Soluble intercellular adhesion molecule-1, E-selectin, vascular cell adhesion molecule-1 and von Willebrand factor in stroke

被引:65
作者
Blann, A [1 ]
Kumar, P
Krupinski, J
McCollum, C
Beevers, DG
Lip, GYH
机构
[1] Univ Birmingham, City Hosp, Dept Med, Haemostasis Thrombosis & Vasc Biol Unit, Birmingham B18 7QH, W Midlands, England
[2] Manchester Metropolitan Univ, Dept Biol Sci, Manchester M15 6BH, Lancs, England
[3] Univ S Manchester Hosp, Dept Surg, Manchester M20 8LR, Lancs, England
关键词
intercellular adhesion molecule-1; von Willebrand factor; vascular cell adhesion molecule-1; E-selectin;
D O I
10.1097/00001721-199907000-00009
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We investigated the role of endothelial cell and leukocyte adhesion in the pathophysiology of acute stroke. The immunocytochemical expression of adhesion molecules in brain tissue from six patients who died following acute ischaemic stroke showed weak endothelial expression of intercellular adhesion molecule-1 (ICAM-1), but intense expression of vascular cell adhesion molecule-1 (VCAM-1) by astrocytes and endothelial cells from the infarcted, but not the non-infarcted areas. We also measured soluble adhesion molecules E-selectin, ICAM-1, VCAM-1 and von Willebrand factor (all by enzyme-linked immunosorbent assay) in 21 patients after an acute ischaemic stroke (ictus <12 h), and again 3 months later. Blood levels in the stroke patients were compared with 82 healthy controls and 22 subjects with carotid atherosclerosis. Compared with healthy controls, both patient groups had raised levels of von Willebrand factor (P < 0.02) but the level of soluble VCAM-1 was raised only in patients with acute stroke (P < 0.02). Levels of von Willebrand factor and soluble VCAM-1 in the stroke patients were still high at 3 months fellow-up. We suggest that there might be changes in adhesion molecule expression and release in the acute and chronic stages of ischaemic stroke, where blood levels are related to immunocytochemical findings on infarcted brain. These changes may perhaps be part of the complex pathophysiological responses to infarction and repair of brain tissue following stroke. Blood Coag Fibrinol 10:277-284 (C) 1999 Lippincott Williams & Wilkins.
引用
收藏
页码:277 / 284
页数:8
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