Simultaneous recording of action potentials from endocardium and epicardium during ischemia in the isolated cat ventricle: relation of temporal electrophysiologic heterogeneities to 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)

[1]  B. Surawicz,et al.  Characteristics and Possible Mechanism of Ventricular Arrhythmia Dependent on the Dispersion of Action Potential Durations , 1983, Circulation.

[2]  A. L. Wit,et al.  Time Course for Reversal of Electrophysiological and Ultrastructural Abnormalities in Subendocardial Purkinje Fibers Surviving Extensive Myocardial Infarction in Dogs , 1975, Circulation research.

[3]  D. Durrer,et al.  The Effect of Acute Coronary Artery Occlusion on Subepicardial Transmembrane Potentials in the Intact Porcine Heart , 1977, Circulation.

[4]  E. Michelson,et al.  Instantaneous and Delayed Ventricular Arrhythmias After Reperfusion of Acutely Ischemic Myocardium: Evidence for Multiple Mechanisms , 1981, Circulation.

[5]  D P Zipes,et al.  Different electrophysiological responses of canine endocardium and epicardium to combined hyperkalemia, hypoxia, and acidosis. , 1980, Circulation research.

[6]  D Durrer,et al.  Mechanism and Time Course of S‐T and T‐Q Segment Changes during Acute Regional Myocardial Ischemia in the Pig Heart Determined by Extracellular and Intracellular Recordings , 1978, Circulation research.

[7]  C W Balke,et al.  Two Periods of Early Ventricular Arrhythmia in the Canine Acute Myocardial Infarction Model , 1979, Circulation.

[8]  N. Saoudi,et al.  Cellular electrophysiologic changes and "arrhythmias" during experimental ischemia and reperfusion in isolated cat ventricular myocardium. , 1986, Journal of the American College of Cardiology.

[9]  M. Prinzmetal,et al.  Myocardial ischemia. Nature of ischemic electrocardiographic patterns in the mammalian ventricles as determined by intracellular electrographic and metabolic changes. , 1961, The American journal of cardiology.

[10]  P. Penkoske,et al.  Disparate Electrophysiological Alterations Accompanying Dysrhythmia due to Coronary Occlusion and Reperfusion in the Cat , 1978, Circulation.

[11]  S. Kimura,et al.  Effects of Verapamil and Lidocaine on Changes in Action Potential Characteristics and Conduction Time Induced by Combined Hypoxia, Hyperkalemia, and Acidosis in Canine Ventricular Myocardium , 1982, Journal of cardiovascular pharmacology.

[12]  W. C. Randall,et al.  Electrophysiology of Coronary Reperfusion: A Mechanism for Reperfusion Arrhythmias , 1980, Circulation.

[13]  R Lazzara,et al.  Characterization and Localization of Ventricular Arrhythmias Resulting from Myocardial Ischemia and Infarction , 1974, Circulation research.

[14]  A. Lukas,et al.  Possible Mechanisms of Ventricular Arrhythmias Elicited by Ischemia followed by Reperfusion Studies on Isolated Canine Ventricular Tissues , 1985, Circulation research.

[15]  J. Boineau,et al.  Slow Ventricular Activation in Acute Myocardial Infarction: A Source of Re‐entrant Premature Ventricular Contractions , 1973, Circulation.

[16]  J. Spear,et al.  Effect of sympathetic tone on ventricular arrhythmias during circumflex coronary occlusion. , 1985, The American journal of physiology.

[17]  A. M. Scher,et al.  Mechanism of S‐T Segment Alteration During Acute Myocardial Injury , 1960, Circulation research.

[18]  A. S. Harris Delayed Development of Ventricular Ectopic Rhythms following Experimental Coronary Occlusion , 1950, Circulation.