A MODEL ANALYSIS OF AFTEREFFECTS OF HIGH-INTENSITY DC STIMULATION ON ACTION-POTENTIAL OF VENTRICULAR MUSCLE

The mechanism for aftereffects of high-intensity de stimulation on ven tricular muscle was studied by using Beeler-Reuter's action potential model, A leak conductance (G(pore), maximal value from 40 to 80 mu S f or 1 cm(2) 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 (tau(pore)) of 5-50 s. The sim ulation results are qualitatively consistent with our experimental obs ervations in guinea pig papillary muscle [1]; they include prolonged d epolarization, diastolic depolarization or oscillation of membrane pot ential leading to a single or multiple spontaneous excitation, The pha se-independence and shock intensity-dependence can also be reproduced, Analysis of current components has revealed that: 1) a large inward l eak current (I-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 depolarizati on or oscillation of membrane potential; 3) spontaneous excitation dep ends on an activation of I-s. These findings support our hypothesis th at strong shocks (>15 V/cm) will produce abnormal arrhythmogenic respo nses in ventricular muscle through a transient rupture of sarcolemmal membrane.