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目的 观察神经元型一氧化氮合酶 (nNOS)及诱导型一氧化氮合酶 (iNOS)在急性一氧化碳 (CO)中毒过程中的变化 ,以探讨CO中毒脑损伤机制。方法 健康Wistar大鼠静式吸入 2 0 0 0～ 2 5 0 0ppmCO 40～ 5 0min以建立实验性急性CO中毒大鼠动物模型 ,采用冰冻切片技术 ,运用免疫组织化学SABC方法 ,分别检测急性CO中毒大鼠中毒后即刻、 1、 3、 6、 12h及1、 3、 7d各时点nNOS及iNOS在大脑皮质及海马CA1区的表达。结果 CO中毒后 1h大脑皮质及海马CA1区nNOS阳性细胞明显增多 (P <0 0 1) ,3h后下降恢复正常 ;iNOS阳性细胞于CO中毒后 3h明显增多 ,6h达高峰 ,12h后缓慢下降 (P <0 0 1) ,至 3d基本恢复正常。结论 急性CO中毒可致大鼠大脑皮质及海马CA1区nNOS与iNOS阳性细胞数增多 ,iNOS的变化较nNOS表现出延迟趋势 ;活性增强的NOS尤其是iNOS可能参与了急性CO中毒所致迟发性脑损伤
Objective To observe the changes of neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) in acute carbon monoxide (CO) poisoning in order to investigate the mechanism of brain injury induced by carbon monoxide poisoning. Methods Healthy Wistar rats were randomly inhaled for 200 ~ 250 mg / L for 40 ~ 50 min to establish experimental animal model of acute CO poisoning. Frozen section technique and immunohistochemical SABC method were used to detect acute CO poisoning Immediately after poisoning, the expression of nNOS and iNOS in cerebral cortex and hippocampal CA1 area were detected at 1, 3, 6, 12h and 1, 3, 7d respectively. Results The level of nNOS positive cells in cerebral cortex and hippocampal CA1 area was significantly increased 1h after CO poisoning (P <0.01), and returned to normal after 3h. The number of iNOS positive cells increased significantly 3h after CO poisoning and reached the peak at 6h, then decreased slowly after 12h P <0 0 1), to the 3d basic return to normal. Conclusions Acute CO poisoning can cause the increase of nNOS and iNOS positive cells in cerebral cortex and hippocampus CA1 area, and the change of iNOS is delayed than that of nNOS. The activity of NOS, especially iNOS, may be involved in the delayed onset of CO poisoning Brain Injury