Tripotassium dicitrato bismuthate (TDB), De-Nol, heals peptic ulcers with an efficacy similar to the H2 antagonists. Tripotassium dicitrato bismuthate may also be effective in decreasing relapse rates. Its mode of action is unknown, but it was recently observed that TDB rapidly increased the number of macrophages in experimental ulcers. This might accelerate reparative processes, accounting for the drug's action. Using more sophisticated techniques we could not demonstrate any macrophage influx in response to single, or multiple, doses of TDB. Electron micrographs did demonstrate that monocytes, the precursors of macrophages, could internalize TDB. This process occurred rapidly in the presence of plasma where an avid TDB-protein interaction was observed. It has been suggested that such an interaction upon the ulcer may form a protective layer allowing mucosal regeneration to occur unhindered beneath. We believe our electron micrographs support this theory.