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作 者:魏燕[1,2] 周京京[1] 杨晶[1] 张娇[1] 张利萍[1] 张翼[1,3]
机构地区:[1]河北医科大学生理学教研室,石家庄050017 [2]泸州医学院心血管病研究所电生理研究室,泸州646000 [3]河北省医学生物技术重点实验室,石家庄050017
出 处:《生理学报》2013年第3期285-292,共8页Acta Physiologica Sinica
摘 要:本研究旨在应用全细胞膜片钳技术观察白藜芦醇甙(polydatin)对大鼠心室肌细胞瞬时外向钾通道电流(Ito)、稳态外向钾通道电流(Iss)和内向整流钾通道电流(IK1)的影响。结果显示:(1)白藜芦醇甙(10μmol/L以上浓度)可通过非浓度依赖性方式增加心室肌细胞IK1。(2)白藜芦醇甙对心室肌细胞Ito无影响,对Ito的激活、失活和失活后的恢复动力学亦无影响。(3)白藜芦醇甙对心室肌细胞Iss无明显影响。以上结果提示,白藜芦醇甙对大鼠心室肌细胞IK1具有激活作用,可增加IK1,但对Ito和Iss无明显影响;白藜芦醇甙对IK1的作用可能是其抗心律失常作用的离子机制之一。The aim of this study was to investigate the effect of polydatin on transient outward potassium channel current (Ito), steady-state outward potassium channel current (Iss) and inward rectifier potassium channel current (IK1) in ventricular myocytes of rat using the whole-cell patch clamp technique. The results showed: (1) Polydatin (above 10 μmol/L) increased IK1 of ventricular myocytes in a non-concentration dependent manner. (2) Polydatin neither had any effect on Ito peak current of ventricular myocytes, nor changed activation, inactivation and recovery kinetics of Ito. (3) Polydatin had no effect on Iss of ventricular myocytes. These results suggest that polydatin enhances IK1 channel activity, but has no effect on Ito and Iss channels in rat ventricular myocytes, which might be one of the ionic mechanisms for antiarrhythmic effect of polydatin.
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