title: Modulation of collision-induced changes in canine heart repolarization by cycle length.
abstract: The possibility that cycle length modulates the electronic effect of activation sequence on repolarization was investigated in experiments using isolated canine cardiac Purkinje strands, in situ canine ventricular myocardium, and computer simulations. Action potential durations and refractory periods during one-way propagation were compared to those obtained during action potential collision. In both the computer simulations and the Purkinje strand experiments, collision decreased action potential duration more at long cycle lengths than at short cycle lengths. Comparably, collision of activation fronts in ventricular myocardium was associated with greater reductions in refractory period during pacing at long cycle lengths than at short cycle lengths. Theoretic considerations indicate that the magnitude of electrotonic effects of activation sequence on repolarization are directly related to action potential height and the square root of membrane resistance during repolarization and are inversely related to conduction velocity. In computer simulations and Purkinje strand experiments, changes in conduction velocity and action potential height elicited by decreasing cycle length could not fully account for the cycle length dependence of collision-induced changes in repolarization. Time-varying membrane resistance of a single cell was calculated in the simulations by briefly hyperpolarizing the membrane and determining the change in total ionic current. Membrane resistance during repolarization was less at short cycle lengths than at long cycle lengths. The results suggest the cycle length dependence of collision-induced changes in repolarization results largely from the effect of cycle length on membrane resistance during action potential repolarization, with changes in action potential height and conduction velocity playing a lesser role.
authors.affiliation: Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City 84112.
authors.forename: K W
authors.initials: KW
authors.lastname: Spitzer
authors.forename: B M
authors.initials: BM
authors.lastname: Steinhaus
authors.forename: M
authors.initials: M
authors.lastname: Hirai
authors.forename: C W
authors.initials: CW
authors.lastname: Haws
authors.forename: M J
authors.initials: MJ
authors.lastname: Burgess
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D003198:Computer Simulation; D004285:Dogs; D004594:Electrophysiology; D006339:Heart Rate / Q000502:physiology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000502:physiology*; D011690:Purkinje Fibers / Q000502:physiology*