Kimura S, Bassett A L, Saoudi N C, Cameron J S, Kozlovskis P L, Myerburg R J
J Am Coll Cardiol. 1986 Apr;7(4):833-42. doi: 10.1016/s0735-1097(86)80345-x.
The cellular electrophysiologic consequences of both regional and global experimental ischemia and reperfusion were studied in the isolated cat myocardium, using conventional microelectrode techniques. Oxygenated Tyrode's solution was perfused through the left anterior descending and circumflex coronary arteries, while the preparation was superfused with Tyrode's solution gassed with 95% nitrogen and 5% carbon dioxide. Electrophysiologic characteristics of endocardial muscle cells were normal during coronary perfusion. When perfusion was discontinued for 30 minutes, resting membrane potential was decreased by 21.6 +/- 4.1%, action potential amplitude was decreased by 29.1 +/- 8.6% and action potential duration was decreased by 54.1 +/- 12.5% (p less than 0.001). Ectopic activity occurred after 5 to 10 minutes of ischemia and was more frequent in regional than in global ischemia (p less than 0.05). Rapid ventricular activity was observed in only 5 (17%) of 29 preparations during ischemia, whereas it occurred in 24 (83%) of 29 preparations during reperfusion. Rapid ventricular activity began 5 to 40 seconds (mean 19) after the start of reperfusion, stopped spontaneously after a mean of 113 +/- 211 seconds and occurred after both regional and global ischemia. The cellular electrophysiologic changes induced by ischemia returned to baseline values within the next 5 minutes. Repeated ischemia and reperfusion runs reproduced the same electrophysiologic changes and rapid ventricular activity. Coronary perfusion with procainamide (20 mg/liter) aggravated the ischemic depressions of action potential amplitude and action potential duration and increased conduction delay during ischemia, but it did not prevent rapid ventricular activity induced by reperfusion. In contrast, verapamil (1 mg/liter) perfusion did not affect the changes in action potential variables during ischemia but prevented reperfusion-induced rapid ventricular activity. Perfusion with calcium ion (Ca2+)-free Tyrode's solution just before ischemia and during reperfusion slowed or prevented reperfusion-induced rapid ventricular activity, without affecting the action potential changes during ischemia. It is concluded that, in these isolated perfused ventricular muscle preparations, different mechanisms may be operative in ischemic and reperfusion arrhythmias and Ca2+ may play an important role in the development of arrhythmias during the reperfusion phase of ischemia/reperfusion sequences.
采用传统微电极技术，在离体猫心肌中研究了局部和整体实验性缺血及再灌注的细胞电生理后果。用含氧的台氏液经左前降支和左旋冠状动脉进行灌注，同时用含95%氮气和5%二氧化碳的台氏液对标本进行表面灌注。冠状动脉灌注期间，心内膜肌细胞的电生理特性正常。当灌注中断30分钟时，静息膜电位下降21.6±4.1%，动作电位幅度下降29.1±8.6%，动作电位时程下降54.1±12.5%（p<0.001）。缺血5至10分钟后出现异位活动，局部缺血时比整体缺血时更频繁（p<0.05）。缺血期间，29个标本中只有5个（17%）观察到快速心室活动，而在再灌注期间，29个标本中有24个（83%）出现快速心室活动。快速心室活动在再灌注开始后5至40秒（平均19秒）开始，平均113±211秒后自发停止，局部和整体缺血后均会出现。缺血诱导的细胞电生理变化在接下来的5分钟内恢复到基线值。重复进行缺血和再灌注实验可重现相同的电生理变化和快速心室活动。用普鲁卡因胺（20mg/升）进行冠状动脉灌注会加重缺血时动作电位幅度和动作电位时程的降低，并增加缺血时的传导延迟，但它并不能预防再灌注诱导的快速心室活动。相比之下，维拉帕米（1mg/升）灌注在缺血期间不影响动作电位变量的变化，但可预防再灌注诱导的快速心室活动。在缺血前和再灌注期间用无钙离子（Ca2+）的台氏液灌注可减缓或预防再灌注诱导的快速心室活动，而不影响缺血期间的动作电位变化。得出的结论是，在这些离体灌注心室肌标本中，缺血性和再灌注性心律失常可能涉及不同机制，并且Ca2+可能在缺血/再灌注序列的再灌注阶段心律失常的发生中起重要作用。
