目的研究硒（Ｓｅ）铁（Ｆｅ）微量元素异常时心肌细胞损害的机理。方法用细胞内微电极技术分别测定饲养１４周后大鼠心肌细胞电生理的改变。结果与对照组相比，单纯高Ｆｅ组无变化；单纯低Ｓｅ组ＲＰ、ＡＰＡ降低、ＡＰＤ５０延长；低Ｓｅ并高Ｆｅ组ＲＰ、ＡＰＡ也降低，但与低Ｓｅ组相比无显著性差异，ＡＰＤ５０则明显延长。提示低Ｓｅ是心肌细胞损害的基本原因，高Ｆｅ对心肌损害有一定的协同作用 Aim To study the mechanism of cardiomyocyte damage induced by trace elements in Se (Fe). Methods The electrophysiological changes of rat cardiomyocytes were measured respectively by intracellular microelectrode technique after 14 weeks of rearing. Results Compared with the control group, there was no change in the group of high Fe alone. The RP and APA of the group with low Se and the group of APD50 were prolonged. The RP and APA of the group with low Se and high Fe were also decreased. However, APD50 was significantly extended. Tip low Se is the basic reason for myocardial cell damage, high Fe on myocardial damage have some synergy