Mast cells are involved in the gastric hyperemic response to acid back diffusion via release of histamine
American Journal of Physiology - Gastrointestinal and Liver Physiology
Grønbech. Mast cells are involved in the gastric hyperemic response to acid back diffusion via release of histamine. Am J Physiol Gastrointest Liver Physiol 280: G1061-G1069, 2001.-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.
... 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 ϩ back diffusion) for 60 min. H ϩ 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 ϩ back diffusion. GBF responses to H ϩ back diffusion were attenuated by H 1 and abolished by H 3 but not H 2 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 GASTRIC MUCOSAL HYPEREMIA in response to acid back diffusion after disruption of the mucosal barrier protects the mucosa against further acid injury (16, 21, 36) mainly by providing enhanced delivery of plasma HCO 3 Ϫ for buffering of H ϩ within the mucosa (18). At least in the rat stomach, sensory afferent neurons appear to be instrumental in mediation of this type of vasodilation (19, 20, 21) . Some evidence suggests that sensory nerves in the stomach may respond directly to local variations in H ϩ concentration (11), whereas it is not known whether increased concentrations of H ϩ per se have any direct effect on, for instance, mast cells, causing release of histamine or other possible mediators for vasodilation in the stomach wall.