微管的差异性重塑引起运动性心肌损伤的机制研究  

The Mechanism Research of the Exercise Myocardial Injury Caused by Diversity Remodeling of Tiny Tubes

作　　者：朱英伟[1] 张晶 

机构地区：[1]渤海大学体育教研部,辽宁锦州121000 [2]辽宁省心脑血管药物基础研究重点实验室,辽宁锦州121001

出　　处：《西安体育学院学报》2014年第6期717-721,共5页Journal of Xi'an Physical Education University

基　　金：辽宁省自然科学基金资助项目(201102002)

摘　　要：目的探讨心肌细胞微管的缺失是否是早期心肌损伤的机制之一。方法跑台法制备大鼠运动性心肌肥厚及运动性心肌损伤模型。利用心电图结合血流动力学指标评价大鼠心功能;HMI评价心脏肥厚程度;激光共聚焦显微镜下观察α-微管形态差异,并进行荧光强度定量分析;RT-PCR法检测心肌组织中ANP和BNP的mRNA表达情况。结果一般训练组心肌细胞骨架无缺损,增生后可恢复正常;心功能可从代偿期恢复至常规状态。过度训练组大鼠心肌细胞骨架出现缺损,增生后不能恢复正常;心功能也不能恢复至状态。结论微管的重构先于心功能改变发生,心肌细胞微管的缺失是早期心肌损伤的机制。Objective To explore the mechanisms of whether the deficiency myocardial cell microtubules as indicators of early myocardial injury. Methods A method of using run for making rats athletic myocardial hypertrophy and athletic myocardial injury model. Evaluation of rat cardiac function use of electrocardiogram combined with hemodynamic parameters ; Evaluation hypertrophy degree on heart--HMI; under the confocal microscope to observe the c~ - microtubules morphological differences and quantitative analysis of fluorescence intensity; use the RT - PCR method to detect the expression of mRNA of ANP and BNP in the myocardial tissue. Results There isn＇t deficiency of the myocardial cytoskeleton of general training group, it can return to normal after hyperplasia; Cardiac function can recover to normal status from compensatory period. There is deficiency of the myocardial cytoskeleton of excessive training group, it cann＇t return to normal after hyperplasia; Cardiac function cannot return to normal state. Conclusions The reconstruction of the microtubules is earlier than cardiac function change, the deficiency of cardiac muscle cell microtubules is the mechanisms of early myocardial injury.

关 键 词：运动性心肌肥厚 微管 细胞骨架 心肌损伤 

分 类 号：G804.53[文化科学—运动人体科学]