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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
Objective: To observe the protective effect of nimodipine on delayed brain injury induced by subacute carbon monoxide poisoning (CO). Methods: mice were injected intraperitoneally with CO 100 mL / kg once daily for 7 days. After the administration of CO was stopped, the mortality of CO-poisoned mice was measured, the ability of passive avoidance learning and memory was measured, the histopathological examination was performed, and the activity of monoamine oxidase-B was measured. Nimodipine (1 mg / kg) was injected intraperitoneally 30 minutes prior to each administration of CO. Results: Nimodipine pretreatment can significantly reduce the mortality of mice with CO poisoning, basically reversing the learning and memory impairment caused by CO poisoning in mice; can prevent the delayed death of hippocampal neurons; and can block CO poisoning caused by monoamine oxidase - B activity increased. Conclusion: Nimodipine has a significant protective effect on delayed brain injury induced by subacute carbon monoxide poisoning