CAJ | 학술논문

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.
목적탐토심기경사후우심실기세포리자통도전류적변화.방법해연구채용결찰토관상동맥좌전강지적방법건립심기경사동물모형,응용막편겸전세포기록방법,기록심기경사후2개월우심실심기세포납통도전류(INa)、L-개통도전류(ICa-L)、순간외향갑전류(Ico)적변화.결과심기경사후2개월,심기경사조INa전류밀도봉치[(20.42±1 73)pA/pF,n=15]교대조조[(35 40±3.43)pA/pF,n=16]명현하강(P＜0.05);심기경사조ICa-L전류밀도봉치[(5.71±0.93)pA/pF,n=12]여대조조[(6.28±1.03)pA/pF,n=10]략하강,단무명현차이(P＞0.05);심기경사조Ito전류밀도(+60 nV시)[(8.61±0.95)pA/pF,n=16]교대조조[(14.38±1.24)pA/pF,n=17]명현하강(P＜0.05).결론심기경사가인기우심실기세포INa화Ito적하강,조성심기전도속도하강화동작전위시정상대연장、복겁이상,가능시도치심기경사후출현실성심률실상적리자궤제.
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.