Guthrie S K, Wilde D W, Brown R A, Savage A O, Bleske B
College of Pharmacy, Department of Psychiatry, School of Medicine, University of Michigan, Ann Arbor 48109-01065.
J Electrocardiol. 1995 Jan;28(1):39-47. doi: 10.1016/s0022-0736(05)80006-8.
The combined effects of ethanol and quinidine on cardiac electromechanical coupling are unknown, but both drugs affect cardiac conduction and can cause myocardial depression. Isolated left ventricular papillary and ventricular myocytes were used to assess the combined effects of quinidine and ethanol on the electrophysiologic and mechanical properties of rat myocardium. The combination of quinidine (1-300 microM) and ethanol (120-240 mg/dL) depressed active papillary muscle tension within the clinically useful concentration range. In electrophysiologic studies of isolated ventricular myocytes, quinidine prolonged the action potential duration at 50% (APD50) and 90% (APD90) repolarization, the absolute refractory period, and the relative refractory period, but decreased the maximum rate of change of depolarization in phase 0 (Vmax). When cells were exposed to ethanol (240 mg/dL) and quinidine (1.5 microM) together, a significant decrease in the quinidine-induced prolongation of the absolute refractory and relative refractory periods was seen. Additional changes in action potential parameters from the quinidine values included slight reductions in Vmax and in APD50 and APD90, but these reductions were not consistently displayed, nor were they statistically significant.
乙醇和奎尼丁对心脏机电耦联的联合作用尚不清楚，但这两种药物都会影响心脏传导并可导致心肌抑制。采用离体左心室乳头肌和心室肌细胞来评估奎尼丁和乙醇对大鼠心肌电生理和机械特性的联合作用。在临床有效浓度范围内，奎尼丁（1 - 300微摩尔）和乙醇（120 - 240毫克/分升）的联合使用降低了活性乳头肌张力。在离体心室肌细胞的电生理研究中，奎尼丁延长了复极化50%（APD50）和90%（APD90）时的动作电位时程、绝对不应期和相对不应期，但降低了0期去极化的最大变化速率（Vmax）。当细胞同时暴露于乙醇（240毫克/分升）和奎尼丁（1.5微摩尔）时，可见奎尼丁诱导的绝对不应期和相对不应期延长显著降低。与奎尼丁单独作用时相比，动作电位参数的其他变化包括Vmax、APD50和APD90略有降低，但这些降低并不一致，也无统计学意义。
