兔心肌梗死后右心室肌细胞离子通道电流的变化

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(Ico)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( 60 nV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.

Alteration of ion channel currents in right ventricular myocytes from infarcted rabbit heart

Objective: To study the current change of right ventricular myocyte ion channel after myocar-dial infarction. Methods: Rabbits were infarcted by ligation of the left anterior descending coronary artery,currents of INa、ICa-L and Ito in cells from the right ventricular myocytes of the 2-month infarcted rabbit heart were recorded using patch-clamp techniques in cells from the right ventricular myocytes from infarcted heart (MI) and compared with the noninfarcted heart (CON). Results: Peak Ina current density(at -30 mV) was sig-nificantly reduced in MI [(20.42±1.73) pA/pF, n=15] compared with CON [(35.40±3.43) pA/pF,n=16],P＜0.05;ICa-1 density was also significantly reduced in MI [(5.71±0.93)pA/pF, n=12], compared with CON [(6.28±1.03)pA/pF, n=10], had no significantly difference (P＜0.05); Ito density (at +60 mV) was also significantly reduced in MI [(8.61±0.95)pA/pF,n=16] compared with CON [(14.38±1.24) pA/pF, n=17], P＜0.05; The ICa-L density in MI was no significantly different from CON. Conclusion: The current density of INa and Ito was significan-tily reduced in MI. These changes may underlie the altered excitability and abnormally long transmembrane action potentials and repolarization of these arrhymogenic right ventricular fibers of the infracted heart, thus contributing to reentrant arrhymias in the infarcted heart.