Increased myothermal economy of isometric force generation in compensated cardiac hypertrophy induced by pulmonary artery constriction in the rabbit. A characterization of heat liberation in normal and hypertrophied right ventricular papillary muscles.

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Abstract
Initial, recovery and resting heat were measured in normal and hypertrophied papillary muscles in order to monitor the energetic consequences of the subcellular changes accompanying hypertrophy. The pulmonary artery was constricted in rabbits 4 wk prior to measurements. Right ventricular papillary muscles were stimulated at 0.2 Hz and 21.degree. C in Krebs-Ringer solution under isometric conditions at optimum length. Peak twitch tension was 5.90 .+-. 0.25 g/mm2 (SEM [standard error of the mean]) in normal muscle (N) and 5.11 .+-. 0.47 g/mm2 (NS [not significant]) in pressure overload muscle (P). The maximal rate of tension generation decreased 26% (P < 0.02) from 15.9 .+-. 0.85 g/mm2 s (N) to 11.7 .+-. 1.37 g/mm2 s (P). Time-to-peak tension increased 30% (P < 0.001) from 627 .+-. 20 m (N) to 816 .+-. 21 m (P). The total activity related heat production per beat decreased 36% (P < 0.001) from 3.92 .+-. 0.26 mcal/g (N) to 2.51 .+-. 0.29 mcal/g (P). Initial heat was reduced 37% (P < 0.001) from 1.66 .+-. 0.10 mcal/g (N) to 1.04 .+-. 0.12 mcal/g (P). The isometric heat coefficient increased 43% (P < 0.005) from 8.76 .+-. 0.54 (N) to 12.5 .+-. 1 (P) showing increased economy in hypertrophy. There was an early fast phase (1.29 .+-. 0.12 mcal/g per) of initial heat lasting 396 .+-. 25 m which was related to tension build-up. A slow phase (1.05 .+-. 0.07 mcal/g per s) accompanied relaxation. In hypertrophy, the fast phase was 32% (P < 0.05) slower than normal and lasted 27% (P < 0.02) longer; the slow phase was 48% (P < 0.001) slower than normal. The ratio of recovery to initial heat (1.37 .+-. 0.09) was not different in N and P muscles. Resting heat was 2.08 .+-. 0.35 mcal/g per beat in N and 1.35 .+-. 0.23 mcal/g per beat in P muscles. Present results and previous enzymatic and mechanical studies suggest that the relation between the compensated pressure overload hypertrophied and normal hearts is similar to the relation between slow and fast skeletal muscle. The changes in the heart that undergoes hypertrophy secondary to pressure overload are beneficial, since they meet the new hemodynamic demands with increased economy of force production.