摘要
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 2 4h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 ,1h达最低值 ,并持续 2 4h ;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
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.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2004年第1期76-79,共4页
Chinese Journal of Pathophysiology
基金
山东省中青年学术骨干基金资助项目
山东省中医药科研基金资助项目 (No .2 0 0 1-81)
