摘要
目的:进一步证实诱导型一氧化氮合酶(iNOS)催化所形成的一氧化氮(NO)在脑缺血/再灌注损伤中具有毒性作用。方法:将S-D大鼠双侧颈总动脉短暂夹闭3分钟,然后分成应用药物组-氨基胍(AG)和非药物组.48小时后取海马脑片,观察顺向群峰电位(oPS)以及组织学改变。结果;给药组大部分可见oPS发放.而对照组只见有突触前排放(pv)无oPS(P<0.05),两组超微结构也有明显差异。结论:本实验证明大鼠海马短暂缺血/再灌注后iNOS抑制剂可减轻神经元损害,即可抑制血由iNOS诱生表达所形成的NO在脑缺血/再灌注损伤中的毒性作用。
Objective: To confirm a neurotoxic action for NO generated by immunologic nitric oxide synthase (iNOS) in the rats exposed to transient foredrain ischemia/reperfusion injury. Methods: The transient forebrain ischemia/reperfusion was induced by transient clipping double side common carotid arteries for 3 mins in rats, then they were divided into non-medicine treatment group and medicine treatment group (Aminoguandine,AG). The hippocampal slices had been made in 48h after the transient forebrain ischemia/reperfusion in rats, the orthodromic population spike (oPS) in hippocampal slices and changes of histology in hippocampus of the rats between two groups were compared. Results: The occurrence rate of oPS obtained in the rats treated with AG after transient forebrain ischemia/reperfusion was higher than that of the control (P<0. 05) and there were marked differences between two groups in histologic ultrastructure. Condusion: NO generated by iNOS in the rats exposed to transient forebrain ischemia/rperfusion had neurotoxic action and iNOS inhibitor-AG could be resistant to NO neurotoxicity.
出处
《脑与神经疾病杂志》
2001年第2期74-76,共3页
Journal of Brain and Nervous Diseases