摘要
目的采用颈交感干离断(TCST)模拟星状神经节阻滞,观察其对局灶性脑缺血再灌注损伤(CIRI)大鼠脑梗死容积及海马诱导型一氧化氮合酶(iNOS)表达等的影响,并探讨其脑保护作用的机制。方法将大鼠随机分成实验组(A组)、对照组(B组)和假手术组(C组);采用线栓法行大脑中动脉栓塞(MCAO)制作大鼠局灶性CIRI模型,A组于TCST后即行MCAO,2h后再恢复灌注;B组为单纯CIRI组;C组仅完成与A组相似的手术步骤但不造成MCAO、不行TCST;再灌注24h后观察各组大鼠神经行为学评分、脑梗死容积及海马iNOS的表达变化。结果A组大鼠脑梗死容积和神经行为学评分均低于B组(P<0.05);与A组、C组相比,B组大鼠海马iNOS的表达增加(P<0.05),而A组与C组间无显著差异(P>0.05)。结论TCST可通过下调大鼠海马iNOS的表达而对局灶性CIRI发挥脑保护作用。
Objective To use transection of cervical sympathetic trunk （TCST） to simulate stellate ganglion block（SGB）, to investigate its effects on cerebral infarct volume, the expressin of induced nitric oxide synthase（iNOS） in Hippocampus of rats during focal cerebral ischemia reperfusion injury（CIRI） ,and analyzing its neuroprotective mechanism. Methods All the animals were randomly divided into three groups： experiment group（group A）,control group（group B）and sham-operation group（group C）. focal cerebral ischemia was induced by middle cerebral artery occlusion（MCAO） with the intraluminal suture method. Group A with MCAO for 2 h followed by reperfusion after TCST;Group B only with CIR;In group C, the similar operation procedure were complete only but on MCAO and no TCST. The neurological deficit scores, the infarct size and the expression of iNOS were detected 24 h after reperfusion. Results The cerebral infarct size and neurological deficit scores of rats in group A were lower than that in group B（P〈0. 05）. The expression of iNOS in Hippocampus of rats in group g increased obviously campared to group A and C （P〈0.05） ,but there were no difference between group A and C（P〉0. 05）. Conclusions TCST was neuroprotective against focal CIRI throught decreasing the expression of iNOS in Hippcampus of rats.
出处
《卒中与神经疾病》
2008年第3期142-144,147,共4页
Stroke and Nervous Diseases
基金
湖北省教育厅优秀中青年人才项目(No2002B03001)
关键词
颈交感干
脑缺血再灌注
一氧化氮合酶
Cervical sympathetic trunk Cerebral ischemia reperfusion iNOS
