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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。
Objective: To observe the changes of Purkinje fiber electrophysiological characteristics after myocardial infarction (MI). Methods: MI model was established by ligation of the left coronary artery in MI group. Left ventricular false tendons (n = 30) were removed after 2 days and were placed in simulated ischemia buffer. The APD 90 and APD 90 were measured with glass microelectrode Refractory period (ERP) and post-depolarization (AD) and other electrophysiological phenomena. Control group without ligating the coronary artery directly removed left ventricular false tendons (n = 30) placed in normal Tyrode’s fluid observed above indicators. Results: Compared with the control group, the APD90 of MI group was significantly shorter than that of the control group (287.4 ± 20.5 ms vs 284.6 ± 13.4 ms, P <0.05; CL = 500 ms, (246.7 ± 15.3) ms vs. ) ms than (268.4 ± 17.8) ms, P <0.05]. ERP in MI group was significantly shorter than that in control group [(207.1 ± 18.3) ms vs (232.3 ± 17.6) ms, P <0.05]. At CL = 200 ms and 300 ms, delayed depolarization (DAD) was observed in 27 of the false chordae in the MI group. In the MI group, all 30 of the false chordae showed an alternation of action potentials (AP). Ryanodine completely inhibits the alternation of DAD and AP in MI tendons. CONCLUSION: The alternation of DAD and AP in the false chordae tendon is related to abnormal calcium regulation in Purkinje cells after MI, and may have potential arrhythmogenic effects.