cardiac function in situ is maintained.