Expression of intercellular adhesion molecule-1 in rat heart with ischemia/reperfusion and limitation of infarct size by treatment with antibodies against cell adhesion …
T Yamazaki, Y Seko, T Tamatani… - The American journal …, 1993 - ncbi.nlm.nih.gov
T Yamazaki, Y Seko, T Tamatani, M Miyasaka, H Yagita, K Okumura, R Nagai, Y Yazaki
The American journal of pathology, 1993•ncbi.nlm.nih.govTo 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 …
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 …
Abstract
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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