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背景:急性心肌梗死(acutemyocardialinfarction,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24hAMI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24h,AMI组INa电流密度峰值犤(28.48±3.53)pA/pF,n=16犦较对照组犤(45.50±5.33)pA/pF,n=12犦明显下降(t=3.026,P<0.01);AMI组ICa-L电流密度峰值犤(3.91±0.95)pA/pF,n=12犦较对照组犤(5.58±1.53)pA/pF,n=10犦明显下降(t=2.985,P<0.01);AMI组IK1电流密度峰值犤(26.93±3.48)pA/pF,n=16犦较对照组犤(34.12±4.21)pA/pF,n=10犦明显下降(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I
BACKGROUND: Myocardial myocardium in the infarct zone and in the peri-infarct peripheral area after acute myocardial infarction (AMI) often plays a key role in arrhythmia. Objective: To study the changes of sodium channel current (INa), L-type calcium channel current (ICa-L), transient outward potassium current (Ito) and inward rectifier potassium current (IK1) Design: Randomized controlled study. Unit: Department of Cardiology, Bethune International Peace Hospital. Materials: This experiment was performed at the Laboratory of Cardiology, Bethune International Peace Hospital from January 2003 to June 2003. Twenty New Zealand purebred rabbits were selected and randomly divided into two groups: AMI group and control group, with 10 in each group. Methods: The animal model of AMI was established by ligating the left anterior descending coronary artery of rabbit. The ventricular myocytes were isolated by enzymatic method. The changes of ion current were recorded by patch clamp whole cell recording. MAIN OUTCOME MEASURES: The changes of INa, ICa-L, Ito and IK1 in cardiomyocytes of AMI group and AMI group at 24 h after AMI. Results: At 24 h after AMI, peak current density of INa (28.48 ± 3.53) pA / pF in n = 16 in AMI group was significantly lower than that in control group (45.50 ± 5.33 pA / pF, n = P <0.01). The peak ICa-L current density (3.91 ± 0.95) pA / pF, n = 12 in AMI group was significantly lower than that in control group (5.58 ± 1.53 pA / pF, , P <0.01). The peak current density of IK1 in AMI group was significantly lower than that in control group (34.12 ± 4.21 pA / pF, n = 10 犤) at 26.93 ± 3.48 pA / pF P <0.05). There was no significant difference in Ito between the two groups (P> 0.05). Conclusion: AMI can induce ventricular myocytes Ⅰ