力竭运动后不同时相大鼠心肌细胞间粘附因子-1的变化

The Change in Rat Myocardial ICAM-1 at Different Time Courses after Exhausted Exercise

目的:探讨力竭运动后不同时相大鼠心肌细胞间粘附因子(ICAM-1)表达的变化特点。方法:100只健康成年雄性SD大鼠,分为一次力竭游泳运动组(n=40)、2周反复力竭游泳运动组(n=40)及相应对照组(n=20),对照组不运动。分别于力竭运动后0、6、12及24小时取材,应用免疫荧光技术和图像分析方法研究大鼠心肌ICAM-1含量的变化。结果:两种力竭运动后,大鼠心肌细胞快速表达,运动后6小时后达到峰值,蛋白含量变化呈先上升后下降的趋势;除反复力竭后24小时组与对照组无显著性差异(P>0.05),其他各时相组与对照组相比均有不同程度升高(P<0.01)。比较两种力竭运动后ICAM-1蛋白含量发现,反复力竭后即刻大鼠心肌各部位ICAM-1蛋白含量均高于一次力竭后即刻组(P<0.01),力竭后6小时组各部位之间无显著性差异(P>0.05),12小时和24小时组,一次力竭后大鼠心肌各部位ICAM-1蛋白含量要高于反复力竭(P<0.01)。结论:不同力竭运动后心肌细胞ICAM-1水平的升高可以诱导细胞因子的激活,介导心肌细胞的粘附和浸润等炎症反应,构成运动性心肌微损伤的发生机制之一。

Objective To investigate the change in the content of intracellular adhesion molecule-1 （ICAM-1）inmyocardium of rats at different time courses after exhausted exercise. Methods One hundred male SD rats were divided into sedentary control group,single bout of exhausted exercise group and 14-day consecutive exhausted exercise group. Rats were killed at 0,6,12 and 24 hours after exhausted exercise. Immunofluorescence technique andimage analysis method were used to study the dynamic changes in the content of ICAM-1 in myocardium. Results Comparing with the control group,following these 2 modes of exhausted exercise,the content of ICAM-1 in ratmyocardium increased and reached its peak value 6 hours after exercise,and then decreased,and ICAM-1 content inall other time courses were significantly increased （P〈0.01）after exhaustive exercise,except 24h after exercise group（P〉0.05）. ICAM-1 content from different parts of myocardium immediately after consecutive exhausted exercisewas significantly higher than that after single bout of exhausted exercise （P〈0.01）,and the differences disappeared 6 hours after exercise （P〉0.05）. ICAM-1 content in 12- and 24-hour single bout of exhausted exercise groups was significantly higher than that in consecutive exhausted exercise groups （P〈0.01）. Conclusion The increase of ICAM-1 level in myocardium after different modes of exhausted exercise can activate cytokine,mediate inflammatory responses of myocytes,such as adhesion and infiltration,which contribute to the exercise-inducedmyocardial micro-injury.