Key result
Activation of K-ATP channels produced a more pronounced reduction in action potential duration in simulated epicardial compared to endocardial myocytes, contributing to APD dispersion in ischemia.
Computer simulations suggest that prominent outward currents in epicardial myocytes exacerbate action potential duration reduction during ischemia, contributing to arrhythmogenic dispersion of repolarization.
Simulations suggest epicardial vulnerability to ischemia; hypothesis-generating and should not change practice.
A computer model has been used to simulate the effects of activation of the ATP sensitive K/sup +/ channels on the action potential morphology and duration of canine-type epicardial myocytes. Simulations were based on a modified version of the Luo-Rudy mammalian action potential model. The authors' formulation of I/sub KATP/ and the transient outward current (I/sub to/) were included in this model. Their results show that the same fraction of open K-ATP channels has a more pronounced effect in epicardium than in endocardium. They conclude that the presence of a prominent outward current in epicardial but not in endocardial myocytes increases the APD reduction produced by the activation of the K-ATP channels and thus contributes to the dispersion of APD observed under ischemic conditions.
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Torres et al. (1997) studied Ischemia. Activation of ATP sensitive K+ channels vs. Endocardial myocytes was evaluated on Action potential morphology and duration. Activation of K-ATP channels produced a more pronounced reduction in action potential duration in simulated epicardial compared to endocardial myocytes, contributing to APD dispersion in ischemia.
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