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目的 通过研究雌雄激素替代法对大鼠离体心室肌细胞单相动作电位 (MAP)的影响及奎尼丁诱导下致心律失常作用性别差异性的机制 ,阐明性激素在尖端扭转型室性心动过速 (TdP)发生中的作用。方法 制造苯甲酸雌二醇、丙酸睾酮替代的大鼠模型 ,Langendorff法灌流离体大鼠心脏 ,采用MAP技术记录 6组大鼠 (①去势雌性大鼠 ;②去势雌性大鼠 +雌激素 ;③去势雌性大鼠 +雄激素 ;④去势雄性大鼠 ;⑤去势雄性大鼠 +雌激素 ;⑥去势雄性大鼠+雄激素 )的MAP ,比较组间的性别差异 ,并观察奎尼丁诱发各组早期后除极 (EAD)、TdP发生率的差异。结果 去势雌性大鼠 +雌激素组的单向动作电位时程 (MAPD)显著长于去势雌性大鼠 +雄激素组 ,去势雄性大鼠 +雌激素组MAPD显著长于去势雄性大鼠 +雄激素组 ;雌激素替代组与单纯去势组相比MAPD也延长 ,雄激素组则相反 ;而去势雌性大鼠组和去势雄性大鼠组无差别。各组在应用奎尼丁后MAPD都有显著延长 ,EAD发生率均较高 ;而雌激素替代组的EAD、TdP发生率都高于雄激素组。结论 雌雄大鼠发生TdP的性别差异性与性别本身无关 ,关键在于性激素的差异 ,雌激素可通过使心肌细胞在复极延长的基础上EAD发生增加 ,导致触发活动 ,从而发生TdP ;雄激素的作用则相反。
Objective To study the effects of estrogen and estrogen replacement on single phase action potential (MAP) of ventricular myocytes in vitro and the mechanism of gender differences induced by quinidine induced arrhythmia, and to clarify the mechanism of sex hormones in torsades de pointes Speed (TdP) in the role. Methods The rat model of estradiol benzoate and testosterone propionate was made. Langendorff’s method was used to perfuse the isolated rat heart. 6 groups of rats (① castrated female rats were recorded by MAP technique; ② castrated female rats + Hormone; ovariectomized female rats and androgen; ④ castration male rats; ⑤ castration male rats + estrogen; ⑥ castration male rats and androgen) MAP, and to compare the gender differences between groups To observe the difference of the incidence of early post-depolarization (EAD) and TdP induced by quinidine in each group. Results The MAPD in ovariectomized female rats + estrogen group was significantly longer than that in ovariectomized female rats + androgenic group. The MAPD in ovariectomized male rats + estrogen group was significantly longer than that in castrated male rats + In the androgen group, MAPD was also prolonged in the estrogen replacement group and in the castration group, while in the androgen group was opposite. In the castrated female group and the castrated male group, there was no difference. In each group, MAPD was significantly prolonged after application of quinidine, and the incidence of EAD was higher; while the incidence of EAD and TdP in estrogen replacement group was higher than that of androgen group. Conclusions The difference of sex of TdP between male and female rats has nothing to do with sex itself. The key lies in the difference of sex hormones. Estrogen may induce TAD by causing cardiomyocytes to increase EAD after prolonged repolarization, resulting in TdP. Androgen The opposite is true.