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目的:观察睡眠剥夺对低压低氧环境急性暴露大鼠认知功能的影响。方法:采用低压低氧舱模拟海拔4 000m低压低氧环境,对S-D大鼠分别进行24h、48h、72h睡眠剥夺,通过水迷宫实验观察认知功能的变化,用免疫荧光法观察海马区Bax、Caspase-3的表达。结果:1与对照组比较,睡眠剥夺24h、48h、72h,均延长了水迷宫实验S-D大鼠的平均逃逸潜伏期(P<0.01),暴露的时间越长,潜伏期越长(P<0.05);2与对照组比较,睡眠剥夺72h组海马CA1/CA3区caspase-3阳性的神经元明显增多(P<0.05),睡眠剥夺48h组海马CA1/CA3区Bax阳性的细胞数明显增多(P<0.01)。结论:睡眠剥夺可加重急性低压低氧暴露大鼠认知功能的损害,其机制可能与海马区细胞的凋亡分子表达有关。
Objective: To observe the effects of sleep deprivation on cognitive function in acute hypoxia-exposed rats. Methods: Low pressure hypoxic chamber was used to simulate hypoxia environment at 4 000 m altitude. SD rats were deprived of sleep for 24 h, 48 h and 72 h respectively. The changes of cognitive function were observed by water maze test. The expression of Bax, Caspase-3 expression. Results: 1 Compared with the control group, sleep deprivation for 24 h, 48 h and 72 h prolonged the mean escape latency of water maze test rats (P <0.01). The longer the exposure time, the longer the incubation period (P <0.05). Compared with the control group, the number of caspase-3 positive neurons in hippocampal CA1 / CA3 area in sleep deprivation 72h group increased significantly (P <0.05), and the number of Bax positive cells in hippocampal CA1 / CA3 area significantly increased after sleep deprivation for 48h ). Conclusion: Sleep deprivation can aggravate the impairment of cognitive function in rats exposed to acute hypobaric hypoxia. Its mechanism may be related to the expression of apoptotic molecules in hippocampal cells.