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目的：研究一氧化氮（ＮＯ）在缺血性脑损伤中的作用。方法：夹闭沙土鼠双侧颈总动脉２０ ｍ ｉｎ 制备前脑缺血性脑损伤模型，分生化组和病理组。每组又分：（１） 假手术组；（２） 缺血对照组； （３） 硝基－Ｌ－精氨酸（ＬＮＮＡ）组，分３种剂量（３，２０，５０ ｍ ｇ／ｋｇ ｉｐ）；（４） Ｌ－精氨酸（Ｌ－Ａｒｇ）组，３００ ｍ ｇ／ｋｇ ｉｐ。第１，２组仅ｉｐ 等量生理盐水。结果：缺血性损伤后脑含水量增加，一氧化氮合酶（ＮＯＳ）活性明显升高，ＬＮＮＡ剂量依赖性抑制ＮＯＳ活性，小剂量能明显减轻脑水肿。小、中剂量ＬＮＮＡ 能减轻缺血性损伤后海马ＣＡ１区和ＣＡ２区锥体细胞缺失，小剂量作用明显，大剂量加重细胞缺失。结论：脑缺血后ＮＯＳ活性明显增加，加重缺血性脑损伤。通过ＬＮＮＡ适当降低脑组织ＮＯＳ活性能明显减轻脑水肿和海马区细胞坏死，对脑损伤有保护作用
Objective: To study the role of nitric oxide (NO) in ischemic brain injury. Methods: The model of forebrain ischemic brain injury was established by clipping the common carotid arteries of 20 min in both sides of gerbils, divided into biochemical group and pathological group. Each group was divided into three groups: (1) sham-operated group, (2) ischemic control group and (3) LNNA group at 3 doses of 3,20 and 50 m g / kg ip); (4) L-arginine (L-Arg) group, 300 m g / kg ip. The first group 1,2 only ip equivalent amount of saline. Results: The brain water content increased, the activity of nitric oxide synthase (NOS) increased significantly after ischemic injury, LNNA dose-dependently inhibited the activity of NOS, while the low dose could significantly reduce cerebral edema. Small and medium doses of LNNA could reduce the pyramidal cell loss in the hippocampal CA1 and CA2 areas after ischemic injury, the effect of low dose was obvious, and the large dose aggravated the cell loss. Conclusion: The activity of NOS after cerebral ischemia is obviously increased, which aggravates the ischemic brain injury. By LNNA appropriate reduction of brain tissue NOS activity can significantly reduce brain edema and hippocampus cell necrosis, has a protective effect on brain injury