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A dynamic action potential model analysis of shock-induced aftereffects in ventricular muscle by rev.pdf

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A dynamic action potential model analysis of shock-induced aftereffects in ventricular muscle by rev

18 IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING, VOL. 49, NO. 1, JANUARY 2002 A Dynamic Action Potential Model Analysis of Shock-Induced Aftereffects in Ventricular Muscle by Reversible Breakdown of Cell Membrane Katsuhiro Ohuchi*, Member, IEEE, Yasuhiro Fukui, Member, IEEE, Ichiro Sakuma, Associate Member, IEEE, Nitaro Shibata, Haruo Honjo, and Itsuo Kodama Abstract—To elucidate the subcellular mechanism underlying the aftereffects of high-intensity dc shocks, a small pore, which mimics reversible breakdown of the cell membrane (electropora- tion), 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 re- polarization 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 ( ) in combi- nation with those of L-type Ca 2+ current ( Ca ( )) and ion flux through the pore ( pore) are responsible for the potential changes. Spontaneous excitation from the oscillation depends on activation of Ca ( ). 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 sponta- neous release of Ca 2+ from the sarcoplasmic reticulum (SR). This delayed afterdepolarization-type oscillation is abolished by com- plete block of Ca 2+ release from the SR. These findings suggest that high-intensity electric field application will cause arrhythmo- genic responses through a transient rupture of sarcolemma with different subcellul