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Am J Physiol Cell Physiol 278: C292-C302, 2000;
0363-6143/00 $5.00
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Vol. 278, Issue 2, C292-C302, February 2000

Hyperbaric oxygen downregulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS

Jon A. Buras1, Gregory L. Stahl2, Kathy K. H. Svoboda3, and Wende R. Reenstra4

1 Department of Emergency Medicine and 2 Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Brigham and Women's Hospital, Boston 02115; 4 Department of Pathology, Boston University School of Medicine, Boston, Massachusetts 02118; and 3 Department of Biomedical Sciences, Baylor College of Dentistry, Dallas, Texas 75246

Hyperbaric oxygen (HBO) is being studied as a therapeutic intervention for ischemia/reperfusion (I/R) injury. We have developed an in vitro endothelial cell model of I/R injury to study the impact of HBO on the expression of intercellular adhesion molecule-1 (ICAM-1) and polymorphonuclear leukocyte (PMN) adhesion. Human umbilical vein endothelial cell (HUVEC) and bovine aortic endothelial cell (BAEC) induction of ICAM-1 required simultaneous exposure to both hypoxia and hypoglycemia as determined by confocal laser scanning microscopy, ELISA, and Western blot. HBO treatment reduced the expression of ICAM-1 to control levels. Adhesion of PMNs to BAECs was increased following hypoxia/hypoglycemia exposure (3.4-fold, P < 0.01) and was reduced to control levels with exposure to HBO (P = 0.67). Exposure of HUVECs and BAECs to HBO induced the synthesis of endothelial cell nitric oxide synthase (eNOS). The NOS inhibitor nitro-L-arginine methyl ester attenuated HBO-mediated inhibition of ICAM-1 expression. Our findings suggest that the beneficial effects of HBO in treating I/R injury may be mediated in part by inhibition of ICAM-1 expression through the induction of eNOS.

cell adhesion molecules; ischemia; reperfusion injury; hyperoxia; neutrophils


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