Toxic dilatation of the colon in a rat model of colitis is linked
to an inducible form of nitric oxide synthase.
Mourelle, Marisabel, Jaime Vilaseca, Francisco Guarner, Antonio Salas,
and Juan-R. Malagelada.
Digestive System Research Unit, Hospital General Vall d'Hebron,
Pathology Department, Hospital Mutua, Barcelona, Spain
APStracts 2:0198G, 1995.
The contribution of nitric oxide to the altered colonic contractility
of acute colitis was investigated in the trinitrobenzenesulfonic acid
model. Nitric oxide-synthase was measured in colonic tissue; the
effects of NO-synthase inhibition on colonic contractility were
studied in vitro and in vivo. Inducible nitric oxide-synthase was not
detected in normal colons, whereas inflamed colons showed high
activity. Acute inflammation was associated with enlarged colonic
perimeter. Nitric oxide-synthase inhibitors or selective inhibitors
of the inducible enzyme prevented colonic dilatation. In vitro,
contractile responses to KCl were lower in muscle from colitic than
control rats. After nitric oxide-synthase inhibition, however, no
difference was observed between colitic and control muscle
contractility. In vivo, intracolonic pressure was lower in colitic
than in control rats. Selective inhibition of inducible NO-synthase
increased intracolonic pressure in colitic but not in control rats.
In conclusion, nitric oxide generation by inducible enzymes impairs
smooth muscle contractility in colitis and may be involved in the
pathogenesis of toxic dilatation of the colon.
Received 3 August 1994; accepted in final form 4 September 1995.
APS Manuscript Number G291-4.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95