Peskar B M
Wien Klin Wochenschr. 1984 Feb 17;96(4):133-8.
Human gastric mucosa synthesizes significant amounts of thromboxane, which has recently been found to be highly ulcerogenic, in addition to protective prostaglandins. The ratio of the various mucosal arachidonic acid metabolites formed may, therefore, exert a modifying influence on the resistance of the mucosa against noxious agents. This hypothesis is supported by the finding that carbenoxolone, a drug accelerating peptic ulcer healing by a mechanism which does not involve inhibition of acid secretion, stimulates gastric mucosal prostaglandin formation and, in parallel, inhibits mucosal thromboxane synthesis. Ulcerogenic non-steroidal anti-inflammatory drugs, on the other hand, usually reduce gastric prostaglandin formation. The inhibitory activity of the various compounds is dependent on their affinity to the gastric mucosal cyclooxygenase, as well as on pharmacokinetic properties. Since gastrointestinal side-effects frequently occur during anti-inflammatory-analgesic therapy, the elucidation of the underlying mechanisms seems of considerable clinical relevance.
人类胃黏膜除了合成具有保护作用的前列腺素外，还能合成大量血栓素，最近发现血栓素具有高度致溃疡作用。因此，所形成的各种黏膜花生四烯酸代谢产物的比例可能会对黏膜抵抗有害因子的能力产生调节作用。这一假说得到了以下发现的支持：甘珀酸是一种通过不涉及抑制胃酸分泌的机制加速消化性溃疡愈合的药物，它能刺激胃黏膜前列腺素的形成，同时抑制黏膜血栓素的合成。另一方面，致溃疡的非甾体抗炎药通常会减少胃前列腺素的形成。各种化合物的抑制活性取决于它们对胃黏膜环氧化酶的亲和力以及药代动力学特性。由于抗炎镇痛治疗期间经常出现胃肠道副作用，阐明其潜在机制似乎具有相当大的临床意义。
