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目的观察阿托伐他汀对急性心肌梗死后非梗死区心肌细胞瞬间外向钾电流(Ito)的影响。方法选用新西兰纯种大耳白兔45只,随机分为3组各15只,分别为正常对照组(CON组);其他两组均采用结扎兔左前降支方法以建立心肌梗死模型后,一组为心肌梗死组(AMI组),分离左心室心肌梗死部位非梗死区(AMI-N)细胞,另一组为阿托伐他汀组,从手术日开始连续口服阿托伐他汀5mg/(kg·d),共7d,后分离AMI-N细胞。采用全细胞膜片钳记录技术分别记录非梗死区(AMI-N)心外膜心肌细胞(Epicardium,Epi)Ito密度。3组均在手术建立模型前抽取静脉血,用生化分析仪测定血清总胆固醇。结果 3组血清总胆固醇水平比较差异无统计学意义(P>0.05)。3组Epi细胞ItoⅠ~Ⅴ曲线均呈电压依赖的线性曲线,电流密度于+70m V电压时达峰值,CON组于+70m V电压时Ito电流密度为(115.83±6.04)p A/p F(n=15cells),AMI组为(72.29±8.74)p A/p F(n=15cells),阿托伐他汀组为(86.15±2.64)p A/p F(n=13cells),3组之间比较有明显差异(P<0.01或P<0.05)。结论 AMI非梗死区Epi细胞Ito密度与正常心肌细胞相比存在差异性,阿托伐他汀对心肌梗死非梗死区Ito密度的异常有部分改善作用。
Objective To observe the effect of atorvastatin on myocardial transient outward potassium current (Ito) in non-infarcted area after acute myocardial infarction. Methods Forty-five New Zealand purebred white rabbits were randomly divided into 3 groups (15 in each), which were normal control group (CON group). The other two groups were established by ligation of the left anterior descending artery to establish a model of myocardial infarction (AMI group). AMI-N cells were isolated from left ventricular myocardial infarction (AMI-N) group and atorvastatin group. Atorvastatin 5 mg / kg · D) for a total of 7 days before AMI-N cells were isolated. Whole cell patch clamp recording technique was used to record the Ito density of epicardium (Epicardium, Epi) in non-infarcted area (AMI-N). All three groups were drawn venous blood prior to the establishment of the model, and serum total cholesterol was measured by biochemical analyzer. Results There was no significant difference in serum total cholesterol between the three groups (P> 0.05). The Ito I ~ V curves of three groups of Epi cells showed a voltage-dependent linear curve, the current density peaked at + 70mV, the Ito current density was + (115.83 ± 6.04) pA / pF n = 15cells), AMI group (72.29 ± 8.74) p A / p F (n = 15cells) and atorvastatin group (86.15 ± 2.64) p A / p F There were significant differences (P <0.01 or P <0.05). Conclusion The Ito density of Epi cells in non-infarcted area of AMI is different from that of normal cardiomyocytes. Atorvastatin can partially improve the abnormality of Ito density in non-infarcted area of myocardial infarction.