心肌梗死后大鼠左心室肌细胞钾通道的重构

Potassium Channel Remodeling of Left Ventricular Myocytes in Infarcted Rats

目的:探讨心肌梗死后大鼠左心室肌细胞钾通道的重构及增加葡萄糖代谢对钾流的作用。方法:取体重200～250 g的雄性Sprague-Dawley(SD)大鼠8只,结扎左冠状动脉建立心肌梗死模型(心肌梗死组),采用酶解法获得单个左心室肌细胞,应用膜片钳全细胞记录技术记录钾电流。对照组5只不结扎冠状动脉。结果:心肌梗死组大鼠心脏重量、心脏／体重比及左心室肌细胞膜电容均较对照组显著增加,但瞬间外向性钾流(Ito)密度则显著降低,分别用1．5 mmol／L二氯乙酸及5 mmol/L丙酮酸在体外预处理心肌梗死后大鼠左心窒肌细胞4～5小时,瞬间外向性钾流密度恢复到对照组水平。结论:心肌梗死后大鼠左心室肌细胞钾通道存在重构,而增加葡萄糖代谢能使之恢复,提示糖代谢和钾通道功能间存在一定关系。

Objective： To investigate the potassium channel remodeling of left ventricular myocytes and the effect of increased glucose metabolism on potassium current in infarcted rats. Methods： The infarction model was established by ligation of left coronary artery＂ of male Sprague-Dawley rats （wt = 200- 250g）. Single left ventricular myocytes were obtained by enzymatic method and the whole-cell patch clamp technique was used to record potassium curreut. Results： Heart weight, heart to body weight ratio and left ventricular myocyte membrane capacitance were significantly high- er in infarcted rats than in the control rats. The Ito density in infarcted rats was significantly decreased compared with the control rats, but it returned to normal after in vitro pretreatment of the left ventricular myocytes with 1.5 mmol/L dichloracetic acid （DCA） or 5 mmol/L pyruvate for 4-5 hours. Conclusion ： There exists potassium channel remodeling in left ventricular myocytes of infarcted rats which can be reversed by increasing glucose metabolism. This suggests that there is some relationship between glucose metabolism and potassium channel function.