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目的:研制慢性疲劳综合征(Chronic Fatigue Syndrome,CFS)动物模型,并观察其血管内皮功能的变化。方法:将Wistar大鼠随机分为正常组与模型组,采用负重力竭游泳的方法建立CFS动物模型并进行评价,检测血管内皮形态及功能变化。结果:模型组大鼠行为出现改变,产生了心理与体力的疲劳状态,基本符合或类似于CFS的临床表现;模型组大鼠光镜、电镜均显示有内皮细胞损伤,血浆内皮素(ET)和血管性假血友病因子(VWF)明显升高(P<0.01);血清一氧化氮(NO)下降(P<0.05)。结论:采用负重力竭游泳制作的CFS大鼠模型与CFS发病机制和临床表现基本符合;模型大鼠存在血管内皮功能障碍,为CFS及“过劳死”的防治提供了实验依据。
Objective: To develop an animal model of Chronic Fatigue Syndrome (CFS) and observe its changes in endothelial function. Methods: Wistar rats were randomly divided into normal group and model group. CFS animal model was established and assessed by negative gravity swimming. The changes of morphology and function of vascular endothelium were detected. RESULTS: The behavior of rats in the model group changed, resulting in mental and physical fatigue, which was basically consistent with or similar to the clinical manifestations of CFS; light microscopy and electron microscopy of rats in the model group all showed endothelial cell injury and plasma endothelin (ET). VWF and von Willebrand disease factor (VWF) were significantly elevated (P<0.01), and serum nitric oxide (NO) was decreased (P<0.05). Conclusion: The CFS rat model produced by negative gravity exhausted swimming is basically consistent with the pathogenesis and clinical manifestations of CFS; model rats have endothelial dysfunction, which provides experimental basis for the prevention and treatment of CFS and overwork death.