离体豚鼠心室肌模拟“缺血”和再灌注的细胞电生理实验表明:(1)迟后除极电位(DAD)在心肌“缺血”时的发生率仅为16.7%,再灌注时增加到50%。如“缺血”台氏液中加入异丙肾素或增加钙含量,对缺血时的DAD 发生率无影响,再灌注时则分别增加到72.3%和57.1%,并见DAD 引发的持续触发活性;(2)早后除极电位(EAD)在心肌“缺血”时的发生率为8.3%,再灌注时为16.7%,且不受“缺血”台氏液中异丙肾素或高钙的影响,均未引发触发活性。 The electrophysiological experiments of ischemia and reperfusion in simulated guinea-pig ventricular myocytes showed that: (1) late onset depolarization potential (DAD) was only 16.7% in myocardial ischemia and increased at reperfusion To 50%. Such as “Ischemic” Tyrode’s solution by adding isoproterenol or increased calcium content, had no effect on the incidence of DAD during ischemia, but increased to 72.3% and 57.1%, respectively, upon reperfusion, as indicated by the sustained triggering of DAD Activity; (2) the earlier incidence of depolarization potential (EAD) was 8.3% in myocardial “ischemia” and 16.7% at reperfusion, and was not affected by “Ischemia” The effect of high calcium, did not trigger the trigger activity.