Effects of an antiulcer drug, sucralfate (A basic aluminum salt of sulfated disaccharide), on experimental gastric lesions and gastric secretion in rats

Abstract

The effects of oral sucralfate, a basic aluminum salt of sulfated disaccharide, on various experimental gastric lesions and on gastric secretion were studied in rats. Sucralfate at 300 mg/kg potently inhibited the development of Shay ulcers and indomethacin- and aspirin-induced erosions. The drug at 1000 mg/kg also potently inhibited histamine-induced erosions. Water-immersion stress-induced erosions were inhibited with 1000 mg/kg of the drug, but the degree of inhibition was weaker than that seen in other types of erosion formation. Sucralfate at 1000 mg/kg given twice daily for 14 days significantly accelerated the spontaneous healing of acetic acid-induced ulcers. Sucralfate at over 300 mg/kg tended to increase the volume of gastric juice but had an insignificant effect on acid and pepsin output of pylorus-ligated rats. As a whole, the effects of sucralfate on experimental gastric lesions appear to be much more potent than Maalox, propantheline bromide, and cimetidine. The mechanism of action of sucralfate remains to be determined.

Effects of 12-sulfodehydroabietic acid monosodium salt (TA-2711), a new anti-ulcer agent, on gastric secretion and experimental ulcers in rats.

“…Sucralfate caused no inhibition of gastric pepsin activity and had no preventive effect against aspirin-induced erosions, while TA-2711 did. The result of sucralfate in gastric pepsin activity was consistent with that re ported by Okabe et al (18). On the other hand, Okabe et al (18) …”

“…The result of sucralfate in gastric pepsin activity was consistent with that re ported by Okabe et al (18). On the other hand, Okabe et al (18) …”

“…The increase in acid secretion (16) and gastric motility (17) has been postulated to be involved in the pathogenesis of the mucosal damage. In addition to the weak effect of TA-2711 on gastric acidity, the possible prompt elimination of this drug from the stomach to the duodenum caused by the increased gastric motility during stressing (18) may explain the low efficacy of TA-2711 on the stress erosions. Sucralfate and carbenox clone, both of which are known to act locally and have no substantial effect on acid secre tion, also did not show any inhibitory effect on the development of the stress erosions, whereas cimetidine, a histamine H2 receptor antagonist, which inhibits gastric acid secre tion, significantly prevented the development of erosions.…”

Effects of KB-5492, 1-(3,4,5-Trimethoxybenzyl)-4-((4-Methoxyphenyl)oxycarbonylmethyl)piperazine Monofumarate Monohydrate, on Gastric Lesions and Gastric Secretion in Rats

“…The pathogenesis of histamine-induced lesions remains un known. In the model of histamine-induced lesions produced by histamine at 100 mg/kg, i.p., propantheline bromide and cimetidine were effective for inhibiting the lesions, thereby indicating the participation of gastric acid and pepsin (13). In another study, it was confirmed that histamine interfered with gastric mucosal circulation in guinea pigs (14).…”

Effects of various agents on prednisolone-induced gastric lesions in rats.

“…The stomach was put into 10% formalin for microscopy. The following agents were given to various groups of 10 were given by oral gastric intubation in a volume of 0.5 ml/100 g of body weight twice (9:00 AM, 6:00 PM) or thrice (9:00 AM, 2:00, 7:00 PM) daily for 4 days during the prednisolone treatment. PG12, firstly dissolved in 1 M Tris buffer and stored in a deep freezer, was diluted with 1.25% NaHCO3 to a desired concentration and given subcutaneously in a volume of 0.2 ml/ 100 g of body weight, 4 times (9:00 AM, 0:00, 3:00, 6:00 PM) daily.…”