Ischemia in isolated cat ventricles caused greater initial reduction in action potential duration and refractory periods in epicardial versus endocardial cells, leading to arrhythmias.
Does ischemia cause differential electrophysiologic changes in endocardial versus epicardial cells in isolated cat ventricles?
Ischemia creates temporal electrophysiologic heterogeneities between endocardium and epicardium that facilitate the development of arrhythmias.
We studied the effects of ischemia on transmembrane action potentials, conduction time, and refractory periods of both endocardial and epicardial muscle cells of coronary-perfused cat left ventricles. Oxygenated Tyrode's solution was perfused through the left anterior descending coronary artery, while the preparation was superfused with Tyrode's solution gassed with 95% N2 and 5% CO2. Transmembrane action potentials recorded simultaneously from endocardial and epicardial cells were normal during coronary perfusion. When perfusion was discontinued ("ischemia"), rapid deterioration of action potentials and prolongation of conduction time were observed in both endocardial and epicardial cells. The magnitude of the reduction of action potential amplitude and action potential duration (APD), and of prolongation of conduction time, was greater in epicardial cells than in endocardial cells, although the change in resting membrane potential was almost the same. However, APD of endocardial cells decreased progressively during 30 min of ischemia, whereas APD of epicardial cells was reduced maximally at 10 min and then partially recovered. Shortening of refractory periods of endocardial cells paralleled APD shortening, whereas refractory periods of epicardial cells decreased for the first 10 min and then increased. At 10 min of ischemia, APD and refractory periods of epicardial cells were significantly shorter than those of endocardial cells. At 30 min of ischemia, refractory periods of epicardial cells exceeded those of endocardial cells because of development of greater postrepolarization refractoriness in epicardial cells. Accompanying these different changes in APD and refractory periods of endocardial and epicardial cells, spontaneous extrasystolic impulses increased and rapid runs of extrasystolic impulses could be induced by extrastimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
Kimura et al. (Fri,) conducted a other in Ischemia and Arrhythmias. Ischemia (discontinuation of coronary perfusion) vs. Normal coronary perfusion was evaluated on Transmembrane action potentials, conduction time, and refractory periods. Ischemia in isolated cat ventricles caused greater initial reduction in action potential duration and refractory periods in epicardial versus endocardial cells, leading to arrhythmias.
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