(Stroke. 1995;26:1361-1364.)
© 1995 American Heart Association, Inc.
Articles |
From the Department of Neurology, Klinikum Mannheim, and Department of Neurology, Klinikum Heidelberg (A.G.), University of Heidelberg, FRG.
Correspondence to Dr K. Fassbender, Department of Neurology, University of Heidelberg, Theodor-Kutzer-Ufer, 68135 Mannheim, FRG.
Background and Purpose Cellular adhesion molecules mediate adhesion between endothelial cells and leukocytes as a precondition for extravasation of leukocytes at sites of tissue injury. The pattern of release of circulating adhesion molecules has been characterized in patients with acute ischemic stroke.
Methods Serum concentrations of soluble selectin-type adhesion molecules (soluble endothelial leukocyte adhesion molecule1 [sELAM-1], soluble lymph node homing receptor [sL-selectin]) and immunoglobulin-type adhesion molecules (soluble vascular cell adhesion molecule1 [sVCAM-1], soluble intercellular adhesion molecule1 [sICAM-1]) were serially determined (at hours 4, 8, and 10 and at days 1, 3, and 5) in 22 patients with acute ischemic stroke. As control subjects, age- and sex-matched individuals with (n=40) and without (n=22) vascular risk factors were studied.
Results We observed increased concentrations of sICAM-1 and decreased levels of sL-selectin in patients with risk factors even in the absence of stroke. Patients with acute stroke had, in addition, an initial transient increase of sELAM-1 and a persistent increase of sVCAM-1.
Conclusions The results suggest a chronic alteration of expression of adhesion molecules sICAM-1 and sL-selectin in subjects with risk factors for atherosclerosis; they also indicate acute changes of levels of sELAM-1 and sVCAM-1 in response to acute ischemic stroke. Determination of soluble adhesion molecules could allow in vivo monitoring of the initial steps of leukocyte-mediated brain damage in acute ischemic stroke.
Key Words: endothelium leukocytes cerebral ischemia
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