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Division of Gastroenterology, Department of Medicine, University of California, San Diego, School of Medicine, San Diego, California 92103
The objective was
to characterize changes in barrier and transport function in an
experimental model of colitis, and to determine whether mast cells
contribute to these changes. Colitis was induced in rats with
intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS, 30 mg) in 50%
ethanol. Controls received 0.9% saline or the ethanol vehicle alone.
In vivo loop perfusion was used to assess colonic water flux (in
µl · cm
1 · h1)
and lumen-to-blood 51Cr-labeled
EDTA clearance (% administered dose) after TNBS. Myeloperoxidase (MPO)
was used as an index of granulocyte influx. TNBS or its vehicle caused
a marked decrease in water absorption and an increase in permeability
at 4 h after administration compared with saline. Neither dexamethasone
(anti-inflammatory control) nor doxantrazole (mast cell stabilizer) was
able to attenuate these early changes likely caused by the vehicle. In
contrast, at later times, TNBS (but not its vehicle) also increased
51Cr-EDTA permeability and
decreased water absorption; both effects were significantly attenuated
by dexamethasone or doxantrazole. These drugs also significantly
reduced TNBS-induced MPO accumulation and release of rat mast cell
protease II. We conclude that experimental colitis is associated with
severe defects in intestinal transport and barrier functions and that
mast cells may contribute to the pathogenesis of these changes.
intestinal transport; permeability; inflammation; doxantrazole; dexamethasone
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