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To elucidate the subcellular mechanism underlying the aftereffects of high-intensity dc shocks, a small pore, which mimics reversible breakdown of the cell membrane (electroporation), was incorporated into the phase-2 Luo-Rudy (L-R) model of ventricular action potentials. The pore size was set to occupy 0.15%-0.25% of the total cell membrane during the 10-ms shock. The pore was assumed to decrease after the shock exponentially with a time constant of 100-1400 ms to simulate resealing process. In normal myocytes, the pore formation results in a delay of repolarization of the shocked action potential, which is followed by prolonged depolarization and oscillation of membrane potential like early afterdepolarization (EAD). Time- and voltage-dependent changes in the delayed rectifier K + currents (I Kr, I Ks) in combination with those of L-type Ca 2+ current (I Ca, (L)) and ion flux through the pore (I pore) are responsible for the potential changes. Spontaneous excitation from the oscillation depends on activation of I Ca, (L). In myocytes overloaded with Na + and Ca 2+ secondary to 90% inhibition of Na +-K + pump, the pore formation results in a delay of repolarization of the shocked action potential, which is followed by slower cyclic depolarization in response to spontaneous release of Ca 2+ from the sarcoplasmic reticulum (SR). This delayed after depolarization-type oscillation is abolished by complete block of Ca 2+ release from the SR. These findings suggest that high-intensity electric field application will cause arrhythmogenic responses through a transient rupture of sarcolemma. with different subcellular events in ventricular cells under normal and pathological conditions.