Objective To quantitatively measure the temporal profiles of intercellular adhesion molecule 1 (ICAM 1) protein in mouse brain after middle cerebral artery occlusion (MCAO) Methods Adult male CD 1 mice received 0, 3, 6, 12, 24, 48 and 72 hour(s) of permanent MCAO with an intraluminal suture technique The degree and the extent of occlusion were determined using a laser Doppler flowmeter ICAM 1 positive expression in ischemic regions was determined immunohisto~chemically and ICAM 1 protein was quantitatively measured using immunoprecipitation and Western blot analysis Results After MCAO, surface cerebral blood flow (CBF) in the ischemic hemisphere decreased to 9%-15% of the baseline in each time point of 7 to 8 animals There were no significant differences in CBF measurement during occlusion between groups Immunohistochemistry showed that ICAM 1 positive microvascular endothelial cells were observed both in the ischemic core and in the perifocal region There was a tendency for increasing expression of ICAM 1 positive microvascular endothelial cells from the ischemic core to the ischemic margin Western blot analysis showed that ICAM 1 expression in the ischemic hemisphere began to increase 3?h after MCAO, peaked at 6?h to 12?h, and persisted to 72?h Conclusions ICAM 1 expression increases in mice with permanent MCAO because ICAM 1 can mediate leukocyte endothelial adhesion and progression of leukocyte infiltration after permanent focal cerebral ischemia ICAM 1 is one of the important factors participating in ischemic cerebral damage and pathogenesis of stroke Objective To quantitatively measure the temporal profiles of intercellular adhesion molecule 1 (ICAM 1) protein in mouse brain after middle cerebral artery occlusion (MCAO) Methods Adult male CD 1 mice received 0, 3, 6, 12, 24, 48 and 72 hour s) of permanent MCAO with an intraluminal suture technique The degree and the extent of occlusion were determined using a laser Doppler flowmeter ICAM 1 positive expression in ischemic regions determined immunohisto ~ chemically and ICAM 1 protein was quantitatively measured using immunoprecipitation and Western blot analysis Results After MCAO, surface cerebral blood flow (CBF) in the ischemic hemisphere decreased to 9% -15% of the baseline in each time point of 7 to 8 animals There were no significant differences in CBF measurement during occlusion between groups Immunohistochemistry showed that ICAM 1 positive microvascular endothelial cells were observed both in the ischemic core and in the perifocal region There was a tendency for increasing expression of ICAM 1 positive microvascular endothelial cells from the ischemic core to the ischemic margin Western blot analysis showed that ICAM 1 expression in the ischemic hemisphere began to increase 3? h after MCAO, peaked at 6? h to 12? h, and persisted to 72? h Conclusions ICAM 1 expression increases in mice with permanent MCAO because ICAM 1 can mediate leukocyte endothelial adhesion and progression of leukocyte infiltration after permanent focal cerebral ischemia ICAM 1 is one of the important factors participating in ischemic cerebral damage and pathogenesis of stroke