左旋硝基精氨酸抗大鼠海马脑片缺氧损伤的电生理研究

THE EFFECT OF NOS INHIBITOR L-NNA AGAINST ANOXIC INJURY IN HIPPOCAMPAL SLICE

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

Objective: To confirm the effect of NOS inhibitor NG-Nitro-L-arginine(L-NNA) against brain injury during anoxia.Methods: By way of the electrophysiological recording technique, we observed the influence of L-NNA on orthodromic population spike(OPS) during anoxia in rat's hippocampal slices. Result: In the hippocampal slices treated with L-NNA, the recovery amplitude and recovery rate of OPS were 104.79±66.25% and 75.00% respectively, significantly higher than those of untreated slices (P<0.05). Conclusion: L-NNA can significantly protect brain from anoxic injury. The mechanism may be that L-NNA inhibits activation of nNOS and decreases the formation of neuronal NO during the early stage of anoxia, and the neurotoxic role of NO on the neurons is then mitigated.