Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: KEGG:D00446 (Sucralfate)
 278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the possible protection of sucralfate with regard to acetylsalicylic acid (ASA)-induced gastric mucosal bleeding as measured by a radiochromium assay of faecal blood loss in a double-blind crossover study involving 16 healthy male volunteers. Medication was given in two combinations during the 2nd and 5th week of the study: 1 g ASA and 1 g sucralfate four times daily, or 1 g ASA four times daily and placebo tablets. Mean faecal blood loss (+/- SEM) was 0.38 +/- 0.04 ml/day in the 1st week (no drugs administered), 7.17 +/- 1.60 ml/day during treatment with ASA + sucralfate, and 9.59 +/- 1.76 ml/day during treatment with ASA + placebo, the difference being not statistically significant. Individual bleeding values registered during sucralfate treatment correlated with those measured in the placebo period. However, three persons with pronounced bleeding after ASA + placebo had minimal bleeding after ASA + sucralfate. Sucralfate may have a protective potential by reducing ASA-induced gastric mucosal bleeding, but further studies are required to evaluate its protective mechanisms and to identify the groups of patients that could benefit from this.
 ...
PMID:Does sucralfate reduce acetylsalicylic-acid-induced gastric mucosal bleeding? 330 91

The effect of luminal application of aluminum sulphate, sucralfate, and bismuth subcitrate on gastroduodenal alkali secretion has been studied with isolated amphibian mucosa. The mucosa, stripped of its external muscle layer, was mounted in chambers that allowed titration of alkali secretion and measurement of transmucosal potential difference and electrical resistance. Neutral aluminum sulphate (3 X 10(-3) M) increased bicarbonate secretion by fundic (mean +/- SEM = 144 +/- 48%, n = 5, P less than 0.05), antral (mean +/- SEM = 214 +/- 63%, n = 4, P less than 0.05), and duodenal (mean +/- SEM = 133 +/- 44%, n = 6, P less than 0.005) mucosa. Sucralfate (0.5 g/l) stimulated fundic (mean +/- SEM = 183 +/- 87%, n = 4, P less than 0.05) and antral (mean +/- SEM = 156 +/- 58%, n = 5, P less than 0.005) alkali secretion and, at a concentration of 1 g/l, duodenal output (mean +/- SEM = 42 +/- 15%, n = 6, P less than 0.05). Bismuth subcitrate (10(-4) M) produced a significant rise in fundic (mean +/- SEM = 80 +/- 21%, n = 5, P less than 0.05) and duodenal (mean +/- SEM = 62 +/- 7%, n = 6, P less than 0.05) alkali secretion. None of these agents altered transmucosal potential difference or electrical resistance. The actions of these agents on gastroduodenal bicarbonate secretion may be important in their ulcer healing effects.
 ...
PMID:Effect of certain ulcer-healing agents on amphibian gastroduodenal bicarbonate secretion. 349 20

Sucralfate, an agent that heals peptic ulcers in humans, has been shown to reduce aspirin-induced gastric mucosal damage in experimental animals. It has been suggested that the protective effect of sucralfate is due to stimulation of local prostaglandin production. The purpose of this study was to establish whether sucralfate was capable of reducing aspirin-induced gastric damage in humans. The effect of 1 g of sucralfate or identical placebo was studied in random order in eight healthy subjects. To determine if the effect of sucralfate was related to local prostaglandin synthesis, a second series of studies was performed in which prostaglandin production was inhibited with indomethacin 50 mg given orally eight hours before sucralfate. In each subject, all studies were performed at least one week apart. Following an overnight fast, upper gastrointestinal endoscopy was performed, with sucralfate or placebo given orally 30 minutes before ingestion of 1,200 mg of soluble aspirin in 50 ml of water. Both endoscopist and subject were unaware of the test agent. Ninety minutes after aspirin ingestion, endoscopy was again performed and gastric mucosal lesions were counted and graded to derive an erosion score. Results are expressed as mean +/- SEM. Aspirin produced endoscopic changes (score of 2.75 +/- 0.49) that were significantly (p less than 0.05) inhibited by sucralfate (score of 1.13 +/- 0.44). The protective effect of sucralfate was abolished by pretreatment with indomethacin (scores of 2.88 +/- 0.55 and 1.88 +/- 0.40, respectively). These results demonstrate that sucralfate significantly protects the human gastric mucosa against the acute damaging effects of aspirin. This effect is abolished by indomethacin, suggesting that the protective action of sucralfate on the gastric mucosa of humans may be related to stimulation of endogenous prostaglandins.
 ...
PMID:Protective effect of sucralfate against aspirin-induced damage to the human gastric mucosa. 366 13