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目的 :为进一步证实一氧化氮合酶 ( NOS)抑制剂左旋硝基精氨酸 ( L -NNA)抗缺血缺氧性脑损伤的作用。方法 :在大鼠离体海马脑片 ,用电生理记录技术 ,观察 L-NNA对缺氧时海马脑片顺向群峰电位 ( OPS)的影响。结果 :使用 L-NNA的海马脑片缺氧后 OPS的恢复程度和恢复率分别为 10 4.79± 6 6 .2 5 %、75 .0 0 % ,与对照组相比有显著性差异 ( P<0 .0 5 )。结论 :L-NNA有明显抗缺氧脑损伤作用 ,作用机理可能是 L -NNA抑制了 n NOS活性 ,降低缺氧时神经源性 NO的形成 ,减轻 NO对神经细胞的毒性作用
Objective: To further confirm the role of nitric oxide synthase (NOS) inhibitor L-NNA against hypoxic-ischemic brain damage. Methods: In vitro rat hippocampal slices, the electrophysiological recording technique was used to observe the effect of L-NNA on cis-group peak potential (OPS) in hippocampal slices during hypoxia. Results: The recovery rate and recovery rate of OPS in hippocampal slices using L-NNA were 10 4.79 ± 6.62.5% and 75.0%, respectively, which were significantly different from those in control group (P < 0 .0 5). CONCLUSION: L-NNA has obvious anti-hypoxic brain injury. The mechanism may be that L-NNA inhibits the activity of nNOS, reduces the formation of neurogenic NO at hypoxia, and reduces the toxic effects of NO on nerve cells