Abstract
Objective To investigate whether intrauterine hypoxia and ischemia can produce long-time effects or NOSI can prevent these damages. Methods Fetal rat intrauterine distress model was constructed. The rats were divided into the normal group, hypoxia and ischemia reperfnsion group and treatment group. Pupa were given to surrogate mothers and the ability of learning and memory at 40 day of age after delivery were examined. Then the water maze test was performed to detect the space learning ability and memory function of rats, and the changing of synaptophysin levels in hippocampns were detected by immunohistochemical staining. Result Behavioral results show that fetal distress produces cognitive impairment demonstrated by Morris water maze performance including a higher escape latency score and a de-creased cross platform time. The COD of Syp positive immunoreactive product in hippocampus were less decreased than that in the normal group or NOSI group. But the behavioral results and the COD of synaptophysin had no difference between normal group and NOSI group. Conclusions Fetal distress produced cognitive impairment and led to the decreasing of synaptophysin in hippocampns. Effective measure can relieve these damages. Key words: Nitric-oxide synthase/AI/PD; Fetal distress/PP; Memory/DE; Synapsins/DE
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