Endogenous prostaglandin E2 synthesis preserved following cytoprotection by Roter (bismuth subnitrate) in the rat alcohol model of gastric ulceration.

The protective effect of the compound preparation Roter, principally bismuth subnitrate and the other base constituents of these tablets, magnesium carbonate and sodium bicarbonate, were assessed using the standard alcohol model of gastric ulceration in the rat. Groups of ten rats were studied with Group A as controls, Group B alcohol alone, Group C pretreatment with base components followed by alcohol, Group D pretreatment with bismuth subnitrate followed by alcohol and Group E pretreatment with full formulation Roter followed by alcohol. The study was assessed by measurement of areas of gastric ulceration and tissue prostaglandin E2 (PGE2) levels. Alcohol alone caused gross ulceration and reduction in PGE2 synthesis compared to controls (P less than 0.001). Pretreatment with tablet base gave only marginal protection whilst bismuth subnitrate gave marked protection against ulceration compared to alcohol alone (P less than 0.001). Full formulation Roter also gave marked protection against ulceration compared to alcohol alone (P less than 0.001) and this was associated with PGE2 synthesis indistinguishable from controls but significantly greater than in the alcohol alone group (P less than 0.001). It was not possible to determine whether the normal PGE2 synthesis was the cause or the result of protective effect of Roter and the accompanying reduction in ulceration. It was possible however to conclude that using this model of experimental ulceration. Roter and bismuth subnitrate are 'cytoprotective' and this was associated with the preservation of normal prostaglandin synthesis.