胺碘酮对大鼠心肌梗死后重构心肌细胞钾电流的作用

Effects of amiodarone on potassium currents in rat remodeling ventricular myocytes after myocardial infarction

目的观察胺碘酮对大鼠心肌梗死后重构心肌钾通道的作用,探讨胺碘酮对心肌梗死后电重构的影响。方法采用脂肪乳灌胃方法建立大鼠高脂血症模型后结扎冠状动脉左前降支建立急性心肌梗死动物模型,应用全细胞膜片钳技术记录急性心肌梗死模型大鼠胺碘酮灌胃1wk后重构区心室肌细胞内向整流钾电流(Ik1)、瞬时外向钾电流(Ito)的变化。结果在实验电压-120mV时,模型组大鼠心室肌细胞Ik1为(-15.66±1.40)PA/PF,较正常组(-21.02±1.95)PA/PF降低(n=4,P<0.01),胺碘酮组(-11.07±1.11)PA/PF,较模型组明显降低(n=4,P<0.05)。在实验电压+50mV时,模型组大鼠心室肌细胞内Ito为(7.29±1.02)PA/PF,较正常组(13.24±1.16)PA/PF降低(n=4,P<0.01),胺碘酮组(4.12±1.01)PA/PF,较模型组降低(n=4,P<0.05)。结论胺碘酮抑制心梗后重构心肌细胞的Ik1、Ito,影响动作电位的复极过程。

Aim To investigate the effect of amiodarone on potassium currents in rat remodeling ventricular myocytes after myocardial infarction, and study the effect of amiodarone on electroremodeling after myocardial infarction. Methods After hyperlipemia model in rat was set up by fat milk intragastric administration, left anterior descending coronary artery was ligated to set up acute myocardial infarction model. Whole cell patch clamp technique was used to record inwardly rectified potassium current（Ik1 ） and transient outward potassium current （Ito） in isolated rat ventricular myocytes of remodeling region. Results Ik1 of model group（ - 15.66 ± 1.40 ）PA/PF was significantly decreased compared with normal group（ -21.02 ± 1.95 ） PA/PF（ n =4 ,P 〈 0. 01 ） , amiodarone group（ - 11.07± 1. 11 ）PA/PF was obviously decreased than model group（ n = 4, P 〈 0.05 ）. I,o of model group （ 7.29 ± 1.02 ）PA/PF was significantly decreased than normal group（ 13.24 ± 1.16） PA/PF （ n = 4, P 〈 0. 01 ）, amiodarone group（4. 12 ± 1.01 ） PA/PF was obviously de- creased than model group（ n = 4, P 〈 0. 05 ）. Conclusion It can be concluded that amiodarone can inhibit potassium currents in rat remodeling ventricular myocytes after myocardial infarction and affect repolariza tion.