Role of mast cell mediators in pathogenesis of anaphylactic gastric ulcer

In an attempt to elucidate the pathophysiological mechanisms of gastric anaphylactic ulcer we measured tritiated thymidine incorporation in gastric cells, their mitotic rate and the degranulation of mast cells in the preulcerous phase. The results showed that there is a highly significant increase in cell turnover and mast cell degranulation in the mucosa of sensitized animals. Changes were found at the site of ovalbumin challenge, where point ulceration occurred within 48-72 h. The tissue culture studies demonstrated that the mucosa of sensitized animals produces significantly more histamine when challenged with ovalbumin than the mucosa of nonsensitized animals. Addition of histamine to the tissue culture medium in which normal gastric mucosa was cultured led to an increase in [3H]-thymidine uptake at low concentration, and a decrease at high concentration. Serotonin added to the culture medium had no significant effect on [3H]-thymidine uptake, but heparin at high concentration was found to have a stimulatory effect. These studies show that anaphylactic gastric ulceration is associated with an increase in mucosal cell turnover, and that the mast cell mediator responsible for this increase may be histamine.