| Objective: Ischemic stroke is a leading cause of death and long-term disability disease.Hyperglycemia has been associated with worse outcome of ischemic stroke in clinical observation and animal studies.However the associations between diabetes,hyperglycemia,and hyperglycemia control and stroke outcome are still controversial issues.The mechanisms for increased neuronal damage include production of cerebral acidosis from enhanced anaerobic metabolism;the toxicity of excitatory amino acids;destruction of blood-brain barrier and promoting hemorrhagic infarct conversion; the toxicity of nitric oxide(NO).The most finding in animal studies is the correlation between hyperglycemia and acidosis,however some authors think that the glucose-lactate coalition protects the ischenic brain.The purpose of this study is to investigate the relationship between the expression of intercellular adhesion molecule-1(ICAM-1) and tumor necrosis factor-α(TNF-α) and leukocyte infiltration and study the effects of pre-hyperglycemia. This experiment aims to study the mechanism of hyperglycemia in cerebral ischemia-reperfusion injury. Methods:36 male SD rats were randomly divided into 3 groups :sham-operation group(n=4) ,normalglycemic group(n=16) and (n=16)(reperfusion for 2,4,6,24,hours post-ischemia; n=4,in normalglycemic group and hyperglycemia group). Sham operation group :sew up the skin after exposing the common carotid artery (CCA)in the right side.Observing group:Hyperglycemia model was made by 50% glucose i.p. before 30 minutes initiation the ischemic insult in hyperglycemic group(normalglycemic group rats received equivalence sterile water i.p.). Cerebral ischemic-reperfusion model was induced by adopting the thread embolism method according to Longa- Zea.Adult male SD rats were anesthetized with 30-40mg/Kg Chloral Hydrate i.p. External carotid artery(ECA) common carotid artery(CCA) in right were divided and ligatured. It is just below of the branching of CCA in the right side that a small mouth was cut and through which a thread (a diameter 0.20mm fishing line of high elasticity was burned a round head at the end of the thread and used after dipping heparin) was inserted from internal carotid artery (ICA) enter the brain to anterior cerebral artery(ACA) ,sew up the ICA and skin. The thread was then pulled out after cerebral ischemia 2 hours.The rats were killed after reperfusion(2,4,6,24 hours; n=4,in each group),the infarcted size was measured by 2,3,5—triphenytetrazolium chloride (TTC) staining technique. Immunohistochemical technique was used to examine the expression of ICAM-1,TNF-α;leukocyte infiltration were measured by HE staining technique.Compare the expression of ICAM-1,TNF-αand leukocyte infiltration with the same reperfusion time in hyperglycemia group with normalglycemia group.Result:(1)Compared with normalglycemia group ,greater infarct volume was found in hyperglycemic group.(2)ICAM-1 and TNF-αexpression and leukocyte infiltration raised obviously and peaked at 24h after the cerebral ischemic-reperfusion .(3) Compared with normalglycemia group in the same reperfusion time,the expression ICAM-1 and TNF-αand leukocyte infiltration in hyerglycemic group were higher than normalglycemic group.(4) The expression ICAM-1 and TNF-αand leukocyte infiltration in hyerglycemic group reached peak earlier than normalglycemia group.(5) There was a positive correlation between ICAM-1 , TNF-αand leukocyte infiltration.Conclusion: ICAM-1 and TNF-αwere involved in the process of leukocyte both adhering to endothelia cell and accumulating around the ischemic area. The expression ICAM-1 and TNF-αand leukocyte infiltration may be play some role of inducing poor outcomes with preischemic hyerglycemia.
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