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目的:评估睡眠剥夺(SD)后大鼠心肌组织损伤程度并探讨其机制。方法:将60只实验大鼠随机分为6组,每组10只。采用改良的多平台SD法(MMPM)建立SD模型,观察SD对心肌组织中缺血修饰白蛋白(IMA)、高敏C反应蛋白(hs-CRP)、还原型谷胱甘肽(GSH)、丙二醛(MDA)、超氧化物酶(SOD)含量的影响。结果:与笼养组(CC组)和大平台组(TC组)相比,SD后大鼠心肌组织中IMA、hs-CRP、GSH及MDA的含量明显升高(P<0.05),且随着SD时间的延长有明显上升的趋势;而SOD的活性随着SD时间的延长有降低的趋势。结论:SD可引起大鼠心肌发生明显的氧化应激和炎症反应,且随着氧化应激和炎症反应的加重,心肌发生进行性缺血缺氧损害。
Objective: To evaluate the degree of myocardial injury in rats after sleep deprivation (SD) and to explore its mechanism. Methods: Sixty experimental rats were randomly divided into 6 groups with 10 rats in each group. SD model was established by modified multi-plate SD method (MMPM). The effects of SD on myocardial ischemia-reperfusion (IMA), high sensitivity C-reactive protein (hs-CRP), reduced glutathione (GSH) Dialdehyde (MDA), superoxide dismutase (SOD) content. Results: The contents of IMA, hs-CRP, GSH and MDA in myocardium of SD rats were significantly higher than those of CC group and TC group (P <0.05) The prolongation of SD time showed a significant upward trend; while the activity of SOD decreased with the extension of SD time. Conclusion: SD can induce obvious oxidative stress and inflammatory reaction in rat myocardium. With the aggravation of oxidative stress and inflammatory reaction, myocardial ischemia / hypoxia damage occurs.