Different electrophysiological responses of canine endocardium and epicardium to combined hyperkalemia, hypoxia, and acidosis.

Abstract

To determine whether canine epicardium and endocardium show intrinsically different electrophysiological responses to metabolic alterations that occur during acute myocardial ischemia in vivo, endocardial, epicardial, papillary muscle tip, and Purkinje fibers (PF) were superfused in vitro with Tyrode's solution containing 8.0 DM KC1 at a pH of 6.85 and a Po 2 < 50 mm Hg.During the initial 10 minutes of superfusion with altered Tyrode's solution, reduction of action potential (AP) amplitude and dV/dtmax and prolongation of activation times were greater in epicardium than in endocardium or in PF, despite similar changes in resting membrane potential.After superfusion for 15 minutes, only 3 of 18 epicardial and 5 of 16 papillary muscle cells were excitable, whereas 14 of 16 endocardial muscle cells and 13 of 13 PF still were responsive.Membrane responsiveness at takeoff potentials < -65mV was lower in epicardium and papillary muscle than in endocardium during superfusion with normal or altered Tyrode's solution.The effects produced by the initial 15 minutes of superfusion with altered Tyrode's solution were partially reversed in endocardium and PF but not in epicardium or papillary muscle, during a subsequent 20-to 60-minute period of continued superfusion.Tetrodotoxin (1'1'X, 5 x 10" 6 M) depressed AP amplitude and dV/dtm., more in epicardium than in endocardium.TTX had only a small effect on the upstroke of PF AP, but shortened AP duration by 30-40%.Verapamil (2 x 10~6 M) had equivalent effects on endocardium and epicardium.These data indicate that excitability is more easily depressed by a combination of hyperkalemia, hypoxia, and acidosis, and by TTX, in epicardium and papillary muscle tip than in endocardium and PF.Responsiveness of endocardial muscle during exposure to altered Tyrode's solution or TTX may be enhanced by contact with PF. drc Res 46: 814-825, 1980IT IS well established that conduction in the subendocardium remains relatively preserved during acute myocardial ischemia in vivo at a time when conduction in the subepicardium has undergone progressive delay and fractionation (Boineau and Cox, 1973;Williams et al, 1974;Scherlag et al., 1974;Elharrar et al., 1977;Ruffy et al., 1979).This difference between the electrophysiological response of endocardium and epicardium is particularly puzzling, considering the established susceptibility of the subendocardium to the necrotizing effects of coronary artery occlusion (Jennings et al., 1957; Rivas.etal., 1976).Various explanations have been offered, including effects of cavity blood (Friedman

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