Man R Y, Dresel P E
J Cardiovasc Pharmacol. 1979 May-Jun;1(3):329-42. doi: 10.1097/00005344-197905000-00005.
Lidocaine and tocainide had no effect on ventricular conduction of extrasystoles with coupling intervals longer than 500 msec in isolated blood-perfused dog hearts, but caused interval-related increases in conduction time of extrasystoles in the range of 250--400 msec, here called mid-range extrasystoles (MRE). Quinidine, procainamide, disopyramide, and methyl lidocaine increased conduction times of extrasystoles at all coupling intervals, and no additional slowing of MRE was observed. The slowing of MRE specific to lidocaine and tocainide was confirmed in the intact dog heart. During acute myocardial ischemia in the intact dog heart, conduction was slowed and additional slowing of MRE was found. Lidocaine and tocainide caused further slowing of conduction of MRE. This unique effect of lidocaine and tocainide on the conduction of MRE may be important in the suppression of reentrant arrhythmias. However, lidocaine and tocainide were also found to be arrhythmogenic when extrasystoles were introduced, after acute coronary occlusion, in those animals in which such occlusion alone did not allow demonstration of arrhythmias due to extrasystoles.
利多卡因和妥卡尼对离体血液灌注犬心脏中配对间期超过500毫秒的室性期前收缩的心室传导没有影响，但却使配对间期在250 - 400毫秒范围内的期前收缩传导时间呈间期相关增加，此处称为中期范围期前收缩（MRE）。奎尼丁、普鲁卡因胺、丙吡胺和甲基利多卡因在所有配对间期均增加期前收缩的传导时间，且未观察到MRE有额外减慢。利多卡因和妥卡尼对MRE的特异性减慢在完整犬心脏中得到证实。在完整犬心脏急性心肌缺血期间，传导减慢且发现MRE有额外减慢。利多卡因和妥卡尼使MRE的传导进一步减慢。利多卡因和妥卡尼对MRE传导的这种独特作用在抑制折返性心律失常方面可能很重要。然而，在急性冠状动脉闭塞后引入期前收缩时，在那些仅这种闭塞本身不会因期前收缩而出现心律失常的动物中，也发现利多卡因和妥卡尼具有致心律失常作用。
