尼莫地平对亚急性一氧化碳中毒致小鼠脑损伤保护作用(英文)

目的:观察尼莫地平对亚急性一氧化碳中毒(CO)致迟发性脑损伤保护作用。方法:小鼠腹腔注射CO100mL/kg,每天1次,连续7天。停止给予CO后,测定CO中毒小鼠死亡率,被动回避性学习记忆能力,进行脑组织病理学检查和测定单胺氧化酶-B活性。尼莫地平(1mg/kg)在每次给予CO前30分钟腹腔注射。结果:尼莫地平预先给予能显著降低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中毒引起的单胺氧化酶-B活性的升高。结论:尼莫地平对亚急性一氧化碳中毒致迟发性脑损伤有明显的保护作用

Protective effect of nimodipine against cerebral injury induced by subacute carbon monoxide intoxication in mice

AIM: To study the effects of nimodipine on delayed cerebral injury in mice from subacute carbon monoxide (CO) exposure. METHODS: Mice were exposed to CO (100 mL/kg, ip) once a day, continuously for 7 d. After 7-d CO-exposure, mortality in mice, changes in learning ability and memory using passive avoidance test, the pathomorphologic observation of brain tissue slices, and changes of monoamine oxide (MAO)-B activities in cerebral tissue were studied. Nimodipine was administered 30 min before CO-exposure every time. RESULTS: The preadministration of nimodipine decreased the mortality in mice, almost reversed the impairment of learning and memory function, prevented the hippocam-pal neurons agaist delayed death and blunted the rise of MAO-B activity after subacute CO poisoning of mice. CONCLUSION: Pretreatment with nimodipine markedly prevented mice from delayed encephalopathy after CO poisoning.