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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。
Objective To investigate the expression of intercellular adhesion molecule-1 (ICAM-1) in brain capillary endothelial cells after cerebral ischemia under overload glucose condition. Methods SD rats were injected streptozotocin through the tail vein to establish a hyperglycemia model. Immunohistochemistry was used to dynamically observe the expression of ICAM-1 in brain capillary endothelial cells at different time points after continuous focal cerebral ischemia in rats. Results The expression of ICAM-1 was significantly increased at 0.5 hour after cerebral ischemia in 1 month. The peak of ICAM-1 expression reached the peak at 1 hour and the expression range was diffuse throughout the ischemic hemisphere. ICAM-1 expression was still significant at 3 to 12 hours of ischemia, But mainly concentrated in the temporal and parietal lobe ischemic area. The expression of ICAM-1 in brain tissue of sham operation group was less than that in ischemia group at 24 hours. No ICAM-1 expression was observed in vascular endothelial cells. Conclusion The expression of ICAM-1 on brain capillary endothelial cells is earlier and more obvious than that of normal blood-glucose-induced SD rats after cerebral ischemia, suggesting that it may be helpful to aggravate the pathological injury after cerebral ischemia Played an important role.