力竭性运动致运动性心肌损伤的产生机制

Pathogenesis of myocardial injury induced by exhausted exercise

目的:研究力竭性运动诱发运动性心肌损伤的产生机制,为心肌损伤预防性措施介入提供理论依据。方法:将Wistar大鼠70只,随机分为空白对照组和力竭性运动组。大鼠运动性心肌缺血模型通过力竭性游泳运动来建立。分别于运动前和力竭性运动后即刻测定心肌酶谱、一氧化氮、内皮素、氧自由基和血液流变学的变化。然后立即处死动物,测定心肌一氧化氮、内皮素和氧自由基,并观察心肌组织病理性变化。结果:大鼠力竭性游泳运动后即刻肌酸激酶、肌酸激酶同功酶、乳酸脱氢酶活性犤(23.20±14.11),(3.94±2.25),(5.11±1.20)μkat/L犦明显高于空白对照组犤(3.72±2.04),(0.74±0.39),(2.76±1.90)μkat/L犦(t=4.3206,4.4358,3.3096,P<0.01);血清一氧化氮、丙二醛、超氧化物歧化酶和血浆内皮素水平也明显高于或低于空白对照组(t=2.7973～6.3741,P<0.05～0.01);心肌组织一氧化氮、丙二醛、超氧化物歧化酶和内皮素含量及血液黏度分别与空白对照组比较,差异也有显著性意义(t=3.4551～5.0690,P<0.01);心肌组织受损。结论:力竭性运动后,机体内一氧化氮和内皮素之间的失衡以及血液黏度的增加引起心肌缺血、缺氧而导致运动性心肌损伤,氧自由基等各种损害因子的产生则加重了这种损伤。

AIM: To study the mechanism of myocardial injury induced by exhausted exercise, so as to provide theoretical basis for the preventative methods of myocardial injury. METHODS: Seventy Wistar rats were randomly divided into control group and exhausted exercise group. The models of exercise-induced myocardial ischemia were established by exhausted swimming. The myocardial enzymogram, nitric oxide(NO), endothelin(ET), oxygen-derived free radical and hemorrheological changes were measured before exercise and immediately after exhaustive exercise. Then the animals were killed and the heart was removed at once for determination of the contents of NO, ET, oxygen-derived free radical in myocardial tissue,pathological changes of myocardial tissue were observed. RESULTS:The activities of creatine kinase(CK), CK MB-isoenzyme and lactic dehydrogenase(LD) immediately after exhausted swimming of the rats[(23.20±14.11),(3.94±2.25),(5.11±1.20) μkat/L] were significantly higher than those in the control group[(3.72±2.04),(0.74±0.39), (2.76±1.90) μkat/L] (t=4.320 6, 4.435 8, 3.309 6,P< 0.01).The serum levels of NO, malondialdehyde(MDA), superoxide dismutase(SOD) and plasma level of ET were significantly higher or lower of rats in the exhausted exercise group than in the control group (t=2.797 3 to 6.374 1, P< 0.05 to 0.01).The levels of NO, MDA, SOD and ET, and blood viscosity in myocardial tissue were significantly different between the two groups (t=3.455 1 to 5.069 0, P< 0.01).The myocardial tissue was damaged. CONCLUSION: After exhausted exercise, the unbalance between NO and ET, and the increase of blood viscosity result in myocardial ischemia and hypoxia, and then lead to exercise-induced myocardial injury, and the occurrence of all kinds of injurious agents such as oxygen-derived free radical aggravates this injury.