【摘要】 探讨应激反应对心肌缺血再灌注损伤的保护作用及其机制。方法：按改良的Ｋａｎｅ方法，制备 心肌缺血再灌注损伤模型。观察结扎左冠状动脉前、后的 １、５、１０ｍｉｎ及再灌注１０ｍｉｎ内心功能指标及再灌注期 间的室速（ＶＴ）、室颤（ＶＦ）发生率及动物死亡率（Ｍ），并测定心肌丙二醛（ＭＤＡ）含量及超氧化物歧化酶（ＳＯＤ）的活 性与对照组比较。结果：实验组的心功能明显的得到了改善；ＶＴ、ＶＦ及Ｍ均明显降低；心肌内ＭＤＡ含量明显减 少，而ＳＯＤ的活性则明显增加.结论：应激反应具有抗心肌缺血再灌注损伤作用，主要作用机制与其增强心肌内 源性抗氧化能力有关。更多还原

【Abstract】 Objective: To study the effect and the mechanism of the protection of stress response on myocardial ischemia reperfusion injury. Methods: According to the modified Kane method, the model of myocardial ischemias-reperfusion injury was made. We observed the cardiac function indexes 1,5, 10 min before and after the ligation of the left coronary artery and 10 min during reperfusion. We also observed the incidences of ventricular tachycaridia, and ventricular fibrillation and the superoxide dismutase activity were determined. Results: The cardiac function were significantly improved, and the ventricular tachycardia, ventricular fibrillation and the animal mortality were significantly lowerd, and the myocardial MDA contents decreased, and the myocardial SOD activity increased in the experiment group. Conclusion: The results indicated that the stress response could against rats myocardial ischemia-reperfusion injury and that the main mechanism was related to enhancement of the myocardial endogenous antiotidative activity.更多还原