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°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 [ΔPd( t), a sustained decrease in pressure that was not at the perturbation frequency] and an in-frequency response [ΔP f ( t), that part at the perturbation frequency]. ΔPd( t) represented the effects of contractile depression. A cross-bridge model was applied to ΔP 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. ΔPd( t) was strongly affected by whether the responses were activated by Ca2+ or by Sr2+. In the Sr2+-activated state, ΔPd( 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 ΔPd( t) or, when it was significant, participated by reducing ΔPd( 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 ΔPd( t) occurred at slower frequencies than those of cross-bridge detachment. Collectively, these results argue against a cross-bridge detachment basis for vibration-induced myocardial depression.