Objective We set up an intermittent hypoxia (IH) animal model by simulating the features of obstructive sleep apnea-hypopnea syndrome (OSAHS) to observe the effects on cognitive function and hippocampus ultra-structure in rats exposed to 50 mL/L IH. Methods Totally 48 mature male Wistar rats were randomly assigned into two groups: 50 mL/L IH (50 mL/L IH) group and unhandled control (UC) group. The compressed air was given to UC group while rats in IH groups suffered from 8-hour IH every day for 2. 4. 6 or 8 weeks, respectively. The cognitive function of rats in 50 mL/L IH and UC groups was assessed with the Morris water maze (MWM) test, and the hippocampus ultra-microstructure was also observed. Results Compared with that in UC group, the synaptic ultra-structure of nerve cell nucleus, mitochondria and rough endoplasmic reticulum was significantly injured in 50 mL/L IH group in a time-dependant manner. MWM test showed that with prolonged hypoxia, the escaping latency was prolonged [(49.17±8.87)s at week 2 and (68.42±7.91)s at week 8], all longer than those in UC group [(25.66+2.97)s at week 2 and (25.29 + 3.07)s at week 8, respectively]. The frequency of crossing the platform was decreased in 50 mL/L IH group (7. 68+ 1. 6 at week 2 and 2. 87 ± 0. 92 at week 8, respectively), all lower than those in UC group (11.57±2.18 at week 2 and 10.65± 1.26 at week 8, respectively). Conclusion Intermittent hypoxia can cause cognitive dysfunction. This damage is related to the neuronal ultra-structure injury from prolonged intermittent hypoxia.%目的 通过模拟阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的发病特征,建立大鼠间歇性低氧(IH)模型,观察重度间歇低氧(50 mL/L)条件下不同暴露时间对大鼠学习记忆功能的影响和海马CA1区超微结构的改变.方法 成年雄性Wistar大鼠48只分为对照(UC)组和50 mL/L间歇性低氧(50 mL/L IH)组.UC组放入舱内仅给予压缩空气,50 mL/L IH组大鼠每日放入自制低氧舱内予间歇低氧暴露8h,分别干预2、4、6、8周.采用Morris水迷宫检测各组大鼠学习记忆功能,电镜观察海马区神经细胞超微结构.结果 与UC组比较,50 mL/L IH组中随低氧时间延长,神经细胞核、线粒体、粗面内质网、突触等超微结构损伤明显,水迷宫检测动物逃避潜伏期时间随缺氧时间增加而延长[从2周(49.17±8.87)s到8周的(68.42±7.91)s],均长于UC组[2周和8周分别为(25.66±2.97)s,(25.29±3.07)s]；50 mL/L IH组的穿台次数也随缺氧时间增加而减少(从2周7.68±1.6到8周的2.87±0.92),均少于UC组(2周和8周分别为11.57±2.18,10.65±1.26).结论 间歇性低氧可造成认知功能障碍,与海马区神经细胞超微结构损伤有关.
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