Pathological Study for Peptic Ulcer-Role of Prostaglandin

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The role of prostaglandins (PGs ) in the gastric mucosa was investigated. Firstly, the release of PGs from the isolated gastric wall of rats was investigated by a tissue incubation method in vitro. The release of PGI2 was higher on the serosal side. The release of PGE2 was, in contrast, higher on the mucosal side. Release of PGs increased in a high calcium medium, and decreased with the addition of EGTA. These results suggest that PGE2 and PGI2 are synthesized in different layers of the gastric wall, and that calcium ion may be required for synthesis or release of PGs in rat stomach. The PGE2 level in the gastric mucosa was increased by histamine or tetragastrin in a dose- related way, and they significantly prevented the gastric mucosal damage caused by 0.6N HCL. These effects were abolished by the pretreatment of indomethacin. These results suggest that secretagogues such as histamine or tetragastrin through increasing endogenous PGE2 protect the gastric mucosa. Secondly, cellular localization of PGE2 producing cells were investigated by the immunoperoxidase technique in rat gastric mucosa.Positive stainings for PGE2 were observed on the luminal surface of the surface epithelial cells and in the cytoplasm of the parietal cells in the deeper layers of the mucosa. These results suggest that parietal cells mainly synthesize PGE2 in rat gastric mucosa. Thirdly, damage caused by ethanol and its prevention by 16,16-dimethyl PGE2 were tested in surface epithelial cells isolated from rat stomach in vitro. Ethanol caused cell damage in a dose-related way, and 16,16-dimethyl PGE2 significantly inhibited the damage caused by 15% ethanol. These results suggest that 16,16-dimethyl PGE2 has direct protective effect on gastric cells.