Selective binding of sucralfate to ulcer lesion. III. Experiments in rats with duodenal ulcer receiving 14C-sucralfate.
To determine whether the previously reported mechanisms of action of sucralfate for gastric ulcer are also operative in duodenal ulcer, a single dose of 14C-labelled sucralfate was administered orally to rats with acetic acid-induced duodenal ulcer. Adhesive coating with sucralfate was visible over the duodenal lesion for 6 h in the majority of animals and found localized increasingly selective to the ulcerous area following administration. Visual observations were supported quantitatively by greater than unity mean within-animal ulcer/non-ulcer ratios of binding by 14C-sucrose fulfate moiety and aluminum, with statistical significance at 3 and 6 h post-administration (P less than 0.01 or 0.05). While the aluminum component was found persistent relative to the sucrose sulfate moiety in the adhesive coating, an additional in vitro study revealed that this was due to the pH of duodenal contents and did not lead to a loss of adhesiveness. In addition to these results, the buffering potential of sucralfate coating to control the local pH condition sufficient for binding to ulcer surface proteins to occur support the conclusion that the same mechanisms of action of sucralfate commonly apply to gastric and duodenal ulcers.
D000085:Acetates; D000535:Aluminum / Q000378:metabolism; D000818:Animals; D004381:Duodenal Ulcer / Q000139:chemically induced / Q000378:metabolism*; D004386:Duodenum / Q000378:metabolism; D008297:Male; D051381:Rats; D013392:Sucralfate; D013395:Sucrose / Q000031:analogs & derivatives; D013997:Time Factors
D000085:Acetates; D013392:Sucralfate; D013395:Sucrose; D000535:Aluminum