Stroke, Vol 25, 869-875, Copyright © 1994 by American Heart Association
M Chopp, RL Zhang, H Chen, Y Li, N Jiang and JR Rusche
BACKGROUND AND PURPOSE: Postischemic cerebral inflammation may contribute
to ischemic cell damage. The CD11b/18 (Mac-1) integrin mediates stimulated
neutrophil binding to endothelia. We therefore investigated the effect of
administration of an anti-Mac-1 monoclonal antibody on cerebral ischemic
cell damage in the rat. METHODS: Rats (n = 10) were subjected to 2 hours of
middle cerebral artery occlusion; the anti-Mac-1 antibody was administered
at a dose of 2 mg/kg i.v. at 1 hour of reperfusion and 1 mg/kg i.v. at 22
hours of reperfusion or an isotype-matched control antibody (n = 10) was
administered using the same experimental protocol. Rats were killed at 46
hours of reperfusion, and brain sections were stained with hematoxylin and
eosin for histological evaluation. In a separate population of rats given
either vehicle (n = 8) or anti-Mac-1 antibodies (n = 9), intraparenchymal
neutrophils were measured by means of a myeloperoxidase assay. RESULTS: The
lesion volume was significantly smaller (28%) in the anti-Mac-1 antibody
group compared with the vehicle control group (P < .01). Numbers of
intraparenchymal polymorphonuclear cells were significantly reduced (P <
.05) in the cortex of the anti-Mac-1 antibody group compared with the
vehicle control group. CONCLUSIONS: Our data demonstrate that
administration of anti-Mac-1 antibody 1 hour after onset of reperfusion
results in significant reductions of ischemic cell damage and
intraparenchymal neutrophils after transient (2-hour) focal cerebral
ischemia in the rat.
ARTICLES
Postischemic administration of an anti-Mac-1 antibody reduces ischemic cell damage after transient middle cerebral artery occlusion in rats
Department of Neurology, Henry Ford Hospital, Detroit, Mich. 48202.
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