兔心肌梗死后2个月肥大心室肌细胞的电生理研究(英文)

Alteration of ion channel currents in hypertrophic ventricular myocytes 2 months after myocardial infarction★

背景:心肌梗死后电重构与梗死后时间和区域相关。目的:研究陈旧性心肌梗死非梗死区肥大心室肌细胞离子通道电流的变化,探讨心肌梗死后肥大心肌发生心律失常的可能的离子机制。设计:随机对照实验研究。地点、材料和干预:所有实验过程在石家庄市白求恩国际和平医院心内科中心实验室完成。新西兰纯种大耳白兔20只,按随机抽签法分为两组:心肌梗死动物模型组和正常对照组。采用结扎兔冠状动脉左前降支的方法建立急性心肌梗死动物模型,应用膜片钳全细胞记录方法。主要观察指标:梗死后2个月心外膜远离梗死区组与梗死区组及正常对照组心室肌细胞L-钙通道电流(L-calciumcurrent,ICa-L)、瞬间外向钾电流(transientoutwardcurrent,Ito)的变化。结果:①远离梗死区组细胞电容犤(155.7±5.8)pF,n=41犦明显大于对照组犤(120.3±6.2)pF,n=35犦和梗死区组犤(130.4±7.8)pF,n=38犦(t=2.642,2.613,P均<0.01)。②ICa-L:远离梗死区组ICa-L电流峰值(0mV)为犤(826.12±121.31)pA,n=21犦,较对照组犤(670.21±183.32)pA,n=10犦和梗死区组犤(629.43±172.12)pA,n=11犦明显增大(t=2.451,2.732,P均<0.05)。但远离梗死区组电流密度峰值为(5.32±0.78)pA/pF,较对照组犤(5.58±1.53)pA/pF犦略下降,与梗死区组犤(4.84±1.48)pA/pF犦和对?

BACKGROUND:The electrical alterations are likely to vary with the stage and the region of the myocardial infarction. OBJECTIVE:To study the alterations of the current of L calcium current(ICa-L) and transient outward current(Ito)in cells from the epicardial zone of the 2 month infarcted rabbit heart,and so as to probe into the cellular basis of the arrhythmias. DESIGN:Randomized controlled trial conducted. SETTING,PARTICIPANTS and INTERVENTION:The experiment was finished in the Central Laboratory of Department of Cardiology,Bethune International Peace Hospital. Twenty New Zealand rabbits(1.5 to 2.0 kg) were randomly divided into two groups:infarcted model group and normal control group.Rabbit models with acute myocardial infarction(AMI) were established by ligation of the left anterior descending coronary artery.Whole cell patch clamp techniques was used.ICa-L and Ito currents were recorded by using whole cell patch clamp techniques. MAIN OUTCOME MEASURES:Two months after infarction,changes of L calcium current(ICa-L) and transient outward current(Ito) were observed. RESULTS:Membrane capacitance of REM myocytes[(155.7±5.8) pF,n=41]was significantly larger compared with CON[(120.3±6.2) pF,n=35]and MI[(130.4±7.8) pF,n= 38](t=2.642,2.613,both P< 0.01).The peak ICa-L current(at 0 mV) was significantly increased in REM[(826.12±121.31) pA,n=21] compared with CON[(670.21±183.32) pA,n=10] and MI[(629.43±172.) pA,n=11](t=2.451,2.732,both P< 0.05). But the peak ICa-L current density in REM[(5.32±0.78)pA/pF]was not significantly different from CON[(5.58±1.53) pA/pF] and MI[(4.84±1.48) pA/pF,n=11],although there was slight reduction in REM and MI compared with CON(t=0.512,1.011,both P >0.05).Ito current density(at +60 mV) was significantly decreased in MI[(10.61±4.12)pA/pF,n=18] and REM[(13.21±4.13)pA/pF,n=23]compared with CON[(17.39±5.24)pA/pF,n=16](t=3.591,2.725,both P< 0.01). Nevertheless,there was a significant increase in REM compared with MI(t=2.429,P< 0.05). CONCLUSION:Exaggeration of cell captiance is found in the myocytes remote from infracted area,indicating myocardial hypertrophy.There is an increase in ICa-L,but the current density of Ito is significantly reduced in REM.These changes may underlie the abnormally long transmembrane action potentials in myocytes of region remote from infarction zone,thus contributing to reentrant arrhymias in the healed infarcted heart.