title: Myocardial contractile depression from high-frequency vibration is not due to increased cross-bridge breakage.
abstract: 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 Pd(t), a sustained decrease in pressure that was not at the perturbation frequency] and an infrequency response [delta Pf(t), that part at the perturbation frequency]. delta Pd(t) represented the effects of contractile depression. A cross-bridge model was applied to delta Pf(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 Pd(t) was strongly affected by whether the responses were activated by Ca2+ or by Sr2+. In the Sr(2+)-activated state, delta Pd(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 Pd(t) or, when it was significant, participated by reducing delta Pd(t) rather than contributing to its magnitude. Furthermore, there was no difference in cross-bridge cycling rate constants when the Ca(2+)-activated state was compared with the Sr(2+)-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 Pd(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.
authors.affiliation: Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman 99164, USA.
authors.forename: K B
authors.initials: KB
authors.lastname: Campbell
authors.forename: Y
authors.initials: Y
authors.lastname: Wu
authors.forename: R D
authors.initials: RD
authors.lastname: Kirkpatrick
authors.forename: B K
authors.initials: BK
authors.lastname: Slinker
mesh_terms: D000818:Animals; D002118:Calcium / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology*; D011817:Rabbits; D013324:Strontium / Q000494:pharmacology; D014732:Vibration
chemical_list: D002118:Calcium; D013324:Strontium