Isselbacher K J
Drugs. 1987;33 Suppl 1:38-46. doi: 10.2165/00003495-198700331-00007.
Metabolites of arachidonic acid have a broad range of physiological functions in the gastrointestinal tract, and seem to be involved in certain disturbances of gastrointestinal integrity and function. Prostaglandins inhibit gastric acid secretion, apparently via an adenylate cyclase-linked receptor, and also stimulate bicarbonate and mucus production by alternative mechanisms. These are all beneficial in treating gastroduodenal ulceration. Moreover, clinical studies have revealed deficient prostaglandin synthesis in the gastric and duodenal mucosa of patients with gastrointestinal ulcers, which suggests that endogenous prostaglandins have a protective role in the gastrointestinal tract. In animal studies, prostaglandin analogues have been shown to protect the gastric mucosa from damage induced by various potent irritants, and this protection seems to involve the deeper layers of the mucosa as well as the epithelium. Indeed, misoprostol and other prostaglandin analogues have proved therapeutically effective in treating gastroduodenal ulceration. Prostaglandins also influence intestinal motility and fluid movement. Prostaglandin E derivatives generally relax circular smooth muscle, contract longitudinal smooth muscle and increase fluid secretion into the intestinal lumen. As a result of these effects, prostaglandins may cause diarrhoea. There is also evidence that prostaglandin synthesis is increased in patients with diarrhoea. Finally, it has been reported that tissue concentrations of prostaglandins are increased in patients with ulcerative colitis, but it is unclear if this is a primary cause, or secondary event. Significantly greater conversion of arachidonic acid to its metabolites was recorded in the mucosa of patients with inflammatory bowel disease compared with the mucosa of healthy subjects. This included a substantial increase in the concentration of leukotriene B4.(ABSTRACT TRUNCATED AT 250 WORDS)
花生四烯酸的代谢产物在胃肠道具有广泛的生理功能，似乎与胃肠道完整性和功能的某些紊乱有关。前列腺素抑制胃酸分泌，显然是通过与腺苷酸环化酶相关的受体，并且还通过其他机制刺激碳酸氢盐和黏液的产生。这些对治疗胃十二指肠溃疡均有益处。此外，临床研究表明，胃肠道溃疡患者的胃和十二指肠黏膜中前列腺素合成不足，这表明内源性前列腺素在胃肠道中具有保护作用。在动物研究中，前列腺素类似物已被证明可保护胃黏膜免受各种强效刺激物的损伤，这种保护作用似乎涉及黏膜的深层以及上皮。事实上，米索前列醇和其他前列腺素类似物已被证明在治疗胃十二指肠溃疡方面具有治疗效果。前列腺素还影响肠道蠕动和液体流动。前列腺素E衍生物通常使环形平滑肌松弛，使纵行平滑肌收缩，并增加肠腔内的液体分泌。由于这些作用，前列腺素可能导致腹泻。也有证据表明腹泻患者的前列腺素合成增加。最后，据报道溃疡性结肠炎患者的组织中前列腺素浓度升高，但尚不清楚这是原发性原因还是继发性事件。与健康受试者的黏膜相比，炎症性肠病患者的黏膜中花生四烯酸向其代谢产物的转化明显更高。这包括白三烯B4浓度的大幅增加。（摘要截选至250词）
