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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 study the injury of rat tail cardiomyocytes and its mechanism. Methods Male Sprague-Dawley rats were randomly divided into five groups. The rats were sacrificed at different times by weight-bearing 30 ° tail-hanging method. The activities of serum LDH and CK-MB and the levels of catecholamine and glucocorticoid in blood were measured. The mitochondrial ATP synthesis rate And mitochondrial membrane permeability transition pore (MPTP) open degree. Results In the 2 weeks after tail suspension, the obvious myocardial ischemic ST segment elevation and T wave rise, the serum LDH and CK-MB activities increased (P <0.05). From the second week after the tail suspension, blood catecholamines and glucocorticoids were significantly increased (P <0.05), and at the third week there was a significant decrease (P <0.05) in mitochondrial ATPase activity and mitochondrial membrane permeability transition pore Open. Conclusion The increase of circulating catecholamines and glucocorticoids may be the important endocrine mechanism of myocardial injury induced by tail-hanging. The disturbance of mitochondrial energy metabolism is an important intracellular mechanism of cardiomyocyte injury.