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Am J Physiol Heart Circ Physiol 276: H984-H992, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 3, H984-H992, March 1999

Role of nitric oxide-derived oxidants in vascular injury from carbon monoxide in the rat

Stephen R. Thom1,2, Donald Fisher1, Y. Anne Xu1, Sarah Garner1, and Harry Ischiropoulos1,3

1 Institute for Environmental Medicine and 2 Departments of Emergency Medicine and 3 Biochemistry and Biophysics, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104-6068

Studies were conducted with rats to investigate whether exposure to CO at concentrations frequently found in the environment caused nitric oxide (NO)-mediated vessel wall changes. Exposure to CO at concentrations of 50 parts per million or higher for 1 h increased the concentration of nitrotyrosine in the aorta. Immunologically reactive nitrotyrosine was localized in a discrete fashion along the endothelial lining, and this was inhibited by pretreatment with the NO synthase (NOS) inhibitor Nomega -nitro-L-arginine methyl ester (L-NAME). The CO-induced elevations of aortic nitrotyrosine were not altered by neutropenia or thrombocytopenia, and CO caused no change in the concentration of endothelial NOS. Consequences from NO-derived stress on the vasculature included an enhanced transcapillary efflux of albumin within the first 3 h after CO exposure and leukocyte sequestration that became apparent 18 h after CO exposure. Oxidized plasma low-density lipoprotein was found immediately after CO exposure, but this was not inhibited by L-NAME pretreatment. We conclude that exposure to relatively low CO concentrations can alter vascular status by several mechanisms and that many changes are linked to NO-derived oxidants.

myeloperoxidase; nitrotyrosine; lipoprotein oxidation; endothelium; xanthine oxidase


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