Reversibility of Electrophysiologic Abnormalities of Subendocardial Purkinje Fibers Induced by Ischemia

Subendocardial Purkinje Fibers. Introduction: During the subacute phase of infarction in the canine heart, the Subendocardial Purkinje fibers subtended by the infarct show depolarization greater than can be accounted for by the decrease in (K), and generate abnormal action potentials and spontaneous rhythms due to abnormal automaticity. We have used pinacidil to hyperpolarize these fibers and evaluate the extent to which an increase in resting potential can normalize action potential generation. Methods and Results: Twenty‐four hours after two‐stage ligation of the canine left anterior descending coronary artery, preparations of Subendocardial Purkinje fibers were studied in vitro by recording transmembrane potentials through standard microelectrodes and exposing the preparation to pinacidil and increases in (K + ) 0 . Pinacidil increased resting potential to the estimated value of E K , abolished the abnormal automaticity, and restored action potentials of normal amplitude with normal values of V max . This effect often persisted after washout of pinucidil. Elevation of (K +) , from 4.0 to 20.0 mM slightly increased maximum diastolic potential, suggesting (hat the excess (over the change in E K ) depolarization was caused by a decrease in g Kl . Conclusion: The ventricular arrhythmias seen during the subacute stage of infarction probably are caused by abnormal automaticity. Our findings support the conclusion that this abnormal automaticity arises in partially depolarized suhendocardial Purkinje fibers. This loss of resting potential is due in large part to a decrease in g K1 . Restoration of resting potential to the value of E k permits the Purkinje fibers to develop essentially normal action potentials. An agent capable of reversing the partial block of 1 K1 , thus might be an effective drug for some types of arrhythmias.