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出 处:《中国应用生理学杂志》2008年第1期71-75,共5页Chinese Journal of Applied Physiology
摘 要:目的:探讨睡眠剥夺对大鼠心肌和抗氧化指标的影响。方法:大鼠随机分为睡眠剥夺2 d组(SD 2 d)、睡眠剥夺4 d组(SD 4 d)、睡眠剥夺6 d组(SD 6 d)、大平台对照组(TC)、正常对照组(CC),利用"小平台水环境法"建立大鼠睡眠剥夺模型,利用BL-410机能实验系统描记体表心电图,采用光镜及透射电镜观察心肌形态学改变,测定心肌线粒体丙二醛含量、超氧化物歧化酶活性。结果:睡眠剥夺组大鼠心率加快,心电图出现缺血性改变;心肌细胞染色质、肌浆网、线粒体、闰盘等亚细胞结构出现损伤性改变,部分心肌纤维溶解、坏死,心肌间质水肿、出血、炎性细胞浸润;心肌线粒体MDA水平升高,SOD活性随睡眠剥夺时间延长有降低趋势。结论:睡眠剥夺能够引起大鼠心肌损伤,其引起的氧化应激可能是心肌损伤的机制。Aim: To explore the effects of sleep deprivation(SD) on myocardium and its antioxygen index. Methods: 35 Sprague-Dawley rats were randomly divided into five groups: Cage control, Tank control, SD 2 d, SD 4 d and SD 6 d. The "flower pot" technique was used to establish rats sleep deprivation model followed by record of surface electrocardiogram, detection of myocardiurn morpholo- gy changes under microscope and transmission electron microscope and investigation of MDA content and SOD activity of myocardial mitochondria. Results: After sleep deprivation, heart rate increased and ECG showed ischemia of myocardium; subcellular organelles such as chromosome, endoplasmic reticulurn, mitochondria, intercalated disk impaired, myofibril lysis or necrosis, and lipid peroxidation reaction effects spread widely; edema, bleeding of the rnicrovessels and invasion of the monocytes could be seen in the lumen. The MDA level increased and SOD activity increased followed by a decreased trend. Conclusion: Sleep deprivation can induce damage on myocardium, and the stress especially oxygen stress caused by SD may be the possible mechanism.
分 类 号:R338.8[医药卫生—人体生理学]
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