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Am J Physiol Heart Circ Physiol 277: H172-H182, 1999;
0363-6135/99 $5.00
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Vol. 277, Issue 1, H172-H182, July 1999

A CD18 monoclonal antibody reduces multiple organ injury in a model of ruptured abdominal aortic aneurysm

A. J. Boyd1, B. B. Rubin1, P. M. Walker1, A. Romaschin1, T. B. Issekutz2, and T. F. Lindsay1

1 Division of Vascular Surgery, Department of Surgery, The Toronto Hospital (General Division), Faculty of Medicine, University of Toronto, Toronto, Ontario M5C 2C4; and 2 Izaak Walton Killam-Grace Health Centre, Division of Microbiology and Immunology, Department of Pediatrics, Dalhousie University, Halifax, Nova Scotia, Canada B3J 3G9

The role of CD18 antibody (anti-CD18) in remote and local injury in a model of ruptured abdominal aortic aneurysm repair was investigated. Rats were divided into sham, shock, clamp, and shock + clamp groups. Shock + clamp animals received anti-CD18 or a control monoclonal antibody. One hour of hemorrhagic shock was followed by 45 min of supramesenteric aortic clamping. Intestinal and pulmonary permeability to 125I-labeled albumin was determined. Myeloperoxidase (MPO) activity, F2-isoprostane levels, and transaminases were also measured. Only shock + clamp resulted in statistically significant increases in pulmonary and intestinal permeability, which were associated with significant increases in MPO activity and F2-isoprostane levels. Treatment with anti-CD18 significantly decreased intestinal and pulmonary permeability in shock + clamp animals. These reductions were associated with significantly reduced intestinal and hepatic MPO activity and pulmonary F2-isoprostane levels and reduced alanine and aspartate aminotransferase levels; however, anti-CD18 had no effect on intestinal or hepatic F2-isoprostane levels or on pulmonary MPO activity. These results suggest CD18-dependent and -independent mechanisms of local and remote organ injury in this model of ruptured abdominal aortic aneurysm.

ischemia-reperfusion; F2-isoprostanes; neutrophils; myeloperoxidase


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