高血糖对大鼠脑缺血再灌注损伤脑梗死体积和ICAM-1表达及白细胞浸润的影响

目的：研究观察高血糖条件下脑缺血再灌注后细胞间粘附分子(intercellular adhesion molecule-1，ICAM-1)表达及白细胞浸润情况，探索高血糖对脑缺血再灌注影响的可能机制。方法：雄性SD大鼠采用缺血前30分钟腹腔注射葡萄糖建立高血糖模型，用Longa——Zea氏线栓法复制脑缺血再灌注模型。采用2％红四氮唑(TTC)染色测量梗死体积；免疫组织化学法和HE染色观察不同再灌注时间点ICAM-1阳性表达及白细胞浸润计数。比较相同再灌注时间点高血糖组和正常血糖组ICAM—1表达和白细胞浸润计数。结果：(1)相同再灌注时间点高血糖组梗死体积明显大于正常血糖组。(2)相同再灌注时间点高血糖组ICAM-1表达及白细胞浸润计数明显高于正常血糖组。(3)高血糖组ICAM-1表达及白细胞浸润计数高峰提前。(4)ICAM-1表达与白细胞浸润呈现明显相关性。结论：ICAM-1介导白细胞和内皮细胞粘附及向脑缺血区浸润过程，ICAM-1表达及白细胞浸润参与了高血糖加重脑缺血再灌注损害过程。

The study on ICAM-1 expression and leukocyte infiltration in hyperglycemic rats after cerebral ischemia-reperfusion

objective: The purpose of this study is to investigate the relationship between the expression of intercellular adhesion molecule? (ICAM-1) 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: male SD rats were randomly divided into 3 groups. Hyperglycemia model was made by 50% glucose i. p. before 30 minutes initiation the ischemic insult in hyper-glycemic group. Cerebral ischemic-reperfusion model was induced by adopting the thread embolism method according to Lon-ga- Zea. The infarcted size was measured by 2, 3, 5 - triphenytetrazolium chloride (TTC) staining technique. Immunohisto-chemical technique was used to examine the expression of ICAM-1; leukocyte infiltration were measured by HE staining technique. Compare the expression of ICAM- 1 and 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 hyperglyce-mic group. (2) Compared with normalglycemia group in the same reperfusion time,the expression ICAM-1 and leukocyte infiltration in hyerglycemic group were higher than normalglycemic group. (3) The expression ICAM-1 and leukocyte infiltration in hyerglycemic group reached peak earlier than normalglycemia group. (4) There was a positive correlation between ICAM-1 and leukocyte infiltration. Conclusion: ICAM-1 were involved in the process of leukocyte both adhering to endothelia cell and accumulating around the ischemic area. The expression ICAM-1 and leukocyte infiltration may be play some role of inducing poor outcomes with preischemic hyerglycemia.