Effect of meciadanol on gastric secretion and aspirin-induced gastric mucosal injury in humans.
The aim of this study was to assess the effects of a newly synthesized flavonoid, meciadanol, on gastric secretion and on aspirin-induced gastric mucosal injury in healthy humans. In vitro experiments have shown that meciadanol (INN proposed) inhibits histidine decarboxylase in gastric cells. In our study meciadanol did not affect either basal or pentagastrin-stimulated gastric acid secretion or pepsin secretion and did not produce any endoscopic or histological changes in the stomach or duodenum. Meciadanol prevented aspirin-induced microbleeding and aspirin-induced DNA loss, suggesting that gastric mucosal histamine is involved in the mucosal injury caused by aspirin.
D000328:Adult; D001241:Aspirin / Q000009:adverse effects*; D001578:Benzopyrans / Q000494:pharmacology*; D002392:Catechin / Q000031:analogs & derivatives / Q000494:pharmacology*; D004247:DNA / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism; D006632:Histamine / Q000378:metabolism; D006801:Humans; D010434:Pepsin A / Q000378:metabolism
D001578:Benzopyrans; C029339:meciadanol; D006632:Histamine; D002392:Catechin; D004247:DNA; D010434:Pepsin A; D001241:Aspirin