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B and AP-1 and
upregulation of ICAM-1 in reperfused canine heart
Division of Cardiology, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21287
We investigated whether oxygen
radicals generated during ischemia-reperfusion trigger
postischemic inflammation in the heart. Closed-chest dogs
underwent 90-min coronary artery occlusion, followed by 1- or 3-h
reperfusion: 10 dogs received the cell-permeant oxygen radical
scavenger N-(2-mercaptopropionyl)-glycine (MPG; 8 mg · kg
1 · h1
intracoronary) beginning 5 min before reperfusion, and 9 dogs received
vehicle. Blood flow (microspheres), intercellular adhesion molecule
(ICAM)-1 protein expression (immunohistochemistry), ICAM-1 gene activation (Northern blotting), nuclear DNA binding activity of nuclear factor (NF)-
B and AP-1 (electrophoretic
mobility shift assays), and neutrophil (PMN) accumulation
(myeloperoxidase activity) were assessed in myocardial tissue samples.
ICAM-1 protein expression was high in vascular endothelium after
ischemia-reperfusion but was markedly reduced by MPG. MPG
treatment also markedly decreased expression of ICAM-1 mRNA and tissue
PMN accumulation. Nuclear DNA binding activities of NF-B and AP-1,
increased by ischemia-reperfusion, were both markedly decreased
by MPG at 1 h of reperfusion. However, by 3 h, AP-1 activity
was only modestly reduced by MPG and NF-B activity was not
significantly different from ischemic-reperfused controls.
These results suggest that oxygen radicals generated in vivo during
reperfusion trigger early activation of NF-B and AP-1,
resulting in upregulation of the ICAM-1 gene in vascular endothelium
and subsequent tissue accumulation of activated PMNs.
reperfusion injury; oxidative stress; neutrophils; vascular endothelium
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