Myocardial contractile depression from high-frequency vibration is not due to increased cross-bridge breakage

Experiments were conducted in 10 isolated rabbit hearts at 25 degrees C to test the hypothesis that vibration-induced depression of myocardial contractile function was the result of increased cross-bridge breakage. Small-amplitude sinusoidal changes in left ventricular volume were administered at frequencies of 25, 50, and 76.9 Hz. The resulting pressure response consisted of a depressive response [Delta P-d(t), a sustained decrease in pressure that was not at the perturbation frequency] and an infrequency response [Delta P-f(t), that part at the perturbation frequency]. Delta P-d(t) represented the effects of contractile depression. A cross-bridge model was applied to Delta P-f(t) to estimate cross-bridge cycling parameters. Responses were obtained during Ca2+ activation and during Sr2+ activation when the time course of pressure development was slowed by a factor of 3. Delta P-d(t) was strongly affected by whether the responses were activated by Ca2+ or by Sr2+. In the Sr2+-activated state, Delta P-d(t) declined while pressure was rising and relaxation rate decreased. During Ca2+ and Sr2+ activation, velocity of myofilament sliding was insignificant as a predictor of Delta P-d(t) or; when it was significant, participated by reducing Delta P-d(t) rather than contributing to its magnitude. Furthermore, there was no difference in cross-bridge cycling rate constants when the Ca2+-activated state was compared with the Sr2+-activated state. An increase in cross-bridge detachment rate constant with volume-induced change in cross-bridge distortion could not be detected. Finally, processes responsible for Delta P-d(t) occurred at slower frequencies than those of crossbridge detachment. Collectively, these results argue against a cross-bridge detachment basis for vibration-induced myocardial depression.