Deficiency of intercellular adhesion molecule 1 attenuates microcirculatory disturbance and infarction size in focal cerebral ischemia

被引:133
作者
Kitagawa, K
Matsumoto, M
Mabuchi, T
Yagita, Y
Ohtsuki, T
Hori, M
Yanagihara, T
机构
[1] Osaka Univ, Sch Med, Dept Internal Med 1, Suita, Osaka 565, Japan
[2] Osaka Univ, Sch Med, Dept Neurol, Suita, Osaka 565, Japan
关键词
intercellular adhesion molecule 1 (ICAM-1); cerebral ischemia; granulocyte; microcirculation; knockout mouse;
D O I
10.1097/00004647-199812000-00008
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Recent evidence has shown crucial roles for cell-adhesion molecules in inflammation-induced rolling, adhesion, and accumulation of neutrophils in tissue. Intercellular adhesion molecule-1 (ICAM-1) is one of these adhesion molecules. Previous studies have shown marked reduction in the size of infarction after focal cerebral ischemia by depletion of granulocytes and administration of the antibody against TCAM-1. In the present study we investigated the role of ICAM-1 in the size of ischemic lesions, accumulation of granulocytes, and microcirculatory compromise in focal cerebral ischemia by using ICAM-1-knockout mice. Ischemic lesions were significantly mitigated in knockout mice after permanent and transient focal ischemia, even though the number of granulocytes in the infarcted tissue was almost the same between knockout and wildtype mice. Depletion of granulocytes further decreased the size of ischemic lesions after transient focal ischemia in ICAM-1-knockout mice. Microcirculation was reduced after focal ischemia. but it was better preserved in the cerebral cortex of knockout mice than that of wild-type mice, The present study demonstrated that ICAM-1 played a role in microcirculatory failure and subsequent development and expansion of infarction after focal cerebral ischemia. However, it is highly unlikely that ICAM-1 played a key role in accumulation of granulocytes after focal cerebral ischemia.
引用
收藏
页码:1336 / 1345
页数:10
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