A model analysis of aftereffects of high-intensity DC stimulationon action potential of ventricular muscle

The mechanism for aftereffects of high-intensity dc stimulation on ventricular muscle was studied by using Beeler-Reuter's action potential model. A leak conductance (G_pore maximal value from 40 to 80 μS for 1 cm² of membrane), which mimics reversible dielectric breakdown of the cell membrane by the shock, was incorporated into the model. To simulate resealing process, G_pore was assumed to decrease after the shock exponentially at a time constant (τ_pore) of 5-50 s. The simulation results are qualitatively consistent with the authors' experimental observations in guinea pig papillary muscle (Amer. J. Physiol., vol. 267, p. H248-58, 1994); they include prolonged depolarization, diastolic depolarization or oscillation of membrane potential leading to a single or multiple spontaneous excitation. The phase-independence and shock intensity-dependence can also be reproduced. Analysis of current components has revealed that: (1) a large inward leak current (l_leak) is responsible for the prolonged depolarization (2) time-dependent decay of outward current (I_X1) in combination with I_leak and slow inward current (I_s) results in diastolic depolarization or oscillation of membrane potential; (3) spontaneous excitation depends on an activation of I_s. These findings support the authors' hypothesis that strong shocks (>15 V/cm) will produce abnormal arrhythmogenic responses in ventricular muscle through a transient rupture of sarcolemmal membrane