Characteristics of IK and its Response to Quinidine in Experimental Healed Myocardial Infarction

作者：Yuan Feng, Judith M.B. Pinto, Quan‐Lin Li, Bernard J. Wasserlauf, Xiangjun Yang, Arthur L. Bassett, Robert J. Myerburg · 发表于：Journal of Cardiovascular Electrophysiology · 年份：1999 · DOI：10.1111/j.1540-8167.1999.tb00265.x · 被引用次数：21 · 研究领域：Cardiac electrophysiology and arrhythmias、Ion channel regulation and function、Cardiac Ischemia and Reperfusion

INTRODUCTION: Mechanisms and drug treatment of serious ventricular arrhythmias in patients with healed myocardial infarction (HMI) are incompletely understood, in part because the electrophysiology and pharmacology of myocytes from noninfarcted regions of HMI hearts are not well characterized. METHODS AND RESULTS: We studied the delayed rectifier potassium current (I(K)) and quinidine responsiveness of single left ventricular subendocardial myocytes isolated from the region remote to the border zone of healed infarct myocardium (4 to 6 mm from scar edge) in cat hearts 2 months after coronary artery occlusion. Subendocardial cells isolated from corresponding regions of normal cat hearts provided controls. I(K) activation and tail currents were recorded using whole cell, voltage clamp techniques. Membrane capacitance of cells remote to HMI (187 +/- 7 pF) was significantly greater than normal (155 +/- 6 pF; P < 0.001). Action potential durations (APDs) recorded from myocytes in remote regions were prolonged (APD90 = 247 +/- 10 msec) compared to normal (214 +/- 11 msec; P < 0.05). Quinidine (1 microM) significantly prolonged APD90 in normal cells but not in remote cells. Density of I(K) (tail current) was significantly decreased in remote cells (3.1 +/- 0.3 pA/pF) compared to normal (3.9 +/- 0.3 pA/pF; P < 0.05), and voltage-dependent activation of I(K) was shifted in the positive direction. Quinidine had significantly less incremental blocking effect on I(K) already blunted by r...