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American Journal of Pathology, Vol 143, 410-418, Copyright © 1993 by American Society for Investigative Pathology
REGULAR ARTICLES |
T Yamazaki, Y Seko, T Tamatani, M Miyasaka, H Yagita, K Okumura, R Nagai and Y Yazaki
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
To elucidate the mechanism(s) of myocardial reperfusion injury, we investigated the roles of cell adhesion molecules on both leukocytes and vascular endothelial cells in the reperfused myocardia. We found that within 2 hours after reperfusion leukocytes began to infiltrate into the rat myocardia subjected to 30 minutes of ischemia and clarified, for the first time, that the expression of intercellular adhesion molecule-1 was enhanced on the capillary and venous endothelial cells from 8 to 96 hours after the start of reperfusion. Furthermore, pretreatment with individual monoclonal antibodies against cell adhesion molecules (CD11a, CD11bc, CD18, and intercellular adhesion molecule-1) reduced not only the infiltration of leukocytes but also the area of infarction in the reperfused hearts. These observations suggest that cell adhesion molecules play a critical role in the pathogenesis of myocardial reperfusion injury.
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