Reduced mechanical efficiency of rat papillary muscle related to degree of hypertrophy of cardiomyocytes.

Isolated rat papillary muscles of the right ventricle were used to discover the origin of reduced myocardial efficiency in chronic heart failure. Right ventricular hypertrophy was induced by monocrotaline injection, causing pulmonary hypertension. Control (n = 7) and hypertrophied (n = 11) papillary muscles were subjected to sinusoidal length changes at 37°C and 5 Hz with a peak-to-peak amplitude of 15% of the length giving maximum force (^L _max) after being stretched to 92.5% of ^L _max Isometric tension at ^L _max was similar in control and hypertrophied muscles. Work was assessed from the area encompassed by force-length 1oops. Work per 1oop was 0.93 ± 0.11 and 0.84 ± 0.11 μJ/mm³ (means ± SE) for control and hypertrophied muscles, respectively (P = 0.591). Suprabasal O₂ uptake per work loop was 5.7 ± 0.7 pmol/mm³ in control muscles and 8.7 ± 1.7 pmol/mm³ in hypertrophied muscles (P = 0.133). Net mechanical efficiency was calculated from the ratio of work output and suprabasal O₂ uptake. The efficiency of hypertrophied muscles was 29.1 ± 3.7% and was smaller than in control muscles (43.7 ± 2.2%, P = 0.016). The right ventricular cardiomyocyte cross-sectional area increased from 272 ± 17 μm² in control muscles to 396 ± 31 μm² in hypertrophied muscles (P < 0.003). Mechanical efficiency correlated negatively with right ventricular wall thickness and cardiomyocyte cross-sectional area [Spearman rank correlation coefficients of -0.50 (P 0.039) and -0.53 (P = 0.024), respectively]. We conclude that efficiency decreases with increasing cardiomyocyte hypertrophy. Thus, the reduced efficiency of diseased whole hearts can be at least partly explained by reduced efficiency at the cardiomyocyte level. [ABSTRACT FROM AUTHOR]