Quadros E, Ramsamooj E, Wilson D E
Department of Medicine, SUNY-Health Science Center at Brooklyn 11203.
Am J Med. 1987 Sep 28;83(3B):19-23. doi: 10.1016/0002-9343(87)90822-9.
This study investigated the relationship between the protective effect of sucralfate against ethanol-induced gastric mucosal injury in the rat and the effects of sucralfate on prostaglandin and mucus synthesis and secretion. Sucralfate at 200, 400, and 800 mg/kg significantly reduced gastric ulceration. Intragastric administration of sucralfate increased luminal mucus and prostaglandin E2 levels but did not affect prostaglandin or mucus synthesis in gastric mucosal biopsy specimens from sucralfate-treated animals. Pretreatment with indomethacin partially reduced the protective effect of sucralfate. However, sucralfate 200 mg/kg, a dose that completely prevented ulceration, did not increase the levels of luminal prostaglandin E2. In vitro incubation with sucralfate did not stimulate mucosal prostaglandin synthesis. Longer-term administration of sucralfate for 48 or 96 hours did not stimulate mucus or prostaglandin synthesis but did increase luminal prostaglandin E2 and mucus. Although sucralfate increased the gastric juice content of prostaglandin E2 and mucus, the two did not appear to be mechanistically related, and only mucus release was consistently associated with mucosal protection.
本研究调查了硫糖铝对大鼠乙醇诱导的胃黏膜损伤的保护作用与硫糖铝对前列腺素及黏液合成和分泌的影响之间的关系。200、400和800mg/kg的硫糖铝显著减少胃溃疡形成。胃内给予硫糖铝可增加腔内黏液和前列腺素E2水平，但不影响硫糖铝处理动物胃黏膜活检标本中前列腺素或黏液的合成。用吲哚美辛预处理可部分降低硫糖铝的保护作用。然而，200mg/kg的硫糖铝（该剂量可完全预防溃疡形成）并未增加腔内前列腺素E2水平。硫糖铝体外孵育不刺激黏膜前列腺素合成。硫糖铝长期给药48或96小时不刺激黏液或前列腺素合成，但确实增加腔内前列腺素E2和黏液。虽然硫糖铝增加了胃液中前列腺素E2和黏液的含量，但二者在机制上似乎并无关联，只有黏液释放始终与黏膜保护相关。
