Priori S G, Mantica M, Napolitano C, Schwartz P J
Centro di Fisiologia Clinica e Ipertensione, Ospedale Maggiore, Milano, Italy.
Circulation. 1990 Jun;81(6):1911-20. doi: 10.1161/01.cir.81.6.1911.
Recent studies in vitro have shown that afterdepolarizations may develop during reperfusion after hypoxia, thus suggesting that these afterdepolarizations may contribute to the genesis of reperfusion arrhythmias. We recorded monophasic action potentials (MAPs) during myocardial ischemia and reperfusion to investigate whether afterdepolarizations develop in vivo when reperfusion arrhythmias occur. In 15 anesthetized cats, 24 trials of 10 minutes of occlusion of the left anterior descending coronary artery were followed by reperfusion. In 13 of 24 (54%) trials, afterdepolarizations developed at the moment of reperfusion, with a mean amplitude of 2.4 +/- 1.1 mV (13 +/- 8% of MAP amplitude). When cycle length was either increased by vagal stimulation or decreased by atrial pacing, early afterdepolarization (EAD) amplitude was modified, according to what has been described for EAD in vitro, with a positive linear correlation between cycle length and EAD amplitude (r = 0.91, p less than 0.0001). The occurrence of EAD was not related to rapid changes in left ventricular pressure. In the eight of 13 (62%) cases in which EAD development was associated with reperfusion arrhythmias, the coupling interval of the EAD and of premature ventricular contractions showed a significant correlation (r = 0.86, p less than 0.0001). However, in five of 13 (38%) cases, occurrence of reperfusion arrhythmias was not accompanied by the presence of EAD on the MAP recording. In two animals, a 2:1 block of EAD conduction was observed, and this was reflected on the intracavitary electrocardiogram as T wave alternans. Thus, EADs occur frequently after reperfusion in vivo, with a time course that parallels the onset of reperfusion arrhythmias. This finding further supports the role of triggered activity in the genesis of reperfusion arrhythmias in vivo.
近期的体外研究表明，缺氧后再灌注期间可能会出现后去极化，因此提示这些后去极化可能与再灌注心律失常的发生有关。我们记录了心肌缺血和再灌注期间的单相动作电位（MAPs），以研究当再灌注心律失常发生时，体内是否会出现后去极化。在15只麻醉猫中，进行了24次试验，每次试验均先阻断左前降支冠状动脉10分钟，随后进行再灌注。在24次试验中的13次（54%）中，再灌注瞬间出现了后去极化，平均幅度为2.4±1.1 mV（占MAP幅度的13±8%）。当通过迷走神经刺激增加周期长度或通过心房起搏缩短周期长度时，早期后去极化（EAD）幅度会发生改变，这与体外EAD的情况一致，周期长度与EAD幅度之间呈正线性相关（r = 0.91，p < 0.0001）。EAD的发生与左心室压力快速变化无关。在13例中有8例（62%）EAD的发生与再灌注心律失常相关，EAD与室性早搏的偶联间期显示出显著相关性（r = 0.86，p < 0.0001）。然而，在13例中有5例（38%），再灌注心律失常的发生并未伴有MAP记录上EAD的出现。在两只动物中，观察到了EAD传导的2:1阻滞，这在腔内心电图上表现为T波交替。因此，EAD在体内再灌注后频繁出现，其时间进程与再灌注心律失常的发作平行。这一发现进一步支持了触发活动在体内再灌注心律失常发生中的作用。
