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作 者:薄冰[1,2] 常芸[1] 杨红霞[1] 温悦萌[1]
机构地区:[1]国家体育总局体育科学研究所,北京100061 [2]上海体育学院
出 处:《中国运动医学杂志》2012年第6期483-489,共7页Chinese Journal of Sports Medicine
基 金:国家体育总局体育科学研究所基本科研业务经费(10-01)
摘 要:目的:探讨力竭运动后不同时相心脏窦房结、房室结和浦肯野氏纤维离子通道相关因子KCNQ1基因和蛋白水平的表达特点,为运动性心律失常发生机制的阐明提供实验依据。方法:100只健康成年雄性SD大鼠随机分为一次力竭组(4组)、反复力竭组(4组)及其相应的安静对照组,每组10只。分别于力竭运动后即刻、4、12及24小时,应用激光显微切割技术定位并收集窦房结、房室结和浦肯野氏纤维细胞团,通过免疫荧光组化及实时荧光定量PCR检测KCNQ1 mRNA和蛋白表达。结果:一次力竭运动后4小时,窦房结、房室结和浦肯野纤维KCNQ1 mRNA与蛋白表达显著高于其对照组(P<0.05);反复力竭运动后4小时、24小时,窦房结和浦肯野纤维KCNQ1 mRNA与蛋白表达显著高于其对照组(P<0.05);反复力竭运动后12小时,房室结KCNQ1 mRNA与蛋白表达显著高于其对照组(P<0.05)。结论:不同力竭运动后心脏传导系统KCNQ1在mRNA和蛋白水平呈异常高表达,除房室结在反复力竭运动后改变略有差异外,窦房结、房室结和浦肯野氏纤维KCNQ1蛋白表达的时相性变化规律基本一致。反复力竭运动后心脏传导系统KCNQ1在mRNA和蛋白水平上变化均较明显,更易诱发运动性心律失常。Objective This paper presents our study on the mRNA and protein expression of KCNQ1 in sinoatrial node(SAN), atrioventricular node(AVN) and Purkinje's fibers at different time phases after exhaustive exercise, in order to provide the experimental evidence for clarifying the mechanism of exercise-induced arrhythmia. Methods One hundred healthy adult male SD rats were grouped into the acute single exhaustive swimming group(n = 40), 2-week repeated exhaustive swimming group(n = 40), and 2 control groups (10 rats for each group). The exercise rats were sacrificed at 0,4, 12, and 24 hours after exhaustive swimming, and rats in the control groups were sacrificed at the same time points as the exercised rats. The ceils of SAN, AVN and Purkinje's fiber were spotted and collected with the approach of laser micro dissection. The mRNA and protein expressions of KCNQ1 were analyzed by real-time fluorescent quantitative PCR,immunochemistry and image analysis. Results As compared to control group, the mRNA and protein expression of KCNQ 1 in cardiac conduction system increased greatly 4 hours after acute single exhaustive exercise (P 〈 0.05). The mRNA and protein expression of KCNQ1 in SAN and Purkinje's fiber increased greatly 4 hours and 24 hours after repeated exhaustive exercise when compared to control group (P 〈 0.05). The mRNA and protein expression of KCNQ1 in AVN increased greatly 12 hours after repeated exhaustive exercise (P 〈 0.05). Conclusion After exhaustive exercise, the abnormally increased expression of KCNQ1 mRNA and protein could cause the activation of potassium channel on cell membrane, and thus increase the outflow of potassium ion and change the process of action potential,which could be the pathological basis and mechanism of exercise-induced arrhythmia.
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