Hawkey C J
Gut. 1986 Dec;27(12):1484-92. doi: 10.1136/gut.27.12.1484.
Because endogenous prostaglandins may protect the gastric mucosa a study was conducted to determine factors influencing the synthesis of immunoreactive prostaglandin (iPG) E2 and thromboxane (iTx) B2 as measured by radioimmunoassay and prostaglandin catabolism measured radiometrically, in human gastric mucosa. Gastric mucosa was obtained at endoscopy. Synthesis of iPE2 and iTxB2 was inhibited in vitro by indomethacin; iTxB2 synthesis was also selectively inhibited by the thromboxane synthesis inhibitor dazmegrel. Prostaglandin catabolism was inhibited by carbenoxolone. Multivariate analysis showed that synthesis of iPGE2 from endogenous precursor during homogenisation was decreased in patients on non-steroidal anti-inflammatory drugs. Mucosal inflammation was associated with significantly increased synthesis of iPGE2 and decreased prostaglandin catabolism. There were no differences between the mucosa of patients with or without gastric ulcers, nor between the ulcer rim and mucosa 5 cm away. Age, sex, smoking history and ingestion of antisecretory drugs appeared to exert no influence. In this study gastritis was the major influence on prostaglandin synthesis. It seems unlikely that prostaglandin deficiency is a strong predisposing factor for gastric ulceration.
由于内源性前列腺素可能对胃黏膜起到保护作用，因此开展了一项研究，旨在确定影响通过放射免疫测定法测得的免疫反应性前列腺素（iPG）E2和血栓素（iTx）B2合成以及通过放射性测量法测得的前列腺素分解代谢的因素，这些研究对象为人类胃黏膜。胃黏膜在内镜检查时获取。吲哚美辛在体外可抑制iPE2和iTxB2的合成；血栓素合成抑制剂达美格雷也可选择性抑制iTxB2的合成。生胃酮可抑制前列腺素的分解代谢。多变量分析显示，使用非甾体抗炎药的患者在匀浆过程中内源性前体生成iPGE2的过程减少。黏膜炎症与iPGE2合成显著增加及前列腺素分解代谢减少相关。患有胃溃疡和未患胃溃疡患者的黏膜之间、溃疡边缘与距溃疡边缘5厘米处的黏膜之间均无差异。年龄、性别、吸烟史及服用抗分泌药物似乎并无影响。在本研究中，胃炎是对前列腺素合成的主要影响因素。前列腺素缺乏似乎不太可能是胃溃疡的一个强有力的诱发因素。
