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目的 探讨硒对大鼠心电图及心肌细胞动作电位的影响。方法 对Ｗ ｉｓｔａｒ雄性大鼠腹腔内注射亚硒酸钠（２ｍ ｇ·ｋｇ－１·ｄ－１），连续９ 周，应用心电图和细胞内玻璃微电极技术，观察正常大鼠和阿霉素致心肌损伤大鼠心电图及心肌细胞动作电位的变化。结果 硒组心电图较实验前及对照组无变化（ Ｐ ＞ ０．０５ ），心肌细胞复极达峰值电位５０％ 所需时间（ＡＰＤ５０）延长（ Ｐ ＜ ０．０５ ）。ＡＤＭ 组和硒＋ ＡＤＭ 组心电图Ｑ－Ｔ 间期及心肌细胞ＡＰＤ５０、ＡＰＤ９０较对照组及试验前均延长（ Ｐ＜ ０．０１）。心率、静息电位（ＲＰ）、动作电位幅度（ＡＰＡ）及动作电位０ 相最大去极化速率（Ｖｍ ａｘ）无变化（ Ｐ ＞ ０．０５）。结论 硒能延长正常大鼠心肌细胞ＡＰＤ５０，不能逆转阿霉素心肌损伤大鼠ＡＰＤ５０、ＡＰＤ９０及Ｑ—Ｔ 间期延长。此结果对于心肌病的防治具有重要意义。
Objective To investigate the effect of selenium on electrocardiogram and action potential of cardiomyocytes in rats. Methods Wistar male rats were injected intraperitoneally with sodium selenite (2 mg · kg-1 · d-1) for 9 weeks. Electrocardiogram and intracellular glass microelectrode technique were used to observe the effects of adriamycin Changes of Electrocardiogram and Action Potential of Myocardial Cells in Rats with Myocardial Injury. Results Electrocardiogram in selenium group showed no change (P> 0.05) compared with those in control group and APD50 (P <0.05). The Q-T interval and the APD50 and APD90 levels of cardiomyocytes in ADM group and selenium + ADM group were longer than those in control group and before experiment (P <0.01). Heart rate, resting potential (RP), action potential amplitude (APA), and maximum potential depolarization rate (Vm ax) did not change (P> 0.05). Conclusion Selenium can prolong the APD50 of normal rat cardiomyocytes, and can not reverse the prolongation of APD50, APD90 and Q-T of rats with adriamycin-induced myocardial injury. This result is of great importance for the prevention and treatment of cardiomyopathy.