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Am J Physiol Gastrointest Liver Physiol 283: G1090-G1097, 2002. First published August 14, 2002; doi:10.1152/ajpgi.00480.2001
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Vol. 283, Issue 5, G1090-G1097, November 2002

NO-flurbiprofen maintains duodenal blood flow, enhances mucus secretion contributing to lower mucosal injury

L. Holm1, M. Phillipson1
M. A. Perry2
(With the Technical Assistance of A. Jägare)

1 Department of Medical Cell Biology, Biomedical Center, Uppsala University, 751 23 Uppsala, Sweden, and 2 Department of Physiology and Pharmacology, University of New South Wales, Sydney, 2052, Australia

This study investigates possible mechanisms behind the reduced gastrointestinal ulcerogenicity of nitric oxide (NO)-flurbiprofen compared with flurbiprofen. The duodenal mucosa of Inactin-anaesthetised rats was exteriorized for intravital microscopy. Blood flow was measured with laser-Doppler flowmetry (LDF), mucus thickness with micropipettes, ICAM-1 and P-selectin expression with dual-labeled antibody technique, and mucosal integrity by 51Cr-EDTA permeability. Exposure of the duodenum to flurbiprofen (1.0 mg/ml) for 90 min significantly reduced LDF to 70 ± 4%, whereas NO-flurbiprofen (1.3 mg/ml) had no significant effect. Mucus accumulation after 60-min exposure was 75 ± 23 µm (control), -1 ± 17 µm (flurbiprofen), and 104 ± 35 µm (NO-flurbiprofen). Mucosal permeability to 51Cr-EDTA was unchanged in the control and NO-flurbiprofen groups but increased significantly from 1.0 ± 0.2 to 3.7 ± 0.7 µl · min-1 · g-1 after 90-min exposure to flurbiprofen. Expression of ICAM-1 was significantly increased after oral flurbiprofen but not by NO-flurbiprofen. Positive effects of NO-flurbiprofen compared with flurbiprofen on mucus formation, blood flow, and adhesion molecule expression likely contribute to the reduced mucosal injury observed with NO-flurbiprofen.

laser-Doppler flowmetry; nonsteroidal anti-inflammatory drugs; nitric oxide; mucosal permeability; adhesion molecules


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