目的建立急性脑缺氧缺血的动物模型。
Objective To replicate the acute hypoxic ischemic brain damaged animal model.
背景：幼鼠脑缺氧缺血后，脑组织水肿加重，脑组织中一氧化氮及丙二醛水平增高。
BACKGROUND: After cerebral tissue ischemia and anoxia in young rats, the cerebral edema gets serious, and the levels of nitric oxide (no) and malondialdehyde (MDA) decrease.
结果表明，对小鼠抗脑缺氧、抗急性脑缺血及抗急性脑栓塞形成等均有显著的保护作用，其药效与腹腔注射尼莫地平溶液接近，显著优于灌胃给药。
Nimodipine liposomes could effectively protect the brain against damage, and were comparable to that after IP nimodipine injection but significantly better than that after ig administration.
结论重型脑损伤后24小时内存在脑缺氧、缺血，伤后第2 - 4天为脑氧合过度、脑充血。
Conclusions When the brain is severely injured, there is cerebral hypoxia or ischemia during the first 24 hours, and cerebral hyperemia in the following second-fourth days.
结论异丙酚可能通过抑制大脑缺氧，抑制神经元的凋亡，从而对大鼠局灶性脑缺血-再灌注损伤发挥保护作用。
Conclusion Propofol may inhibit hypoxia in the brain and the apoptosis of nerve cells in result of protecting the cerebral ischemia and reperfusion damage in rats.
新生儿中早产儿患上癫痫病的比例较高，围产期窒息、慢性功能性脑缺氧、先天性脑发育不良、脑缺血等是致病原因。
Preterm newborn child suffering from epilepsy in a higher proportion of perinatal asphyxia, chronic functional brain hypoxia, congenital dysplasia, and so is the cause of cerebral ischemia.
新生儿中早产儿患上癫痫病的比例较高，围产期窒息、慢性功能性脑缺氧、先天性脑发育不良、脑缺血等是致病原因。
Preterm newborn child suffering from epilepsy in a higher proportion of perinatal asphyxia, chronic functional brain hypoxia, congenital dysplasia, and so is the cause of cerebral ischemia.
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