实验性超负荷血糖大鼠脑缺血后脑毛细血管内皮细胞ICAM-1表达的研究

目的　了解超负荷血糖条件下，脑缺血后，脑毛细血管内皮细胞细胞间粘附分子１（ＩＣＡＭ－１）表达的情况。方法　采用ＳＤ大鼠尾静脉注射链脲霉素，建立超负荷血糖模型。用免疫组化方法动态观察大鼠超负荷血糖１ 月条件下以尼龙线栓堵大鼠大脑中动脉造成持续性局灶性脑缺血后不同时间，脑毛细血管内皮细胞ＩＣＡＭ－１ 的表达。结果　超负荷血糖１月脑缺血０．５ 小时ＩＣＡＭ－１ 的表达明显升高；１小时达高峰，表达范围弥漫整个缺血半球；缺血３～１２ 小时， ＩＣＡＭ－１表达仍很明显，但主要集中在颞、顶叶缺血区；缺血２４ 小时表达不明显；假手术组大鼠脑组织毛细血管内皮细胞ＩＣＡＭ－１只有较少的表达；正常血糖对照组及阴性对照者脑毛细血管内皮细胞均未见ＩＣＡＭ－１ 表达。结论　与正常血糖ＳＤ大鼠脑缺血相比，超负荷血糖大鼠脑缺血后， ＩＣＡＭ－１ 在脑毛细血管内皮细胞上表达出现的早而明显，提示对加重脑缺血后的病理损伤起到了重要作用。

The study on ICAM 1 expression of brain capillary endotheliocyte in experimental hyperglycemic rats after cerebral ischemia

Objective To investigate imtercellular abhension modecule 1 (ICAM 1) expression on brain capillary endotheliocyte under hyperglycemic condition after cerebral ischemia. Methods Hyperglycemia model was made by intravenous injection of streptozocin in SD rats and the hyperglycemia in rats was observed for 1 month by immunohistochemical method, permanent focal cerebral ischemia was made by occluding the middle cerebral artery with nylon line in streptozocin induced hyperglycemic rats. Results Focal cerebral ischemia for 0.5 h based on 1 month hyperglycemia,ICAM 1 expression raised obviously and peaked in 1h, cerebral ischemia for 3~12h, ICAM 1 expression was still obvious, but in 24h a slight expression of ICAM 1 was observed in hyperglycemic rats, brain capillary endotheliocyte ICAM 1 in false operative group had fewer expression, but there was no ICAM 1 expression in normal control group and negative control. Conclusion ICAM 1 expression on brain capillary endotheliocyte was earlier and clearer in hyperglycemic rats than normal glucose in SD rats. ICAM 1 might play an important role in worsening the pathological injury after cerebral ischemia under hyperglycemic condition.