小鼠腹腔注射CO 10 0ml/kg,每天 1次 ,连续 7天 ,尼莫地平 (Nimodipine) 1mg/kg在每次给予CO前 30分钟腹腔注射。停止给予CO后 ,以CO中毒小鼠死亡率 ,被动回避性学习记忆能力改变 ,脑组织病理学和单胺氧化酶 -B活性改变为指标观察尼莫地平对一氧化碳中毒致小鼠迟发性脑损伤保护作用。结果显示 ,给予尼莫地平能显著降低CO中毒小鼠死亡率 ;基本逆转小鼠CO中毒引起的学习记忆能力的损害 ;能防止海马神经元细胞延迟性死亡 ;并能阻遏CO中毒引起的小鼠脑组织单胺氧化酶 -B活性的病理性升高。提示 ,尼莫地平对一氧化碳中毒致小鼠迟发性脑损伤有明显的保护作用 The mice were injected intraperitoneally with CO 10 0 ml / kg once daily for 7 days. Nimodipine 1 mg / kg was injected intraperitoneally 30 minutes prior to each administration of CO. After stopping the administration of CO, the protective effect of nimodipine on carbon monoxide poisoning-induced delayed brain injury was observed in mice with CO poisoning, the changes in passive avoidance learning and memory ability, brain histopathology and monoamine oxidase-B activity as indexes . The results showed that the administration of nimodipine can significantly reduce the mortality of CO poisoning mice; basically reversing the learning and memory impairment caused by CO poisoning in mice; preventing the delayed death of hippocampal neurons; and inhibiting CO poisoning-induced mice Pathological increase of monoamine oxidase-B activity in brain tissue. Tip, nimodipine on carbon monoxide poisoning induced delayed brain injury in mice have a significant protective effect