Electrophysiological Properties of Canine Purkinje Cells in One-Day-Old Myocardial Infarction

Abstract

Electrophysiological mechanisms which underlie the ectopic ventricular beats occurring 1 day after occlusion of the anterior descending coronary artery of dogs were explored. In intact dogs, bipolar electrograms were recorded in the infarcted and normal zones. Both Purkinje and ordinary myocardial potentials were recorded from the endocardial surface of the normal zone, but only Purkinje potentials were recorded from the infarcted zone. The Purkinje potentials in the infarcted zone were diminished in amplitude and rapidity. The threshold for endocardial pacing was higher in the infarcted zone than it was in the normal zone. The refractory periods of Purkinje cells were longer in the infarcted zone than they were in the normal zone. Excised specimens of endocardial surface containing the infarcted zone were superfused with Tyrode's solution. No ordinary myocardial cells were electrically active at the endocardial surface of the infarcted zone. Purkinje cells showed diminished resting and action potentials, reduced upstroke velocity, enhanced automaticity and phase 4 depolarization, and long action potentials with prolonged phase 3. Excitability was depressed within the infarcted zone. During superfusion, even with Tyrode's solution poor in oxygen and free of dextrose, Purkinje cells recovered toward normal with respect to amplitude of resting and action potentials, upstroke velocity, automaticity, and excitability. The prolonged action potentials persisted. Repetitive firing was easily elicited within the infarcted zone. Various types of pacemaker activity were detected within the infarcted zone. Thus Purkinje cells in the infarcted zone showed distinctive alterations in electrophysiological properties which were probably related to deleterious factors that accumulated in that zone. It is likely that the arrhythmia which occurred in the intact dogs at this time originated within the altered Purkinje cells of the infarcted zone. KEY WORDSprolonged action potentials enhanced automaticity recovery hypoxia working myocardium pacemaker reentry

Activation becomes highly organized during long-duration ventricular fibrillation in canine hearts

“…The following findings suggest that LSVF is maintained by activation spreading from the PF network to the WM: 1) the endocardium, the location of the PF-WM junctions, had the highest activation rate in our canine study, as opposed to previously reported findings that the activation rate during VF is high transmurally in porcine hearts (1,15), in which the PF-WM junctions are distributed intramurally almost to the epicardium (10, 11); 2) PF activation was coupled to and preceded WM activation during LSVF; 3) the activation sequences from the endocardium to the epicardium and the PF activation properties in LSVF were similar to sinus rhythm; and 4) the canine PF network is more resistant to the global ischemia caused by VF than is WM (2,8,9,13), so that during long-duration VF, it was possible for activation to initiate in the PF network and propagate through the PF-WM junctions and then spread in the WM. During LSVF, the WM activations have multiple initiation sites on the endocardium (Figs.…”

Intramural Foci During Long Duration Fibrillation in the Pig Ventricle

“…(5) Enhanced automaticity has been observed in Purkinje fibers of ischemic hearts. 35,36 (6) Microreentry has been suggested to be a possible driving force of focal arrhythmia. 37 In addition, a modeling study suggested Purkinje-muscle reentry as a possible mechanism for polymorphic ventricular arrhythmia.…”

Mechanisms Contributing to Malignant Dysrhythmias Induced by Ischemia in the Cat

“…In animals with ventricular fibrillation, cyclic AMP was significantly elevated in normal and ischemic zones compared to animals with PVCs only. Electrical from the relatively benign dysrhythmias occurring later (1)(2)(3)(4)(5). Thus, elucidation of factors contributing to dysrhythmias associated with sudden death in man may require analysis of processes occurring during the interval immediately after the onset of myocardial ischemia.…”