Alterations of cross-bridge kinetics in human atrial and ventricular myocardium

Open Access
Publisher Website
Google Scholar
Abstract
Condensed abstract: We analyzed actomyosin cross-bridge kinetics in human atrial and ventricular muscle strip preparations by using sinusoidal length changes from 0.1 to 60 Hz. The minimum stiffness frequency was higher in atrial than in ventricular human myocardium and lower in failing than in non-failing left ventricular human myocardium. β-Adrenergic stimulation increased the minimum stiffness frequency by 18±3% (p10 of at least 2.7. Background: Dynamic stiffness measurements have revealed acute and chronic alterations of actomyosin cross-bridge kinetics in cardiac muscles of a variety of different animal species. We studied dynamic stiffness in right atrial and left ventricular preparations of non-failing and failing human hearts and tested the influence of the temperature and β-adrenergic stimulation on cross-bridge kinetics. Methods and Results: Muscle strips were prepared from right atria and left ventricles from human non-failing and failing hearts. After withdrawal of calcium, steady contracture tension was induced by the addition of 1.5 mM barium chloride. Sinusoidal length oscillations of 1% muscle length were applied, with a frequency spectrum of between 0.1 and 60 Hz. Dynamic stiffness was calculated from the length change and the corresponding force response amplitude. The specific minimum stiffness frequency, which indicates the interaction between cross-bridge recruitment and cross-bridge cycling dynamics, was analyzed for each condition: (1) The minimum stiffness frequency was 0.78±0.04 Hz in left ventricular myocardium and 2.80±0.31 Hz in right atrial myocardium (p10 of at least 2.7. (4) β-Adrenergic stimulation significantly (ppConclusions: The contractility of human heart muscle is not only regulated by excitation–contraction coupling but also by modulation of intrinsic properties of the actomyosin system. Acute and chronic alterations of cross-bridge kinetics have been demonstrated, which play a significant role in the physiology and pathophysiology of the human heart.