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目的 探讨大鼠局灶性脑缺血再灌流后细胞间粘附分子 - 1(ICAM- 1)表达规律与白细胞浸润。方法 采用大鼠 MCA线栓闭塞 /再通法建立局灶性缺血 /再灌流模型 ,动态观察 ICAM- 1、髓过氧化物酶 (MPO)变化情况。结果 (1)鼠脑缺血 /再灌流后 MCA供血区皮质及梗死周边区的微血管 ICAM- 1表达于再灌流 6 h已增强 ,36～ 48h达高峰 ,以后逐渐减弱 ,但第 7天表达仍强于假手术组。(2 )坏死周边区神经元也表达 ICAM- 1。(3)再灌流 6 h出现白细胞浸润 ,浸润高峰在 2 4～ 36 h,6 d后恢复正常。结论 (1)缺血再灌流使微血管表达 ICAM- 1上调 ,同时也伴随坏死周边区的神经元表达 ICAM- 1。 (2 )白细胞浸润与 ICAM- 1表达规律同步。
Objective To investigate the expression of intercellular adhesion molecule - 1 (ICAM - 1) and leukocyte infiltration after focal cerebral ischemia / reperfusion in rats. Methods The model of focal ischemia / reperfusion was established by MCA occlusion / reperfusion in rats. The changes of ICAM-1 and MPO were observed dynamically. Results (1) The expression of ICAM-1 in the cortex and infarct peripheral area in the MCA-supplying area after cerebral ischemia / reperfusion increased at 6 h after reperfusion and reached the peak at 36-48 h, then gradually decreased, but on the 7th day Stronger than sham group. (2) Peripheral neurons in necrosis also expressed ICAM-1. (3) Leucocyte infiltration was observed at 6 h after reperfusion, and the infiltration peak peaked at 2-4 h and returned to normal after 6 d. Conclusions (1) ICAM-1 is up-regulated by ischemia / reperfusion in the microvessels and is also accompanied by ICAM-1 expression in neurons in the peripheral area of necrosis. (2) leukocyte infiltration and ICAM-1 expression synchronization.