[Objective] To investigate whether pretreatment with flunarizine hydrochlorid could relieve the injury of local cerebral ischemia - reperfusion in rats with hyperglycemia. [Method] Thirty six healthy male SD rats (weight from 180 g to 220 g) were randomly divided into 2 groups; hyperglycemia group (n = 18) and flunarizine + hyperglycemia group (flunarizine group n= 18 ). The rats in each group were divided into 3 subgroups according to reperfusion 3 h ( re = 6 ) , .6 h (n=6) and 24 h (n=6) after ischemia for 90 minutes. The differences of cerebral pathological changes and the expressions of ICAM - 1 among these groups. [Result] Compared with hyperglycemia group, the number of degenerative and necrosis neurons were less and tissue edema became was weaker. In the flunarizine group, the expression of ICAM - 1 can be seen at 3 hours from reperfusion, and increase in 24 hours from reperfusion, P <0. 05. Compared with hyperglycemia group at every reperfusion time; ICAM - 1 expressions were decreased in flunarizine group, P <0. 01. [ Conclusion] The pretreatment of flunarizine hydrochlorid could decrease the expression of ICAM - 1 and the focal ischemia - reperfusion damage of the ras with hyperglycemia.%[目的]探讨预防性应用盐酸氟桂利嗪对高血糖条件下SD大鼠局灶性脑缺血再灌注损伤是否有保护作用及其可能机制.[方法]雄性健康SD大鼠36只,建立高血糖模型后随机分为两组:高血糖组(n=18)与盐酸氟桂利嗪+高血糖组(简称氟桂利嗪组,n=18),各组按脑缺血90 min再灌注3 h(n=6)、6h(n=6)、24 h(n =6)分为3个亚组.比较氟桂利嗪组与高血糖组各再灌注时间点脑组织病理形态改变及ICAM -l表达的动态变化.[结果]脑组织病理形态观察:氟桂利嗪组随着再灌注时间的延长,脑组织受损程度逐渐加重,但与高血糖组各时间点比较,变性、坏死的神经元较少,组织间水肿较轻.ICAM -1表达:氟桂利嗪组于再灌注3h可见IAM -1阳性表达,24h内逐渐增高(P＜0.05).氟桂利嗪组与高血糖组比较各时间点缺血区ICAM -1表达均减少(P＜0.01).[结论]预防性应用盐酸氟桂利嗪能减轻高血糖条件下的局灶性脑缺血再灌注损伤.
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