Abstract
This paper reports on a comparison of the extent of length-dependent activation of contraction in the right ventricle myocardium in healthy rats and rats with monocrotaline-induced heart failure on two levels of heart-tissue organization, that is, muscle stripes and isolated cardiomyocytes, within the framework of a single study. It has been shown that a deficiency in the length-dependent increase in the contractile force produced by failing myocardium when expressed in quantitative terms is similar at both levels of organization of myocardial tissue. These findings indicate that the mechanisms of length-dependent regulation of myocardial contractility in the failing heart are suppressed mainly at the cellular level. In muscle strips, the deficiency of the length–tension relationship appears to be more pronounced, most likely because the spatial organization of myocytes affects the integral contractile response of the muscle.
Published Version
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