Bigger J T
Department of Medicine, Columbia University, New York, New York.
Am J Cardiol. 1990 Feb 20;65(8):15D-20D; discussion 68D-71D. doi: 10.1016/0002-9149(90)91412-y.
Moricizine is a class I antiarrhythmic drug. In preclinical studies, it produces a concentration-dependent decrease in the maximal rate of phase 0 depolarization, speeds repolarization of phases 2 and 3, and decreases the action potential duration and effective refractory period duration in cardiac Purkinje fibers. It has no effect on the slope of phase 4 depolarization, but suppresses normal automaticity in vitro and in vivo and suppresses abnormal automaticity in depolarized Purkinje fibers. Also, it suppresses early afterdepolarizations, delayed afterdepolarizations and triggered activity. In patients, moricizine has minimal effects on the normal sinus node, slows conduction in the atrium, atrioventricular node, His-Purkinje system and ventricular myocardium and has little effect on the atrial and ventricular refractoriness. The intensity of moricizine action on the atrioventricular node, His-Purkinje system and JT interval are dose-related. Co-administration of digoxin and moricizine intensified the lengthening of the PR, AH and HV intervals, and produced more shortening of the JT interval. Patients in whom moricizine was efficacious had a significantly greater lengthening of the AH and QRS intervals than those in whom moricizine was not efficacious. In some patients with sinus node dysfunction, moricizine produced sinus bradycardia, increased sinus node recovery time, and produced second-degree or complete sinoatrial block.
莫雷西嗪是一种Ⅰ类抗心律失常药物。在临床前研究中，它使0期去极化的最大速率呈浓度依赖性降低，加速2期和3期复极化，并缩短心脏浦肯野纤维的动作电位时程和有效不应期时程。它对4期去极化斜率无影响，但在体外和体内均能抑制正常自律性，并抑制去极化浦肯野纤维的异常自律性。此外，它还能抑制早期后除极、延迟后除极和触发活动。在患者中，莫雷西嗪对正常窦房结影响极小，减慢心房、房室结、希氏-浦肯野系统和心室肌的传导，对心房和心室的不应期影响很小。莫雷西嗪对房室结、希氏-浦肯野系统和JT间期的作用强度与剂量相关。地高辛与莫雷西嗪合用会增强PR、AH和HV间期的延长，并使JT间期缩短得更多。莫雷西嗪有效的患者，其AH和QRS间期的延长明显大于莫雷西嗪无效的患者。在一些窦房结功能障碍患者中，莫雷西嗪会引起窦性心动过缓，延长窦房结恢复时间，并导致二度或完全性窦房阻滞。
