title: Selective binding of sucralfate to ulcer lesion. II. Experiments in rats with gastric ulcer receiving 14C-sucralfate or potassium 14C-sucrose sulfate.
abstract: 14C-Sucralfate, a basic aluminum salt of 14C-sucrose sulfate, or potassium 14C-sucrose sulfate was administered orally to rats with acetic acid-induced gastric ulcer. The radioactivities representing specific binding of the sucrose sulfate moiety were found significantly higher in ulcer sections of the stomach, with the mean within-animal ulcer/non-ulcer ratio attaining 6, 7, 12 and 2.5, respectively, at 1, 3, 6 and 24 h after 14C-sucralfate administration. Microautoradiography provided direct in vivo evidence for binding of the 14C-sucrose sulfate moiety to exuded proteins resulting in effect in formation of a pepsin-resistant barrier over the surface of an ulcer crater. No comparable findings were obtained in the area of normal mucosa. The administration of 14C-sucralfate was associated with much greater and longer-sustained binding to the ulcer lesion and retention in the stomach and duodenum than simple administration of the soluble potassium salt. These findings not only demonstrate therapeutically significant effects of basic aluminum compoundation but also substantiate likely differences from pepsin inhibitors such as amylopectin sulfate in terms of presence or absence of adhesiveness, local barrier effects, and long duration of actions.
mesh_terms: D000085:Acetates; D000535:Aluminum / Q000378:metabolism; D000818:Animals; D001345:Autoradiography; D004064:Digestive System / Q000378:metabolism; D004386:Duodenum / Q000378:metabolism; D007420:Intestine, Large / Q000378:metabolism; D008297:Male; D051381:Rats; D013276:Stomach Ulcer / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D013392:Sucralfate; D013395:Sucrose / Q000031:analogs & derivatives / Q000378:metabolism; D013997:Time Factors
chemical_list: D000085:Acetates; D013392:Sucralfate; D013395:Sucrose; D000535:Aluminum