Actions of halothane on the electrical activity of Purkinje fibers derived from normal and infarcted canine hearts.

Abstract

The effects of 0.39 mM halothane (approx. 1.1 vol%) on the action potentials of proximal (false tendon) and distal (apical) left ventricular Purkinje fibers were compared in analogous in vitro preparations derived from normal dogs and animals surviving 1 day following acute myocardial infarction. In ten noninfarcted hearts, halothane reduced regional differences in repolarization by decreasing action potential duration (APD90, mean +/- SE) in proximal fibers from 300 +/- 7 to 277 +/- 6 msec (P less than or equal to 0.01) without decreasing APD90 in distal fibers (control 240 +/- 4 msec, halothane 249 +/- 5 msec). In ten infarcted hearts, halothane accentuated pathologic differences in repolarization by decreasing APD90 in the non-ischemic proximal fibers from 311 +/- 8 to 287 +/- 7 msec (P less than or equal to 0.01), while increasing APD90 in the ischemic distal fibers from 375 +/- 15 to 406 +/- 18 msec (P less than or equal to 0.01). Halothane also decreased the overshoot from 32.9 +/- 1.0 to 28.4 +/- 0.8 m V (P less than or equal to 0.01) and Vmax from 356 +/- 28 to 300 +/- 22 V/s (P less than or equal to 0.05) in ischemic fibers. In seven infarcts evaluated by extrastimulus techniques, halothane slowed the conduction of premature impulses and prolonged refractoriness, while, in five of the seven hearts, it reversibly increased the range of coupling intervals which induced probable reentrant responses. In a separate study of seven infarcts, halothane decreased the rate of spontaneous activity originating in the ischemic region. It is concluded that halothane facilitates the occurrence of re-entry while inhibiting the initiation of abnormal impulses in the in vitro canine infarction model.