Decreased parietal cell acid secretion after vagotomy is not associated with altered gastric prostaglandin levels.

In a previous investigation we demonstrated that after vagotomy there is a decreased ability of parietal cells to use intracellular cyclic adenosine monophosphate (cAMP). Prostaglandins are present in gastric mucosa and have been demonstrated to be inhibitors of in vivo and in vitro acid secretion through a cAMP-mediated mechanism. In the present study we have examined in vitro acid secretion and prostaglandin E2 levels in rabbits 8 weeks after vagotomy and pyloroplasty compared with control animals to investigate the possible role of prostaglandins in postvagotomy-impaired cAMP use. In vitro acid secretion was assessed in isolated gastric glands by 14C-labeled aminopyrine uptake and prostaglandin E2-generating capacity measured by high-pressure liquid chromatography. After vagotomy, there was a decrease in basal aminopyrine uptake (p less than 0.05), as well as that simulated by histamine and 8-bromo-cAMP (p less than 0.007). No differences were observed in prostaglandin E2 levels in either gastric glands or intact fundic mucosa (p greater than 0.5). These data suggest that impaired cAMP use observed in parietal cells after vagotomy is not the result of alterations in gastric prostaglandin levels.