Role of nitric oxide in restitution of injured guinea pig gastric
mucosa in vitro.
Yanaka, Akinori, Hiroshi Muto, Hisayuki Fukutomi, Susumu Ito, and
William Silen.
Department of Gastroenterology, Institute of Clinical Medicine,
University of Tsukuba, Ibaraki, 305 Japan, Department of
Neurobiology, Harvard Medical School, Boston, MA 02115, Department of
Surgery, Beth Israel Hospital, Harvard Medical School, Boston, MA
02215
APStracts 2:0025G, 1995.
The role of nitric oxide (NO) in restitution was examined in intact
sheets of in vitro guinea pig gastric mucosae after mucosal injury
induced by exposing the luminal surface to 1.25 M NaCl for 10 min.
The recovery of transmucosal electrical resistance and 3H-mannitol
flux after the injury were significantly greater at luminal pH (pHL)
7.0 than at 3.0. The recovery was abolished by pretreatment with 1 mM
NG-nitro-L-arginine methyl ester (L-NAME), only at pHL 3.0, an effect
reversed by 1 mM L-arginine. Enhancement of the recovery by L
-arginine at pHL 3.0 was abolished by 50 [mu]M methylene blue, an effect
restored by 1 mM N2, 2'-O-dibutyrylguanosine 3',5'-cyclic
monophosphate (dbcGMP). In L-arginine-treated, but not in L-NAME
-treated tissues, recovery was enhanced further by an increase in
[HCO3-]s, and was inhibited either by 5 % N-acetyl-L-cysteine
in the luminal solution, or by the removal of serosal HCO3-.
Morphological examination showed the formation of a thick "mucoid
cap" in L-arginine-treated, but not in L-NAME-treated tissues. These
results suggest that, in the presence of luminal acid, endogenous NO
contributes to restitution in injured gastric mucosa at least in part
by facilitating the formation of the "mucoid cap".
Received 6 July 1994; accepted in final form 27 January 1995.
APS Manuscript Number G262-4.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 February 1995.