目的 观察鼠神经生长因子早期干预对大鼠急性一氧化碳中毒迟发性脑病的防治疗效，并初步探讨迟发性脑病的发病机制。方法 将92只180～230 g、雄性Wistar大鼠随机分成2个实验组(每组n=40)和健康对照组(n=12)，即一氧化碳中毒组(COP组);鼠神经生长因子组(NGF组);健康对照组(NC组)。实验组按150 mL·kg^-1腹腔内注射一氧化碳制备急性一氧化碳中毒动物模型，对照组注射等体积空气。神经生长因子组在中毒后30 min内给予肌肉注射鼠神经生长因子(18 μg·kg^-1·d^-1，共7 d)，而对照组和一氧化碳中毒组则注射等剂量生理盐水。监测中毒后90 min和7、14、21 d各组大鼠血清中髓鞘碱性蛋白(MBP)的含量，并在上述各时间点处死动物取脑组织，常规制备冰冻病理切片，行HE及MBP免疫组化染色。分别在中毒后7、14、21 d各时间点采用Morris水迷宫评估动物的智力状态，以正确穿越平台次数少于3次判定为迟发性脑病。结果 中毒后所有大鼠呈现典型一氧化碳中毒表现。实验组大鼠共死亡29只，其中一氧化碳中毒组15只，NGF组14只，死亡率分别为37.50%、35.50%。Morris水迷宫结果显示:一氧化碳中毒组中有8只大鼠被判定为迟发性脑病;神经生长因子组中有5只被判定为迟发性脑病;一氧化碳中毒组大鼠血清中髓鞘碱性蛋白含量增高显著，神经生长因子组接近正常。差异在中毒后7、14 d最明显。病理学检查结果显示一氧化碳中毒组出现迟发性脑病大鼠在中毒90 min~21 d内在脑海马、皮层下出现神经元损伤、髓鞘碱性蛋白脱失等病理改变。上述病理改变在各组中均可观察到，一氧化碳中毒组大鼠病变程度重，神经生长因子组则较轻。结论 鼠神经生长因子可显著降低大鼠迟发性脑病的发生率，而不能降低其死亡率。髓鞘碱性蛋白在迟发性脑病的发病机制中可能起着重要作用。

OBJECTIVE To observe the mouse nerve growth factor on early intervention in rats with acute carbon monoxide intoxication delayed encephalopathy control effects, and preliminarily discuss the pathogenesis of delayed encephalopathy. METHODS Ninety-two weight only 180-230 g, male Wistar rats were randomly divided into two experimental groups (n=40), and a healthy control group (n=12), namely the CO poisoning group (COP) of the group; mouse nerve growth factor (NGF plays group); healthy controls (NC group). Experimental group was according to 150 mL·kg^-1 intraperitoneal injections of CO in the preparation of animal model of acute carbon monoxide poisoning, in the control group rats were injected with equal volume of air. NGF group rats were injected within 30 min after poisoning muscle injection of mouse nerve growth factor, once a day, every time 18 μg·kg^-1, total 7 days; Control group and the COP were given intramuscular isodose physiological saline. NGF group rats were treated with 18 μg·kg^-1·d^-1 NGF (total 7 times); NC group and COP group treated with the same dose saline. 90 min, 7 day,14 day and 21 day groups of rats serum myelin basic protein (MBP) levels were monitored. The routine preparation of brain tissue frozen pathology slice, line HE and MBP immunohistochemical staining. Animal intelligence is assessed by Morris water maze experiment, in the 120 s in rats to determine correctly through the platform number less than 3 times DEACMP. RESULTS All rats showed typical toxic after CO poisoning. Experimental group rats died 29, including COP death cases in the group, the model NGF group of 15, 14, mortality rates were 37.50%, 35.00% respectively. Morris water maze experiment results showed that the COP in the group 8 rats were judged to be delayed encephalopathy; model NGF group has 5 only be judged to be delayed encephalopathy; COP group rats serum MBP content increased significantly, model NGF group close to normal.Differences were obvious in poisoning after 7 days, 14 days.Pathological examination showed the COP group delayed encephalopathy rats in poisoning 90 min-21 d in hippocampus, subcortical neurons damage, such as myelin basic protein depigmentation pathological changes.The above pathological changes can be observed in each group, the COP group rats lesion severity is heavy, model NGF group was lighter. CONCLUSION Mouse nerve growth factor can significantly reduce the incidence of delayed encephalopathy in rats, but can't reduce the mortality. Myelin basic protein (MBP) in the pathogenesis of delayed encephalopathy may play an important role.