触发活性在实验性心肌“缺血”和再灌注心律失常中的作用  

The Role of Triggered Activity in the Experimentally Generated Ischemia of Myocardium and Reperfusion Arrhythmias

作　　者：沈坚冰[1] 蒋文平[1] 

机构地区：[1]苏州医学院附属第一医院心血管病研究室

出　　处：《江苏医药》1992年第5期240-243,共4页Jiangsu Medical Journal

摘　　要：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。Cellular Electrophy Siologic experiment of simulated ischemia and reperfusionischemia of isolated guinea pig ventricular muscles was carried out.The result showedthat:(1)incidence of delayed afterdepolarizations(DAD)was 16.7% during simulatedcardiac ischemia and 50% during reperfusion,When ischemic Tyrode solution containing isoproterenol or high Ca^++ level,the incidence of DAD did not change during simulatedischemia,but it increased to 72.3% and 57.1% respectively during reperfusion.Sustainedtriggered aclivity induced by DAD was also observed during reperfusion;(2)incidence ofearly afterdepolarizations(EAD)was 8.3% during simulated cardiac ischemia and 16.7%during reperfusion.The induction of EAD was not influenced by isoproterenol or highCa^++ level containing in ischemic Tyrode solution.Triggered activity induced by EADwas not observed in this experiment.

关 键 词：心肌缺血 再灌注 心律失常 

分 类 号：R541.7[医药卫生—心血管疾病]