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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
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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] |
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