Kabell G, Scherlag B J, Brachmann J, Harrison L, Lazzara R
J Electrocardiol. 1985 Jan;18(1):87-96. doi: 10.1016/s0022-0736(85)80039-x.
We studied the effects of reperfusion in 60 dogs following a 30-45 minute period of left anterior descending coronary artery occlusion using electrocardiograms and composite electrogram recordings. One-stage reperfusion in 14 of 15 dogs produced ventricular arrhythmias which degenerated into ventricular fibrillation within 60 seconds. The onset of ventricular arrhythmias was associated with continuous electrical activity in epicardial and intramural electrograms recorded from the reperfused zone. Vagal slowing during reperfusion (64 +/- 8/min) did not prevent ventricular fibrillation (eight of eight dogs) and escape beats were often followed by one or more coupled ectopic beats associated with continuous electrical activity. Rapid atrial pacing (270/min) also did not prevent the appearance of ventricular arrhythmia with associated continuous electrical activity and ventricular fibrillation (six of six dogs) nor did 4 mg/kg lidocaine (15 of 16 dogs). In another group of 15 dogs reperfusion was performed in two stages resulting in no ventricular fibrillation but in 8 of 15 dogs ventricular arrhythmias were observed beginning within two minutes after reperfusion and lasting 20-30 minutes. These ventricular arrhythmias were not associated with continuous electrical activity in any of the recorded leads. Atrial pacing suppressed ventricular arrhythmias and idioventricular rate averaged 157 +/- 10/min versus 55 +/- 10/min pre-reperfusion control. The earliest site of activation indicated automatic foci arising in the subendocardium of the reperfused zone. Lidocaine (2-4 mg/kg) rapidly (less than 90 sec) restored normal sinus rhythm and suppressed automaticity (72 +/- 11/min) as did left anterior descending artery reocclusion (52 +/- 6/min). We conclude that both reentry and enhanced automaticity play a role in ventricular arrhythmias due to reperfusion. Lidocaine (2-4 mg/kg) suppresses automatic but not reentrant ventricular arrhythmias in this experimental setting.
我们使用心电图和复合心电图记录,研究了60只犬在左前降支冠状动脉闭塞30 - 45分钟后的再灌注效应。15只犬中有14只进行一期再灌注,均出现室性心律失常,并在60秒内恶化为心室颤动。室性心律失常的发作与再灌注区记录的心外膜和心内膜电图中的持续电活动有关。再灌注期间迷走神经减慢(64±8次/分钟)并不能预防心室颤动(8只犬全部发生),逸搏后常跟随一个或多个与持续电活动相关的耦合异位搏动。快速心房起搏(270次/分钟)也不能预防伴有相关持续电活动和心室颤动的室性心律失常的出现(6只犬全部发生),4mg/kg利多卡因(16只犬中有15只)同样不能预防。在另一组15只犬中,进行两阶段再灌注,未出现心室颤动,但15只犬中有8只在再灌注后两分钟内开始出现室性心律失常,持续20 - 30分钟。这些室性心律失常与任何记录导联中的持续电活动均无关。心房起搏可抑制室性心律失常,心室自主心律平均为157±10次/分钟,而再灌注前对照为55±10次/分钟。最早的激动部位表明自动兴奋灶起源于再灌注区的心内膜下层。利多卡因(2 - 4mg/kg)可迅速(小于90秒)恢复正常窦性心律并抑制自律性(72±11次/分钟),左前降支动脉再次闭塞(52±6次/分钟)也有同样效果。我们得出结论,折返和增强的自律性在再灌注导致的室性心律失常中均起作用。在本实验环境中,利多卡因(2 - 4mg/kg)可抑制自律性但不能抑制折返性室性心律失常。