AJP - GI Information on EB 2010
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Gastrointest Liver Physiol 280: G1061-G1069, 2001;
0193-1857/01 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (9)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rydning, A.
Right arrow Articles by Grønbech, J. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rydning, A.
Right arrow Articles by Grønbech, J. E.
Vol. 280, Issue 6, G1061-G1069, June 2001

Mast cells are involved in the gastric hyperemic response to acid back diffusion via release of histamine

Astrid Rydning1, Oddveig Lyng1, Birgitte Lid Adamsen1, Sture Falkmer2, Arne K. Sandvik3, and Jon Erik Grønbech1

Departments of 1 Surgery, 2 Laboratory Medicine, and 3 Physiology, Norwegian University of Science and Technology, N-7006 Trondheim, Norway

Acid back diffusion into the rat stomach mucosa leads to gastric vasodilation. We hypothesized that histamine, if released from the rat mucosa under such conditions, is mast cell derived and involved in the vasodilator response. Gastric blood flow (GBF) and luminal histamine were measured in an ex vivo chamber. Venous histamine was measured from totally isolated stomachs. Mucosal mast cells (MMC), submucosal connective tissue mast cells (CTMC), and chromogranin A-immunoreactive cells (CgA IR) were assessed morphometrically. After mucosal exposure to 1.5 M NaCl, the mucosa was subjected to saline at pH 5.5 (control) or pH 1.0 (H+ back diffusion) for 60 min. H+ back diffusion evoked a marked gastric hyperemia, increase of luminal and venous histamine, and decreased numbers of MMC and CTMC. CgA IR cells were not influenced. Depletion of mast cells with dexamethasone abolished (and stabilization of mast cells with ketotifen attenuated) both hyperemia and histamine release in response to H+ back diffusion. GBF responses to H+ back diffusion were attenuated by H1 and abolished by H3 but not H2 receptor blockers. Our data conform to the idea that mast cells are involved in the gastric hyperemic response to acid back diffusion via release of histamine.

sensory neurons; thioperamide; pyrilamine; enterochromaffin-like cells


This article has been cited by other articles:


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
A. Rydning, O. Lyng, S. Falkmer, and J. E. Gronbech
Histamine is involved in gastric vasodilation during acid back diffusion via activation of sensory neurons
Am J Physiol Gastrointest Liver Physiol, September 1, 2002; 283(3): G603 - G611.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online