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采用犬全脑缺血动物模型，研究脑缺血／再灌注损伤对脑组织Ｌ－Ａｒｇ∶ＮＯ通路的影响。９只家犬随机分为全脑缺血／再灌注组和对照组。结果显示犬全脑缺血／再灌注８ｈ，与手术对照组比较，脑皮质ＮＡＤＰＨ阳性神经元和阳性纤维明显增加，脑皮质Ｎｉｔｒｉｔｅ含量显著增加（Ｐ＜０．０１），提示犬脑组织中存在一氧化氮合成酶，全脑缺血／再灌注损伤能激活脑组织Ｌ－Ａｒｇ∶ＮＯ通路，ＮＯ可能在脑缺血／再灌注损伤中发挥重要作用。
To investigate the effect of cerebral ischemia / reperfusion injury on the L-Arg: NO pathway in the brain of a canine model of global cerebral ischemia. Nine dogs were randomly divided into two groups: cerebral ischemia / reperfusion group and control group. The results showed that the NADPH positive neurons and positive fibers in cerebral cortex were significantly increased and the Nitrite content in cerebral cortex was significantly increased (P <0.01) 8 h after cerebral ischemia / reperfusion in dogs, suggesting that there was Nitric oxide synthase, global cerebral ischemia / reperfusion injury can activate L-Arg: NO pathway in brain tissue. NO may play an important role in cerebral ischemia / reperfusion injury.