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Differences in the Effect of Metabolic Inhibition on Action Potentials and Calcium Currents in Endocardial and Epicardial Cells

BackgroundIschemia-induced electrophysiological changes are more prominent in epicardial cells than in endocardial cells. Epicardial action potentials shorten more than endocardial action potentials during ischemia. Since the L-type Ca2' current plays an important role in the maintenance of action potential duration, we hypothesized that the Ca2' current is affected more in epicardial cells than in endocardial cells during ischemia. Methods and ResultsTo test this hypothesis, we examined the effect of metabolic inhibition, a major component of ischemia, on action potentials and the Ca2' current in single cells isolated from the endocardial and epicardial layers of the feline left ventricle. The membrane voltage and current were measured by using the whole-cell mode of the patch-clamp technique. During control periods, action potentials recorded from epicardial myocytes had lower amplitude, a prominent notch between phases 1 and 2, and shorter action potential duration compared with those recorded from endocardial myocytes. However, the amplitude and current-voltage relation of the Ca2' current were similar in endocardial and epicardial cells at test potentials of −30 to 60 mV elicited from a holding potential of −40 mV. The time course of inactivation of the Ca21 current also was identical in the two cell types. After 15 minutes of superfusion with glucose-free Tyrode's solution containing 1 mM CN-, action potential duration was reduced by 13 ± −7% in endocardial cells and by 80 ± 9%o in epicardial cells (p < 0.01). The peak Ca21 current was reduced by 21 ± 9% in endocardial cells and by 37 ± 6% in epicardial cells (p < 0.01). ConclusionsWe conclude that enhanced depression of the Ca21 current may account in part for the greater action potential shortening in epicardial cells during ischemia and metabolic inhibition.