中文摘要：

目的：观察心肌梗死（MI）后浦肯野纤维电生理特性的改变。方法：MI组结扎左冠状动脉造成MI模型,2d后取出左心室假腱索（n=30）置于模拟缺血缓冲液中用玻璃微电极测定动作电位90%复极时间（APD90）和有效不应期（ERP）,并观察后除极（AD）和其他电生理现象。对照组不结扎冠状动脉直接取出左心室假腱索（n=30）置于正常Tyrode’s液中观测上述指标。结果：慢频率刺激时,MI组APD90明显短于对照组[心动周期（CL）=800ms,（247.4±20.5）ms比（284.6±13.4）ms,P〈0.05;CL=500ms,（246.7±15.3）ms比（268.4±17.8）ms,P〈0.05]。MI组ERP明显短于对照组[（207.1±18.3）ms比（232.3±17.6）ms,P〈0.05]。CL=200ms和300ms时,MI组27根假腱索观察到迟后除极（DAD）;CL=200ms,MI组30根假腱索均出现动作电位（AP）交替现象。Ryanodine全面抑制MI组假腱索的DAD和AP交替现象。结论：MI后假腱索DAD和AP交替现象与浦肯野细胞钙调控异常有关,且可能有潜在的致心律失常作用。

英文摘要：

Objective： To investigate the dynamic changes of electrophysiological characteristics of purkinje fibers after myocardial infarction（MI）.Methods： MI was produced in MI group by ligating the left coronary artery.The false tendons of MI group（n=30） were excised after two days of MI,and conserved in ischemia solution for determining the action potential duration at 90% repolarization（APD90） and effective refractory period（ERP）,and for observing the after depolarization（AD） and other electrophysiological phenomena.After having been excised,the false tendons of control group（n=30） were conserved in normal Tyrode＇s solution and the same indexes were determined.Results： During low frequency pacing,APD90 and ERP of MI group were shorter than these of control group signifcantly,（APD90： CL=800 ms,247.4±20.5 ms vs 284.6±13.4 ms,P0.05;CL=500 ms,246.7±15.3 ms vs 268.4±17.8 ms,P0.05;ERP： 207.1±18.3 ms vs 232.3±17.6 ms,P0.05）.At CL of 200 ms or 300 ms,delayed after depolarizations（DADs） presented in 27 of all 30 false tendons of MI group.At CL of 200 ms,the active potential（AP） amplitude and duration of all 30 false tendons of MI group altered beat-to-beat.Ryanodine deprived all DADs and AP alternans in MI group under all conditions.Conclusion： After MI,the DADs and AP alternans of false tendon play a potential role in the arrhythmogenesis,and might be related to the abnormal calcium handling.