兔急性心肌梗死后24小时心室肌细胞离子通道电流的变化

背景急性心肌梗死(acute myocardial infarction ,AMI)后梗死区内部和梗死周边区尚存活的心肌,往往在心律失常的发生上起关键作用.目的研究 AMI后梗死区心肌细胞钠通道电流( INa)、 L型钙通道电流(ICa-L)、瞬间外向钾电流( Ito)和内向整流性钾电流 (IK1)活性的变化.设计随机对照研究. 单位白求恩国际和平医院心内科. 材料本实验于2003- 01/2003- 06在白求恩国际和平医院心内科中心实验室完成.选择新西兰纯种大耳白兔20只,按随机抽签法分为两组即 AMI组和对照组,每组 10只. 方法结扎兔冠状动脉左前降支建立AMI动物模型,采用酶解的方法分离心室肌细胞,应用膜片钳全细胞记录方法记录离子电流的变化.主要观察指标 AMI后 24 h AMI组和对照组心外膜梗死区心肌细胞 INa,ICa-L, Ito和 IK1的变化. 结果 AMI后 24 h, AMI组 INa电流密度峰值 [(28.48±3.53) pA/pF, n=16]较对照组 [(45.50± 5.33) pA/pF, n=12]明显下降( t=3.026,P<0.01); AMI组 ICa-L电流密度峰值 [(3.91± 0.95 ) pA/pF, n=12]较对照组 [(5.58±1.53) pA/pF, n=10]明显下降( t=2.985 ,P< 0.01); AMI组 IK1电流密度峰值 [(26.93±3.48 ) pA/pF, n=16]较对照组 [(34.12± 4.21) pA/pF, n=10]明显下降( t=2.706 , P<0.05);两组 Ito差异无显著性意义 (P >0.05). 结论 AMI可引起心室肌细胞INa 、 ICa-L和 IK1的下降,造成心肌传导速度下降和动作电位时程缩短、复极异常,可能是导致AMI后出现折返性室性心律失常的离子机制.

Alteration of ionchannel currents in ventricular myocytes of the rabbit 24 hours after acute myocardialinfarction

BACKGROUND:After acute myocardial infarction(AMI),there is still surviving myocardium in and around the infarcted area,which plays an important role in the occurrence of arrhythmia. OBJECTIVE:To study the alterations of the activities of Na+ channel current(INa),L-calcium current(ICa-L),transient outward K+ current(Ito) and inward rectifying K+ current(IK1) in the cardiomyocytes in the infarcted area after AMI. DESIGN: A randomized controlled study. SETTING:Department of Cardiology,Bethune International Peace Hospital. PARTICIPANTS:The experiment was finished in the Central Laboratory of the Department of Cardiology,Bethune International Peace Hospital from January to June 2003.Twenty New Zealand pure big-ear rabbits were randomly divided into AMI group(n=10) and control group(n=10). INTERVENTIONS:Rabbit AMI models were established by ligation of the left anterior descending coronary artery.The ventricular myocytes were separated with the method of enzymatic dissociation technique,and the changes of the ion currents were recorded with the whole cell patch-clamp techniques. MAIN OUTCOME MEASURES:The changes of INa,ICa-L,Ito and IK1 in the cardiomyocytes taken from the infarcted area of epicardium 24 hours after AMI in both the AMI and control groups. RESULTS:Twenty-four hours after AMI,the peak current densities of INa,ICa-L and IK1 in the AMI group [(28.48± 3.53) pA/pF,n=16;(3.91± 0.95) pA/pF,n=12;(26.93 ± 3.48) pA/pF,n=16]were all significantly reduced as compared with those in the control group [(45.50± 5.33) pA/pF,n=12;(5.58± 1.53) pA/pF,n=10;(34.12± 4.21) pA/pF,n=10] (t=3.026,P< 0.01;t=2.985,P< 0.01;t=2.706,P< 0.05).There was no significant difference in the Ito density between the AMI group and control group (P >0.05). CONCLUSION:The reduce of INa,ICa-L and IK1 caused by AMI can result in the decrease of myocardial conduction velocity,the shortening of action potential-time,abnormal repolarization,which is possibly the ionic mechanism for the reentrant ventricular arrhythmia after AMI.