胞间粘附分子1对大鼠脑缺血再灌注损伤的作用

目的 观察大鼠脑缺血再灌注不同时相不同脑区胞间粘附分子1（ICAM－1）的方法。方法 采用双侧颈总动脉阻断＋全身低血压法建立SD大鼠脑缺血模型，随机分为假手术组、缺血再灌注（24，48，72，96，168h）组，于规定时间取脑组织石蜡包埋切片，常规苏木精－伊红染色、亚甲蓝染色及ICAM－1免疫组织化学染色对标本进行检测。结果 与假手术组相比，缺血组海马CA1区神经元尼氏体缺失明显，缺血脑区微血管肿胀变形，白细胞粘附、浸润；缺血再灌注后24h皮质及海马ICAM－1表达均显著升高，48h达高峰。可维持7d。结论 ICAM－1在脑缺血再灌注时表达明显上调，介导白细胞和脑血管内皮细胞粘附，参与缺血再灌注损伤。

Effects of Intercellular Adhesion Molecules-1 on Forebrain Ischemia-Reperfusion Damage in Rats

Objective To investigate the expression of intercellular adhesion molecules|1(ICAM|1) in the different areas of the brain following forebrain ischemia|reperfusion in rats. Methods Transient forebrain ischemia was induced by bilateral common carotid artery(CCA) occlusion and bleeding to lower the mean arterial blood pressure to 30|35 mmHg. Sprague|Dawley rats were randomly divided into sham|operated group, ischemia|reperfusion 24, 48, 72, 96 and 168 h groups. The expression of ICAM|1 was measured by immunohistochemical methods. At the same time, the methylene blue staining and hematoxylin|eosin staining were done for histological analyses. Results The number of neurons in CA1 area of hippocampous were significantly reduced in the ischemia group compared with the sham|operated group. In the ischemia group, immunohistochemical stainings demonstrated a marked increase of {ICAM|1} in both cortex and hippocampous occured at 24 hours, peaked at 48 hours, and elevated up to 7 days. The deformation of the microvascular endothelium and transmigration of the neutrophils were observed at 24 hours, then they deteriorated at 48 to 72 hours. Conclusion The upregulation of {ICAM|1} induced by the forebrain ischemia mediated the adhesion of the neutrophils to the microvascular endothelial cells which contributed to the inflammatory ischemic injuries. ICAM|1 on brain capillary endothelium play an important role after brain ischemia. ;