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在缺氧－再给氧条件下，观察了体外分离培养的大鼠脑微血管内皮细胞表面粘附分子ＩＣＡＭ－１的表达及中性粒细胞与内皮细胞粘附作用的改变。结果表明，单纯缺氧１０ｈ不引起内皮细胞ＩＣＡＭ－１的上调，再给氧６ｈＩ－ＣＡＭ－１的表达升高（Ｐ＜０．０１），再给氧１２ｈ表达量增加了１００％（Ｐ＜０．０１），此时中性粒细胞与内皮细胞的粘附作用也明显增强（Ｐ＜０．０１）。缺氧前用盐酸川芎嗪（２ｍｇ／ｍｌ）预处理内皮细胞可阻断ＩＣＡＭ－１的表达（Ｐ＜０．０１），同时也可降低ＰＭＮ与内皮细胞的粘附（Ｐ＜０．０５）。结果提示，脑微血管内皮细胞在缺氧－再给氧刺激下可自身调节Ｉ－ＣＡＭ－１的表达，为中性粒细胞与内皮细胞的粘附提供特异的结合位点。
Under hypoxia-reoxygenation conditions, the expression of ICAM-1 on the surface of rat brain microvascular endothelial cells cultured in vitro and the change of neutrophil adhesion to endothelial cells were observed. The results showed that the ICAM-1 upregulation was not induced by endothelial hypoxia alone for 10 h, but the expression of 6 hI-CAM-1 in reoxygenation group was increased (P <0.01), and the expression of ICAM-1 increased by 100% 0.01). At this time, the adhesion of neutrophils and endothelial cells was also significantly enhanced (P <0.01). Pretreatment of endothelial cells with ligustrazine hydrochloride (2mg / ml) before hypoxia blocked the ICAM-1 expression (P <0.01) and also decreased the adhesion of PMN to endothelial cells (P <0.05) . The results suggest that brain microvascular endothelial cells can regulate the expression of I-CAM-1 under hypoxia-reoxygenation and provide a specific binding site for the adhesion of neutrophils and endothelial cells.