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Department of Neurology (Drs. Zhang, Chopp, Li, and Jiang, and C. Zaloga), Henry Ford Health Sciences Center, Detroit, MI; the Department of Physics (Dr. Chopp), Oakland University, Rochester, MI; the Department of Pathology (Drs. Jones and Ward), University of Michigan Medical School, Ann Arbor, MI; and the Department of Immunology (Dr. Miyasaka), Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Intercellular adhesion molecule-1 (ICAM-1) is a glycoprotein expressed on endothelial cells that facilitates leukocyte adhesion. To test the hypothesis that reduction of leukocytes in an ischemic lesion reduces ischemic brain damage, we measured the effect of administration of an anti-ICAM-1 monoclonal antibody on ischemic brain damage after transient middle cerebral artery occlusion in the rat. ICAM-1 expression increased in the ischemic lesion, and the lesion volume was significantly reduced by 41% in the anti-ICAM-1 antibody group compared with the control group (p < 0.05). Numbers of polymorphonuclear leukocytes (PMNs) were significantly reduced in the cortices of the anti-ICAM-1 antibody group compared with the control animals (p < 0.05). Our data indicate that administration of anti-ICAM-1 antibody results in a significant reduction of ischemic brain damage concomitant with a reduction of PMNs in the lesion after transient focal cerebral ischemia in the rat.
Address correspondence and reprint requests to Dr. Michael Chopp, Department of Neurology, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI 48202.
Supported by NIH grants NS23393 and NS29463.
Received December 9, 1993. Accepted in final form February 21, 1994.
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