Protection of the gastric mucosa against the lesions caused by reserpine through degranulation of mucosal mast cells.

Abstract

AbstractThe ulcerating effects of reserpinisation in the gastric mucosa of rats were studied by special observation of the function of the gastric mucosal mast cells and the changes in mitotic activity of the epithelial cells. The significance of degranulation of the mucosal mast cells for the ulcerating effect of reserpine was also studied after the pretreatment of rats with dexamethasone. Immediately after the dexamethasone treatment there was a pronounced decrease in mitotic count of the gastric mucosal epithelium which 2—3 days later when the mast cells of the gastric mocusa were almost completely degranulated was followed by a 2—3 fold increase in mitotic activity as compared with controls. 10 and 20 days later the mitotic count in the gastric mucosal epithelium decreased below the controls values, the mucosal mast cells being re‐granulated over the control values. The changes in mitotic count in the epithelium of duodenum. ileum and colon under the same conditions were scanty. The degranulation of the mast cells was markedly slighter in the intestinal than in the gastric mucosa. In the reserpinized rats the number of mitoses in the gastric epithelium decreased simultaneously with the degranulation of the mast cells. The degranulation of the mast cells in the duodenal mucosa was slighter and no changes in mitotic activity occurred in the duodenal epithelium. Lesions appeared during reserpinisation in the ventricular mucosa. Reserpinisation after the dexamethasone treatment did not cause ulcer formation in the gastric mucosa, nor did it in this phase cause inhibition in the mitotic activity, typical of which was an overshooting 2—3 days after dexamethasone treatment. The mechanism of gastric mucosal ulceration is discussed.