Normal Myocardial Function and Energetics in Volume-Overload Hypertrophy in the Cat

Depressed contractility with a paradoxically increased myocardial oxygen consumption has been associated with pressure-overload hypertrophy. The present experiments investigated myocardial hypertrophy induced by volume overload. Right ventricular volume overload was produced in 19 cats by surgically creating atrial septal defects (ASD); these cats were compared with 10 sham-operated control cats. The ASD cats showed an increase in the ratio of pulmonary blood flow to systemic blood flow from 1.04 ± 0.01 ( SE ) (control) to 3.30 ± 0.28 (ASD) ( P 0.9). The myocardial oxygen consumption of isotonic contractions was normal for ASD muscles. The length-tension curves were comparable, with developed tensions at Lmax of 6.20 ± 0.31 g/mm 2 for ASD muscles and 6.34 ± 0.23 g/mm 2 for control muscles ( P > 0.7). Myocardial oxygen consumption pergram of tension development at Lmax was 0.66 ± 0.06 µliters/mg beat -1 x 10 -3 in the ASD muscles and 0.65 ± 0.05 µliters/mg beat -1 x 10 -3 in the control muscles ( P > 0.8). The mitochondrial oxidative indexes from control and hypertrophied right ventricles were similar, with respiratory control indexes of 14.3 ± 0.8 for ASD hearts and 12.8 ± 1.6 for control hearts ( P > 0.1). These data demonstrate that contractility and energetics are normal in volume-overload hypertrophy, although these same factors are abnormal in pressure-overload hypertrophy. Thus, hypertrophy alone is not a common denominator for abnormal myocardial function and energetics.