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机构地区:[1]武汉科技大学医学院心脏电生理研究室,湖北武汉430080
出 处:《中国病理生理杂志》2006年第4期696-699,共4页Chinese Journal of Pathophysiology
基 金:湖北省自然科学基金资助项目(No.2003ABA189);湖北省教育厅科研基金项目(No.2002A01011)
摘 要:目的:研究缺氧对急性心肌梗死(AMI)大鼠心室肌细胞持续性钠电流的影响,以期更进一步探讨急性心肌梗死后心律失常的发生机制。方法:采用结扎大鼠冠状动脉左前降支建立AMI动物模型,应用膜片钳全细胞记录方法,观察AMI3周心室肌外膜梗死区细胞持续性电流(INap)的变化。结果:常氧条件下,假手术组(n=9)的INap电流密度为0·144±0·022(pA/pF),心梗组(n=9)的INap电流密度为0·121±0·013(pA/pF),明显低于假手术组(P<0·01),以上两组的INap均可被河豚毒素(TTX)阻断。缺氧条件下,假手术组和心梗组的INap均随着缺氧时间的延续而增大,但假手术组INap的增大明显大于心梗组,两组的INap均可被谷胱甘肽(1mmol/L)所阻断。结论:急性心肌梗死后,无论是在常氧或是再次缺氧情况下,心肌梗死区与非梗死区细胞INap的大小均存在差异,造成心肌复极离散度增大,可能是导致AMI后出现折返性室性心律失常的原因之一。AIM: To investigate the effect of hypoxia on persistent sodium current (INap) in single ventricular myocyte isolated from acute myocardial infarction (AMI) heart of rats and to study the mechanisms of cardiac arrhythmias that occur after AMI. METHODS: AMI model was induced by ligating the left anterior descending ceronary artery in rats. The whole-cell patch clamp technique was used to record the current in epicardial myocytes in infarcted region from rats at 3 week after AMI. RESULTS: In normoxic conditions, .the current density of INapin cardiomyocytes of fake operation (FO) and AMI hearts was 0.144 ± 0.022 pA/pF ( n = 9), 0.121 ± 0.013 pA/pF ( n = 9, P 〈 0.01 ), respectively, which was blocked by tetredotoxin (TTX). The amplitude of INap was gradually increased with the prolongation of hypoxia time, but the increase in extent of INap in FO cells was significant bigger than that in AMI cells. The INap was blocked by 1 mmol/L glutathione. CONCLUSIONS: After AMI, the amplitude of INap, in infarcted and noninfarcted myocardium showed differences both in normoxic and hypoxie conditions, which increased dispersion of repolarization. This may be one of the reasons of reentrant ventricular arrhythmias that occur after AMI.
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