尾吊对大鼠心肌损伤及其机制探讨

Research on Injury of Myocardium in Rats Induced by Tail Suspension and It’s Mechanism

目的研究尾吊对大鼠心肌细胞的损伤作用及其机制。方法雄性SD大鼠分为5组,采用鼠头低位30°尾吊方法模拟失重不同时间,测定各组动物血清LDH和CK-MB活性和血液儿茶酚胺和糖皮质激素浓度;检测线粒体ATP合成的速率和线粒体膜通透性转换孔(MPTP)开放程度。结果尾吊2周出现明显的心肌缺血性ST段升高和T波高耸、血清LDH和CK-MB活性升高(P<0.05)。尾吊第2周开始血液中儿茶酚胺和糖皮质激素显著升高(P<0.05),第3周开始出现心肌线粒体ATP酶合成活力的显著下降(P<0.05)和线粒体膜通透性转换孔的开启。结论循环血中儿茶酚胺和糖皮质激素的升高可能是尾吊致心肌损伤的重要内分泌机制,线粒体能量代谢的紊乱是介导心肌细胞损伤的重要细胞内机制。

Objective To investigate the injury of myocardium in rats induced by tail suspension and it＇s mechanism. Methods Tail-suspended SD rat model was used to simulate weightlessness. The activity of LDH and CK-MB were determined with biochemical methods. High pressure liquid phase and radioimmunoassay were used to detect the concentration of catecholamine and glucocorticoid,respectively. ATP synthesis rate of mitochondria was measured with luciferin-luciferase luminescent technique. The opening of MPTP was measured by fluorescent probe fluid dialysis setting. Results After 2 weeks of tail suspension, Specific change, ST segment shift and T wave height of myocardial ischemia was detected by electrocardiogram. The activity of LDH and CK-MB in serum increased significantly （P 〈 0.05） after 3 weeks of tail suspension. Two weeks of tail suspension later, catecholamine and glucoeorticoid concentration in serum increased significantly （ P 〈 0.05）. Three weeks of tail suspension later, ATP synthesis rate of myocardial mitochondria decreased significantly （P 〈0.05） and the opening of mitochoudrial membrane permeability transition pore （MPTP） emergened. Conclusion Increasing of catecholamine and glucocorticoid concentration in serum maybe is the important mechanism of myocardial damage induced by tail suspension. Disorder of mitochondrial energy metabolism is the important intracellular mechanism.