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

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Abstract
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 < 0.001). Hypertrophy was evidenced by a ratio of right ventricular weight to body weight of 0.59 ± 0.03 g/kg for control cats and 0.97 ± 0.03 for ASD cats (P < 0.001). A polarographic muscle bath was used to study papillary muscles from 8 control and 8 ASD cats. ASD muscles demonstrated normal force-velocity curves, with maximal measured preload velocities of 1.32 ± 0.05 muscle lengths/sec: control velocities were 1.33 ± 0.05 muscle lengths/sec (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/mm2 for ASD muscles and 6.34 ± 0.23 g/mm2 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.