Mechanism for the Abnormal Energetics of Pressure-Induced Hypertrophy of Cat Myocardium
Depressed myocardial contractility with paradoxically increased oxygen consumption has been demonstrated in previous studies of pressure overload hypertrophy. To determine whether altered mitochondrial respiration participates in the abnormal energetics of this muscle, right ventricular hypertrophy (RVH) was produced in 12 cats by pulmonary artery banding. A polarographic muscle bath was used to study eight control and eight RVH papillary muscles, and the respiration of mitochondria isolated from these right ventricles was characterized. RVH muscles demonstrated depressed force-velocity and length-tension curves. The myocardial oxygen consumption per gram of peak active tension was increased from 0.65 ± 0.05 nliters/mg beat-1 (control) to 1.10±0.07 nliters/mg beat-1 (RVH) (P<0.001). Abnormal mitochondrial respiration was shown by an increase in the rate of state 4 oxygen consumption from 12.5±0.8 natoms/mg min-1 (control) to 19.9±0.8 natoms/mg min-1 (RVH) (P < 0.001). The altered oxygen cost of active isometric tension in the RVH muscles was linearly correlated with the altered rate of mitochondrial state 4 oxygen consumption (r = 0.91). Ruthenium red, a compound that blocks mitochondrial calcium uptake, reduced the rate of RVH state 4 oxygen consumption to the control level. The present study suggests a mechanism for the abnormal myocardial oxygen consumption in pressure overload hypertrophy and relates it to nonphosphorylating mitochondrial respiration linked to calcium transport.
- abnormal cardiac muscle states
- cat papillary muscles force-velocity relationship
- length-tension relationship mitochondrial oxidative indexes
- mitochondrial calcium transport myocardial contractility
- Received January 30, 1973.
- Accepted May 24, 1973.
- © 1973 American Heart Association, Inc.