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.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2008年第1期71-75,共5页
Chinese Journal of Applied Physiology
