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The Protective Effect of Stellate Ganglion Block or Transection of Cervical Sympathetic Trunk on the Cerebral Ischemia-reperfusion Injury

Author: XiongLiangZhi
Tutor: ZhouQingShan；WangQingXiu
School: Wuhan University
Course: Anesthesiology
Keywords: SGB TCST brain ischemia-repermsion injury IL-8 iNOS Bax/Bcl-2 behavioral deficit scores Hippocampus
CLC: R743.3
Type: Master's thesis
Year: 2005
Downloads: 111
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Abstract


Objective To investigate the effects of stellate ganglion block （SGB） on the serum Interleukin-8 （IL-8）,the expression of Bax and Bcl-2 in Hippocampus CA1 of rabbits during global cerebral ischemia reperfusion （IR）,and the eflFects of transection of cervical sympathetic trunk （TCST） on cerebral infarct volume,the expression of induced nitric oxide synthase （iNOS） in Hippocampus of rats during focal cerebral IR,analyzing the neuroprotective mechanism of SGB and TCST.Methods The study was divided into two parts:In part Ⅰ ,twenty-one healthy adult Japan White rabbits were randomly divided into three groups of 7 rabbits each: experiment group （group A）,control group （group B） and sham-operation group （group C）.Group A with cerebral ischemia induced by clipping bilateral external,internal carotid arteries and vertebral arteries for 15min and then declamping for 24h,0.25% bupivacaine with the rate of 0.5ml · h-1 was injected continuously following a bonus of 0.5ml to left stellate ganglion （SG） through epidural catheter before the occlusion; Group B with cerebral ischemia but no SGB; Group C without vessels occlusion and SGB. Blood samples of all animals were collected to measure the serum concentration of IL-8 at 10min before the occlusion （T0）, at 1h （T1）,2h （T2）,4h （T3） after reperfusion.the neurological deficit scores of all rabbits were evaluated at 24h after reperfusion,the expression of Bax and Bcl-2 were detected with immunohistochemistry staining.In part Ⅱ,fifty healthy Wistar rats were randomly divided into three groups: experiment group （group A, n=20）, control group （group B, n=20） and sham-operation group （group C, n=10）.Focal cerebral ischemia was induced by middle cerebral artery occlusion （MCAO） with the intralurninal suture method.Group A with MCAO for 2h followed by reperfusion after cervical sympathetic trunk were transected; Group B only with cerebral ischemia and reperfusion;In group C,the similar operation procedure were completed only but no MCAO and no TCST.after the behavioral deficit scores of all rats were evaluated 24h after reperfusion,randomly selected half rats, detected the infarctsize with 2,3,5-triphenyltetrazolium chloride（TTC）.Another half rats were detected the expression of iNOS with immunohistochemistry staining.Results （DThe neurological deficit scores of rabbits in group A were lower than that in group B （P<0.05）.?The serum IL-8 levels of rabbits in group A only increased markedly at T3 compared to To and group C, （P<0.05）, but increased significantly in group B at every time points compared to group A and C （P<Q.05）.?ftbe expression of Bax in Hippocampus CA] of rabbits in group A and B increased markedly compared to group C （P<0.01）,there were higher increase in group B man group A （P<0.05）.The expression of Bcl-2 in group A increased obviously compared to group C （P<0.05）,the increase in group B was not significant compared to group C （PX）.Q5）.?The cerebral infarct size and behavioral 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 B increased obviously compared to group A and C（PO.05）,but there were no difference between group A and C （P>0.05）.Conclusion (DSGB can decrease the neurological deficit scores and the serum IL-8 concentration,improve the expression of Bcl-2 ,and depress the expression of Bax of rabbits during global cerebral IR,and these were probably involved in its neuroprotective mechanism. ?TCST can decrease the cerebral infarct volume and the behavioral deficit scores of rats during focal cerebral IR,these suggested mat TCST was neuroprotective.and TCST can also depress the expression of iNOS in hippocampus of rats,that might contribute to the neuroprotective mechanism.

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