Impairment of the gastric hyperemic response to luminal acid in
cirrhotic rats.
Nishizaki, Yasuhiro, Paul H. Guth, Catia Sternini, and Jonathan D.
Kaunitz.
Medical Service, West Los Angeles Veterans Affairs Medical Center,
Los Angeles, CA 90073, Department of Medicine, UCLA School of
Medicine, Los Angeles, CA 90024, Department of Anatomy, UCLA School
of Medicine, Los Angeles, CA 90024, CURE: VA/UCLA Gastroenteric
Biology Center, Los Angeles, CA 90073, Current address: 3rd
Department of Internal Medicine, School of Medicine, Tokai
University, Bouseidai, Iseharashi, Kanagawaken 259-11, JAPAN
APStracts 2:0126G, 1995.
Liver cirrhosis impairs gastric mucosal resistance to luminal acid in
humans and in animal models. Since we have previously shown that
pentagastrin enhances defensive as well as aggressive factors
implicated in mucosal injury, we examined the hypothesis that the
pentagastrin-mediated enhancement of mucosal defense mechanisms may
be impaired in cirrhotic rats. Increased acid back-diffusion and
susceptibility to gross mucosal injury, associated with an
elimination of the hyperemic response to gastric barrier disruption,
was observed in cirrhotic rats. In in vivo microscopic studies in
anesthetized rats, cirrhosis had no effect on pentagastrin-associated
enhancement of mucus gel thickness or baseline gastric mucosal blood
flow, although baseline mucus gel thickness was decreased. Cirrhosis
did, however, abolish the luminal acid-related hyperemic response to
pentagastrin, which was associated with impaired pHi homeostasis
during acid superfusion. Cirrhosis did not alter submucosal
calcitonin-gene related peptide immunoreactive nerves. We conclude
that acid back-diffusion and pentagastrin-associated hyperemic
responses are important mucosal defensive factors that are
specifically impaired by cirrhosis.
Received 30 March 1995; accepted in final form 19 June 1995.
APS Manuscript Number G129-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 11 July 1995.