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目的探讨心肌梗死后右心室肌细胞离子通道电流的变化。方法该研究采用结扎兔冠状动脉左前降支的方法建立心肌梗死动物模型,应用膜片钳全细胞记录方法,记录心肌梗死后2个月右心室心肌细胞钠通道电流(INa)、L-钙通道电流(ICa-L)、瞬间外向钾电流(Ito)的变化。结果心肌梗死后2个月,心肌梗死组INa电流密度峰值[(20.42±1.73)pA/pF,n=15]较对照组[(35.40±3.43)pA/pF,n=16]明显下降(P<0.05);心肌梗死组ICa-L电流密度峰值[(5.71±0.93)pA/pF,n=12]与对照组[(6.28±1.03)pA/pF,n=10]略下降,但无明显差异(P>0.05);心肌梗死组Ito电流密度(+60mV时)[(8.61±0.95)pA/pF,n=16]较对照组[(14.38±1.24)pA/pF,n=17]明显下降(P<0.05)。结论心肌梗死可引起右心室肌细胞INa和Ito的下降,造成心肌传导速度下降和动作电位时程相对延长、复极异常,可能是导致心肌梗死后出现室性心律失常的离子机制。
Objective To investigate the changes of ion channel currents in right ventricular myocytes after myocardial infarction. Methods The animal model of myocardial infarction was established by ligation of the left anterior descending coronary artery in rabbits. Whole-cell patch-clamp recording was used to record the changes of sodium channel current (INa) and L-calcium channel in right ventricular myocardium 2 months after myocardial infarction Current (ICa-L), transient outward potassium current (Ito) changes. Results At 2 months after myocardial infarction, the peak current density of INa in myocardial infarction group was significantly lower than that in control group [(20.42 ± 1.73) pA / pF, n = 15] (35.40 ± 3.43 pA / pF, n = 16) <0.05). The ICa-L peak current density in myocardial infarction group [(5.71 ± 0.93) pA / pF, n = 12] was slightly lower than that in the control group [(6.28 ± 1.03) pA / pF, n = 10] P <0.05). Compared with the control group [(14.38 ± 1.24) pA / pF, n = 17], the Ito current density in myocardial infarction group was significantly higher at +60 mV [(8.61 ± 0.95) pA / pF, n = 16] Decreased (P <0.05). Conclusions Myocardial infarction can cause the decrease of INa and Ito in the right ventricular myocytes, leading to the decrease of myocardial conduction velocity and the prolongation of action potential duration. The repolarization may be the ion mechanism of ventricular arrhythmia after myocardial infarction.