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The relationship between gastric mucosal prostaglandin (PG) and acute gastric mucosal lesions caused by oral administration of phenylbutazone 200mg/kg was examined in rats. PGE and PG (A+B) were extracted, separated from the PG group on silicic acid column chromatography, and converted into PGB by alkaline treatment. Following above procedures, the PG was measured with the RIA double antibody method using anti-PGB1 serum.In the control rats, PGE was found approximately 10 times higher in concentration compared to PG (A+B). PG quantities in the experimental rats given the phenylbutazone were, both PGE and PG (A+B), significantly lower (p<0.001) at 6 hours after administration. And the PG remained low at 54 hours after, by which time the lesions had healed. These data shows that recovery from gastric mucosal lesions and the increase of endogenous PG are not related to each other.Furthermore, proglumide, an agent that promotes healing of ulcers, was administrated to determine whether or not the increase of gastric mucosal PG facilitates the recovery from gastric ulcer lesions. The accompanying increase of endogenous gastric mucosal PG was not observed. Therefore, proglumide did not cause the increase of gastric mucosal PG.These results proved that the decrease of endogenous gastric mucosal PG is related directly to the cause of acute gastric mucosal lesions. But, recovery from acute gastric mucosal lesions is not necessarily accompanied by the PG increase.
財団法人日本消化器病学会の論文

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