Konturek S J, Obtulowicz W, Kwiecien N, Oleksy J
Scand J Gastroenterol Suppl. 1984;101:75-7.
Human fundic mucosa generates various prostaglandins (PGs), particularly PGE2, and tromboxanes. This generation appears to be significantly lower in gastric ulcer patients than in duodenal ulcer patients or normal subjects. Nonsteroidal antiinflammatory compounds (NOSAC), such as aspirin or indomethacin, greatly reduce the PG biosynthesis and cause mucosal damage, including mucosal erosions and hemorrhages observed at endoscopy, increased gastric microbleeding and DNA loss. In contrast, paracetamol or carprofen, a novel NOSAC, fails to affect mucosal generation of PGs and does not influence gastric mucosal integrity. This study indicates that endogenous PGs may be involved in the pathogenesis of gastric ulcer and that normal generation of mucosal PGs is essential for the mucosal integrity.
人胃底黏膜能产生多种前列腺素（PGs），尤其是前列腺素E2（PGE2）和血栓素。胃溃疡患者的这种生成量似乎明显低于十二指肠溃疡患者或正常受试者。非甾体类抗炎化合物（NOSAC），如阿司匹林或吲哚美辛，会大幅降低PG生物合成，并导致黏膜损伤，包括内镜检查时观察到的黏膜糜烂和出血、胃微出血增加以及DNA丢失。相比之下，对乙酰氨基酚或新型NOSAC卡洛芬不会影响PG的黏膜生成，也不会影响胃黏膜完整性。这项研究表明，内源性PGs可能参与胃溃疡的发病机制，黏膜PG的正常生成对黏膜完整性至关重要。
