Pathological Study for Peptic Ulcer-Role of Prostaglandin

探讨前列腺素在胃粘膜中的作用。首先，采用组织培养法研究离体大鼠胃壁pg的体外释放情况。浆膜侧PGI2的释放量较高。相比之下，PGE2在粘膜侧的释放量更高。PGs的释放在高钙培养基中增加，随着EGTA的加入而减少。这些结果表明，PGE2和PGI2是在不同的胃壁层中合成的，大鼠胃中PGs的合成或释放可能需要钙离子。组胺和四甲黄素均能使胃黏膜PGE2水平呈剂量相关升高，并能显著预防0.6N盐酸对胃黏膜的损伤。经吲哚美辛预处理后，这些影响被消除。这些结果表明，分泌剂如组胺或四甲黄素通过增加内源性PGE2来保护胃粘膜。其次，利用免疫过氧化物酶技术研究大鼠胃粘膜中PGE2生成细胞的细胞定位。表面上皮细胞的管腔表面和粘膜深层壁细胞的细胞质中可见PGE2阳性染色。提示大鼠胃粘膜壁细胞主要合成PGE2。第三，研究乙醇对大鼠胃表面上皮细胞的损伤及16,16-二甲基PGE2的预防作用。乙醇引起细胞损伤呈剂量相关，16,16-二甲基PGE2显著抑制15%乙醇引起的细胞损伤。说明16,16-二甲基PGE2对胃细胞具有直接的保护作用。

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.