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

Histamine is involved in gastric vasodilation during acid back diffusion via activation of sensory neurons

“…2). Furthermore, in two recent studies (37,38) using the same experimental model as in the present investigations, we showed that mast cell-stabilizing ketotifen and sodium cromoglycate, which, to our knowledge, cannot protect against lysis, were able to completely protect against reduction of the mast cell mass associated with acid back diffusion. Therefore, it is reasonable to suggest that the reduction of stainable mast cells could be attributed to degranulation, although we acknowledge the possibility that lysis of mast cells could be part of it.…”

“…As in our recent study (38), exposure of the gastric mucosa to saline pH 1.0 after hypertonic injury led to a substantial reduction of stainable mast cells, an effect that could be attributed to acid back diffusion, because it was not evident when the mucosa was exposed to neutral saline after hypertonic injury (Table 1). It might be pertinent to consider whether or not the decrease of stainable mast cells could be a result of damage of the mucosa and thereby lysis of mast cells.…”

“…Therefore, it is reasonable to suggest that the reduction of stainable mast cells could be attributed to degranulation, although we acknowledge the possibility that lysis of mast cells could be part of it. It is also reasonable to assume that the increased luminal release of histamine in response to acid back diffusion in the present study at least mainly comes from mast cells because: 1) a detailed morphometric analysis of ECL cells (evaluated as chromogranin-A immunoreactive cells) in our recent study (38) using the same experimental model did not reveal any changes whatsoever during acid back diffusion; 2) luminal release of histamine associated with acid back diffusion was closely correlated with preservation of stainable mast cells by a mast cellstabilizing agent (38); and 3) in the present study no increase of the ECL cell marker pancreastatin was detected during acid back diffusion.…”

“…Blockade of H 1 or H 3 receptors, either attenuated or abolished, respectively, the hyperemic response to acid back diffusion. These findings led to the conclusion that mast cells are involved in the gastric hyperemic response to acid back diffusion via release of histamine (38). However, the question still remains whether the mast cells are directly influenced by back-diffusing protons or whether they are degranulated by, for example, activated sensory neurons.…”

“…We (38) recently showed that histamine released from mast cells is involved in the vasodilator response to acid back diffusion in the chambered stomach of the rat. The reason for this contention was that rats with either pharmacologically depleted or stabilized mast cell mass showed almost abolished release of histamine and hyperemia in response to acid back diffusion into the mucosa.…”