Abstract: ［Abstract］ Objective〖HTSS〗〓To observe the effect of dexmedetomidine on neuronal apoptosis in neonatal rats with cerebral ischemia and hypoxia, and to explore the effect of dexmedemidine on neurological function and longterm learning and memory ability.
〖HTH〗〖WTHZ〗Methods〖HTSS〗〓Hypoxicischemic encephalopathy(HIE) was built for the model of cerebral ischemia and hypoxia. Ninety sevendayold(P7) SpragueDawley rats were randomized into five groups: sham operation group(S), the HIE group(R), the dexmedetomidine(25 μg/kg) group(D1), the dexmedetomidine(50 μg/kg) group(D2), the yohimbine group(5 μg)(Y). P7 rats were operated without hypoxia in S group, and continued hypoxia for 2 h in R group. After HIE 2 h, P7 rats were pretreated with different concentrations of dexmedetomidine(25 μg/kg,) in D1 group, and pretreated with dexmedetomidine(50 μg/kg) in D2 group and yohimbine(5 μg) in Y group. After 24 h, the expression of caspase3 was detected. Neurological deficit scores were used to evaluate neurological function. For 4 weeks after the intervention, Morris water maze test was used to evaluate the changes in learning and memory ability.
〖HTH〗〖WTHZ〗Results〖HTSS〗〓HIE in R group induced the upregulation of caspase3 and neurological deficit scores, compared with S group（P＜005）. Dexmedetomidine(25 μg/kg, 50 μg/kg) and yohimbine pretreatment markedly downregulated the expression of caspase3 and neurological deficit scores, compared with R group（P＜005）. The escape latency of R group was increased compared with S group, and reduced with D1, D2, Y group at 2th,3th,4th and 5th day after training（P＜005）. The escape latency of both D1 and D2 group were reduced at 2th,3th,4th and 5th day, and increased time of target quadrant compared with R group, and reduced compared with S group（P＜005）. Neurological deficit scores and the expression of caspase3 were significantly reduced in Y group compared with D1 and D2 group（P＜005）. There were not significant differences between D1 and D2 group in neurological deficit scores, the expression of caspase3 and Morris water maze test.
〖HTH〗〖WTHZ〗Conclusion〖HTSS〗〓 HIE causes neuronal apoptosis in the hippocampus of neonatal rats, and decrease the ability of learning ang memory in longterm neonatal rats. The expression of caspase3 was inhibited by dexmedetomidine pretreatment(25 μg/kg, 50 μg/kg), which reduced the apoptosis of neurons . Dexmedetomidine treatment for neonatal rats during HIE could improve the longterm learning and memory ability of neonatal rats.

Key words: hypoxicischemic, brain, modes, animal, dexmedetomidine