Vera Z, Pride H P, Zipes D P
Division of Cardiology, University of California, Davis School of Medicine, USA.
J Cardiovasc Electrophysiol. 1995 Jul;6(7):532-43. doi: 10.1111/j.1540-8167.1995.tb00426.x.
The precise mechanism of reperfusion arrhythmias is not established. The role of early afterdepolarizations (EADs) and triggered activity in the genesis of reperfusion ventricular arrhythmia was investigated.
Monophasic action potentials (MAPs) were recorded in the canine heart using Ag-AgCl contact electrodes from the left and right ventricular endocardium and the left ventricular epicardial border zone during 10 minutes of occlusion of the proximal left anterior descending coronary artery followed by 2 minutes of reperfusion. Ventricular arrhythmias during ischemia and reperfusion were studied in three autonomically varied groups. Group 1 (n = 8) had intact autonomic neural innervation; group 2 (n = 8) had bilateral transection of ansae subclavii and vagi; and group 3 (n = 8) underwent bilateral transection of ansae subclavii and vagi with bilateral ansae subclavii stimulation during reperfusion. Ventricular fibrillation (VF) on reperfusion occurred in 2, 3, and 5 animals in the innervated, denervated, and sympathetically stimulated groups, respectively. Rapid ventricular tachycardia during ansae subclavii stimulation, antecedent to VF, occurred in 4 of 5 episodes in the sympathetically stimulated group. The frequency of premature ventricular complexes, couplets, and triplets on reperfusion was not significantly different among the three groups. Phase 2 or phase 3 EADs were noted during the acute ischemic phase in 6 of 8, 7 of 8, and 7 of 8 animals in the three groups, respectively (and persisted during reperfusion in the majority). Thus, these EADs were not a de novo phenomenon during reperfusion. Of the 72 MAP recording sites, only one demonstrated de novo phase 2 EADs during reperfusion. EADs disappeared during reperfusion in 6 animals (prior to the onset of VF in 4), and 5 dogs developed reperfusion VF without EADs being recorded. There was no direct correlation between the presence of EADs during reperfusion and the development of VF. The prevalence and onset of reperfusion VF was not significantly different in the presence of sympathetic stimulation.
This study demonstrates that EADs can be recorded in the majority of dogs during both ischemia and reperfusion and do not appear to be a major mechanism responsible for reperfusion ventricular tachycardia and VF.
再灌注心律失常的确切机制尚未明确。本研究探讨了早期后除极（EADs）和触发活动在再灌注性室性心律失常发生中的作用。
使用银 - 氯化银接触电极记录犬心脏的单相动作电位（MAPs），记录部位为左、右心室心内膜以及左心室心外膜边缘区，记录过程包括左前降支冠状动脉近端闭塞10分钟，随后再灌注2分钟。在三个自主神经状态不同的组中研究缺血和再灌注期间的室性心律失常。第1组（n = 8）自主神经支配完整；第2组（n = 8）双侧切断锁骨下袢和迷走神经；第3组（n = 8）双侧切断锁骨下袢和迷走神经，并在再灌注期间对双侧锁骨下袢进行刺激。再灌注时发生心室颤动（VF）的动物在有神经支配组、去神经支配组和交感神经刺激组中分别为2只、3只和5只。交感神经刺激组中，5次VF发作前有4次在锁骨下袢刺激时出现快速室性心动过速。再灌注时室性早搏、成对早搏和三联律的频率在三组之间无显著差异。三组中分别有8只动物中的6只、8只中的7只和8只中的7只在急性缺血期出现2相或3相EADs（大多数在再灌注期间持续存在）。因此，这些EADs并非再灌注期间的新生现象。在72个MAP记录部位中，只有1个在再灌注期间出现新生的2相EADs。6只动物在再灌注期间EADs消失（4只在VF发作前），5只犬发生再灌注VF时未记录到EADs。再灌注期间EADs的存在与VF的发生之间无直接相关性。交感神经刺激时，再灌注VF的发生率和发作情况无显著差异。
本研究表明，大多数犬在缺血和再灌注期间均可记录到EADs，但其似乎并非再灌注性室性心动过速和VF的主要机制。
