Amioka I, Arima T, Nagashima H
Gastroenterol Jpn. 1987 Jun;22(3):273-9. doi: 10.1007/BF02774252.
The role of endogenous mucosal prostaglandins (PGs) in the production of acute gastric mucosal lesions (AGML) was examined in rats. Aspirin, ethanol or 0.6 N-HCl was given intragastrically and 20% acetic acid was injected into the gastric wall. Endogenous gastric mucosal PG (A + B), PGE and PGF were determined by radioimmunoassay. Their gastric contents were markedly reduced by aspirin administration (p less than 0.001). The level of gastric mucosal PGs still remained low (p less than 0.001) after the aspirin-induced AGML began to heal. Furthermore, rats with AGML induced by ethanol, HCl or acetic acid, showed no decrease in endogenous gastric mucosal PGs compared with the controls. These findings indicated that endogenous PGs are not necessary for either the induction or healing of experimental AGML.
在大鼠中研究了内源性黏膜前列腺素（PGs）在急性胃黏膜损伤（AGML）产生中的作用。通过胃内给予阿司匹林、乙醇或0.6N盐酸，并向胃壁注射20%乙酸。采用放射免疫分析法测定内源性胃黏膜PG（A+B）、PGE和PGF。给予阿司匹林后，它们的胃内容物显著减少（p<0.001）。在阿司匹林诱导的AGML开始愈合后，胃黏膜PGs水平仍保持较低（p<0.001）。此外，与对照组相比，由乙醇、盐酸或乙酸诱导AGML的大鼠内源性胃黏膜PGs没有降低。这些发现表明，内源性PGs对于实验性AGML的诱导或愈合并非必需。
