The rat heart develops a compensatory hypertrophy after infarction which is secondary to volume overload in the left ventricle (LV) and to pressure overload in the right ventricle (RV). This study was undertaken to determine whether the reduced inotropic response to Ca2+ presented by the LV of infarcted rats extends to the RV and whether this hemodynamic profile in vivo affects the contractile performance of the ventricles assessed in vitro. 2. Male adult rats were submitted to left coronary artery ligation to produce infarction (Inf) or to a sham surgery (SO) and used 4 to 5 weeks later. The hemodynamic data were recorded in the anesthetized animals and the systolic performance of both ventricles was evaluated in vitro in the hearts perfused by the Langendorff technique. The isovolumic systolic pressure (ISP) developed by both ventricles was measured at various diastolic pressures (0 to 30 mmHg) and Ca2+ concentrations (0.62, 1.25, and 2.50 mM). 3. The RV systolic pressure was higher in Inf (N = 12) than in SO (N = 12) rats (42 +/- 5 vs 26 +/- 1 mmHg, P < 0.05). A positive and linear correlation (r = 0.86, P < 0.01) between RV systolic pressure and the RV weight to body weight ratio in Inf rats was observed. 4. Length-dependent activation, evaluated by using normalized ventricular function curves, was unchanged in the RV of Inf hearts. In the Inf LV, however, a slight improvement of the normalized systolic performance was observed in relation to SO hearts for diastolic pressures higher than 15 mmHg. 5. A similar depression of the inotropic response to Ca2+ was observed in both ventricles of Inf hearts. Moreover, for Inf hearts the increase of the ISP to Ca2+ flattened at lower Ca2+ concentrations in relation to the SO group. 6. The present results demonstrate that LV infarction in rats depresses the contractile performance of both ventricles. The reduced inotropic response to Ca2+ presented by both ventricles may contribute to the reduced capacity of the Inf heart to generate external work under conditions of higher metabolic demand.
