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本研究采用液氮冷冻Wistar大鼠一侧大脑制成血管源性脑水肿模型，将大鼠全脑沿冷冻中心制成冠状面冰冻切片，运用免疫组化染色观察脑水肿组及对照组白质血脑屏障内皮细胞ICAM-1蛋白表达量的变化。对此进行图像分析．并将脑组织冰冻切片与大鼠T淋巴细胞悬液共同孵育后，常规HE染色、显微镜下观察，求出T淋巴细胞与血管壁的特异性粘附率，发现大鼠内皮细胞在正常情况下表达少量的ICAM－1蛋白分子，冷冻后3小时有明显的升高（P＜0．001），3～12小时达高峰，以后逐渐恢复，至24小时后基本降至冷冻前表达量水平，ICAM－1蛋白表达量的高峰时间与脑水肿达高峰的时间一致；T淋巴细胞的特异性粘附率在事先未满加抗ICAM-1单抗组较高，而在事先满加抗ICAM－1单抗组则明显下降（P＜0.0001），但并未完全被抑制，说明ICAM－1并不是唯一介导T淋巴细胞特异性粘附的分子。
In this study, a model of vasogenic brain edema was made by freezing the brain of one side of a liquid nitrogen-frozen Wistar rat. The whole brain of the rat was made into a coronal frozen section along the freezing center, and the cerebral edema group and the control group were observed by immunohistochemistry. Changes of ICAM-1 protein expression in brain barrier endothelial cells. Do this for image analysis. The frozen sections of brain tissue were co-incubated with T lymphocyte suspension of rats. The cells were stained with HE and observed under a microscope. The specific adhesion rate of T lymphocytes to the blood vessel wall was obtained. Under normal conditions, Expression of a small amount of ICAM-1 protein molecules, 3 hours after freezing significantly increased (P <0.001), 3 to 12 hours peaked, then gradually recovered to 24 hours after the basic reduced to the level of expression level before freezing, ICAM-1 protein expression peak time consistent with the peak time of cerebral edema; T lymphocyte specific adhesion rate in the prior under the anti-ICAM-1 monoclonal antibody group was higher, and in advance with anti-ICAM- 1 mAb was significantly decreased (P <0.0001), but not completely inhibited, indicating that ICAM-1 is not the only molecule that mediates T lymphocyte-specific adhesion.