力竭运动对大鼠β-肾上腺素能受体介导的心肌细胞收缩的影响  

Effects of exhaustive exercise on contractile responses mediated by β-adrenoceptor in rat cardiac myocytes

作　　者：高利平[1] 刘颖[1] 孙红[1] 

机构地区：[1]徐州医学院生理学教研室,江苏徐州221002

出　　处：《中国应用生理学杂志》2013年第5期437-440,共4页Chinese Journal of Applied Physiology

基　　金：江苏省徐州市社会发展项目(XM08C063);徐州医学院院长专项人才基金项目(09KJZ31)

摘　　要：目的:观察力竭运动对β-肾上腺素能受体(β-AR)介导的心肌细胞收缩的影响;探讨力竭运动后心肌收缩功能障碍的产生机制。方法:16只SD大鼠随机分为静坐组和运动组(n=8),运动组大鼠经过一周(共5次)的力竭运动训练后,分离培养心肌细胞,阻断α1-AR后测定去甲肾上腺素(NE)刺激引起的细胞收缩幅度、收缩时间(TTP)及舒张95%时间(R95)的变化及不同浓度NE刺激下心肌细胞的收缩幅度。结果:与静坐组相比,运动组大鼠心肌细胞收缩幅度显著降低;β-AR介导的心肌细胞收缩幅度明显降低、TTP和R95延长;β-AR对NE的反应性减弱。结论:力竭运动后β-AR介导的心肌细胞收缩功能减弱,导致心肌收缩功能障碍。Objective： To investigate the effects of exhaustive exercise on contraction mediated by β-adrenoceptor （β-AR） in rat cardiac myocytes and to analyze the mechanism by which cardiac systolic dysfunction is caused after exhaustive exercise. Methods： Sixteen SD rats were divided randomly into sedentary group and trained group. Cardiac myocytes were isolated from sedentary group and trained group after five times of exhaustive exercise in one week. Shortening response to norepinephrin（NE）, time-to-peak contraction （TIP） and time-to-95 % relaxation （R95） were measured after α1-AR were blocked. Also shortening responses to different levels of NE were observed. Results： Shortening amplitudes in trained rat cardiomyocytes were lower than that in sedentary group. Compared with sedentary group, shortening amplitudes in- duced by β-AR stimulation were significantly decreased, meanwhile TIPs and R95 were prolonged when β-AR were activated in trained rat cardiomyocytes. β-AR responsiveness to NE was weakened in trained group compared with that in sedentary group. Conclusion： Decreased shortening cardiomyocyte systolic function stimulating by β-AR could result in cardiac systolic dysfunction after exhaustive exercise.

关 键 词：力竭运动 Β-肾上腺素受体 心肌细胞 收缩 

分 类 号：R331.3[医药卫生—人体生理学]