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

Abstract

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 ( Lmax) after being stretched to 92.5% of Lmax. Isometric tension at Lmaxwas similar in control and hypertrophied muscles. Work was assessed from the area encompassed by force-length loops. Work per loop was 0.93 ± 0.11 and 0.84 ± 0.11 μJ/mm3(means ± SE) for control and hypertrophied muscles, respectively ( P = 0.591). Suprabasal O2uptake per work loop was 5.7 ± 0.7 pmol/mm3in control muscles and 8.7 ± 1.7 pmol/mm3in hypertrophied muscles ( P = 0.133). Net mechanical efficiency was calculated from the ratio of work output and suprabasal O2uptake. 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 μm2in control muscles to 396 ± 31 μm2in 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.