一氧化氮与脑血管痉挛性神经元损伤和L-精氨酸的作用

目的:探讨一氧化氮(NO)与蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)所致神经元损伤的关系及L-精氨酸(L-Arg)的保护作用。方法: 应用血管内穿刺法建立大鼠SAH模型,将动物随机分为假手术组(SO组)、SAH组和SAH+L-Arg组。动态检测24 h内大脑顶叶皮层局部脑血流量(rCBF),测量基底动脉(BA)管径变化,测定不同时点血清NO(NO^-₂/NO^-₃)水平和血浆ET-1含量,并行海马神经元形态学观察。 结果: 假手术对各项指标无显著影响。SAH组术后rCBF迅速降低,1 h达最低值,并持续24 h;SAH后BA管径明显缩小;血清NO^-₂／NO^-₃含量明显减少,血浆ET-1含量逐渐增加,海马神经元显著损伤。与SAH组比较,SAH+L-Arg组rCBF下降的速度减慢、程度减轻;BA管径缩小的程度减轻;血清NO^-₂／NO^-₃水平降低和血浆ET-1含量增高的变化减轻;海马神经元损伤的程度减轻。结论: 血清NO浓度的降低参与了CVS性神经元损伤,L-Arg对之具有一定减轻作用。

Role of nitric oxide in cerebral vasospasm-inducedneuronal damage in rats

AIM: To investigate the role of nitric oxide in neuronal damage induced by cerebral vasospasm (CVS) following subarachnoid he morrhage (SAH) in rats. METHODS: Noncraniotomy models of SAH by a endovascular puncture method in Wistar rats were used and animals were divided i nto sham-operated group, SAH group and SAH L-arginine group. Dynamic changes of regional cerebral blood flow (rCBF) within 24 hours were monitored. Diameters of basilar artery (BA) were measured. Serum NO(NO - 2/NO - 3) and plasma endo thelin-1 content at different time points within 24 hours were also detected. RESULTS: Sham operation did not affect all of above parameters. In SAH group, rCBF reduced immediately after induction of SAH, reaching its lowe st at 1 h, persisting within 24 h. Diameter of BA significantly decreased after S AH. Serum NO - 2/NO - 3 decreased and plasma endothlin-1 increased statisti cally after SAH. In SAH L-arginine group, decline of rCBF was not as rapid and s evere as that in SAH group. L-arginine also effectively antagonized vasospasm of BA and damage of hippocampal neurons. Decrease of serum NO - 2/NO - 3 and increase of plasma endothlin-1 were not so obvious in SAH L-arginine group comp ared to SAH group. CONCLUSION: Decrease in NO is involved in the development of CVS- induced neuronal damage following SAH, and L-arginine partly increases serum NO and thus protectes ischemic brain neurons.