16-16-dimethylprostaglandin-e2 and meciadanol

Flavonoids reportedly inhibit histidine decarboxylase and reduce gastric mucosal histamine content. We studied the effects of acute and chronic intragastric administration to rats of meciadanol, a new synthetic flavonoid (Zyma S.A., Nyon, Switzerland). The action of meciadanol was compared to that of 16,16-dimethyl PGE2. Meciadanol did not affect acid or pepsin output at any dose used. High doses of 16,16-dimethyl PGE2 reduced both acid and pepsin output. Meciadanol partially prevented aspirin-induced lesions but the prevention required chronic administration of meciadanol. In contrast, a single dose of meciadanol completely prevented ethanol-induced lesions. Chronic administration of meciadanol also completely prevented ethanol-induced lesions. 16,16-Dimethyl PGE2 prevented both aspirin-induced and ethanol-induced lesions in doses that did not affect acid or pepsin output. Meciadanol did not influence the effect that either aspirin or ethanol had on endogenous mucosal PGI2. Thus, the dose range of meciadanol that protected against ulcerogens did not affect either gastric acid secretion or pepsin output. Therefore, we conclude that meciadanol's action represents true cytoprotection, which was previously attributed only to prostaglandins.

Topics: 16,16-Dimethylprostaglandin E2; Animals; Anti-Ulcer Agents; Aspirin; Benzopyrans; Carboxy-Lyases; Catechin; Epoprostenol; Ethanol; Female; Gastric Acid; Gastric Mucosa; Histidine Decarboxylase; Male; Rats; Rats, Inbred Strains; Stomach Ulcer; Time Factors