预防性应用盐酸氟桂利嗪对高血糖SD大鼠局部脑缺血再灌注损伤保护作用的研究

目的 采用高血糖条件下Sprague-Dawley（SD）大鼠局灶性脑缺血再灌注模型，观察神经功能缺损评分、脑梗死体积、脑组织病理形态改变及抑凋亡基因bcl-2的表达情况，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。方法36只雄性健康SD大鼠，建立高血糖模型后随机分为2组：高血糖组（n=18）、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90min再灌注3h（n=6）、6h（n=6）、24h（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神经功能缺损评分、脑梗死体积和脑组织病理形态的改变。结果相同再灌注时间点，氟桂利嗪组比高血糖组神经功能缺损程度减轻，P〈0．05；相同时间点氟桂利嗪组较高血糖组梗死体积缩小，其中再灌注3、6h组间比较P〈0．05，再灌注24h组间比较P〈0．01；脑组织病理形态观察：氟桂利嗪组与高血糖组各再灌注时间点比较，变性、坏死的神经元减少，空泡化改变减轻，组织间水肿减轻。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，减轻神经功能缺损症状，缩小梗死体积，减轻神经细胞变性、坏死及组织水肿。

Research for protective effect of pretreatment by flunarizine hydrochlorid on focal cerebral ischemia reperfusion damage in SD rat with hyperglycemia

Objective Applying focal ischemia-reperfusion model of SD rat on the condition of hyperglycemia, through observing the state of neurologic impairment score, cerebral pathomorphology and infarction volume after focal ischemia-reperfusion damage in SD rat on the condition of hyperglycemia. Method :36 healthy male SD rats(weight from 180 g to 220 g) with normal blood glucemia( ＜6 mmol/l)were randomly divided into 2 groups : hyperglycemia group ( n = 18 ) and flunarizine + hyperglycemia group ( namely flunarizine group n =18 ). Each group was divided into 3 subgroups according to reperfusion 3 h ( n = 6 ), 6 h ( n = 6), 24 h ( n = 6 ) after ischemia for 90 minutes. Compare the differences of neurologic impairment score, cerebral infarction volume and pathomorphology. Results 1. There are great difference of the neurologic impairment score between the flunarizine group and hyperglycemia group(P ＜0. 05) ,The infarction volume can be seen at flunarizine group,and the peak was at reperfusion 24 hours. Compared 6 h with 3 h and 24 h with 6 h in flunarizine group, P ＜0. 01. The infarction volume in the flunarizine group was lower than that in the hyperglycemia group,P ＜0. 01 at reperfusion 3 hours and 6 hours, P ＜ 0. 05 at reperfusion 24 hours. Cerebral tissue pathomorphology:In flunarizine group, the injury of cerebral tissue became serious with time went by, but compared with hyperglycemia group, the number of neuron which became degeneration and necrosis decreased, vacuolization and intertissue edema became relieved. Conclusion On the condition of hyperglycemia, pretreatment of flunarizine could decrease focal ischemia-reperfusion damage, relieve the neurologic impairment symptoms; reduce infarction volume, reduce the neuron degeneration, necrosis and tissue edma.