Controlled clinical trials have shown that
tripotassium dicitrato bismuthate healed duodenal and
gastric ulcers significantly better than placebo. One mechanism suggested is that it forms a protective coat at the
ulcer base. We studied this coating action in rats with chronic
gastric ulcers produced by a standardized technique for mucosal wounding at the fundoantral junction.
Bismuth was identified by histochemical staining using Castel's
reagent, the specificity of which was verified in vitro against 13 other metallic compounds and chemicals. Our results showed that
tripotassium dicitrato bismuthate had a coating affinity for the
ulcer base, but not for the adjacent normal mucosa. All rats treated with
tripotassium dicitrato bismuthate 1, 2, 4, and 6 h previously, but not the control rats treated with water or those treated with four other
bismuth compounds, manifested a layer of
bismuth that coated the
ulcer base. Light and electron microscopy of the
tripotassium dicitrato bismuthate-treated
ulcers--but not their controls-revealed an abundance of macrophages, which had ingested the
bismuth. This unique
bismuth coat may insulate the
ulcer base from
acid-
pepsin digestion, while the influx of macrophages may expedite reparative processes.