Crampton J R, Gibbons L C, Rees W D
Department of Gastroenterology, University of Manchester School of Medicine, Hope Hospital, Salford.
Scand J Gastroenterol Suppl. 1987;140:15-8.
The effect of sucralfate on gastroduodenal bicarbonate secretion has been examined using isolated amphibian mucosa. Significant increases in gastric bicarbonate secretory rate were seen following addition of 0.5 milligram sucralfate to the luminal solution. Duodenal alkali secretion was stimulated only by a higher concentration of 1 milligram. Pretreatment with indomethacin prevented the increases in gastric and duodenal bicarbonate secretion observed after sucralfate. Other experiments indicated that sucralfate caused stimulation of prostaglandin E2 formation by mucosal homogenates. These studies demonstrate that sucralfate is a potent stimulant of gastroduodenal bicarbonate secretion and that the action is dependent on mucosal prostaglandin formation. These effects are likely to play an important role in the mode of action of the drug.
已使用离体两栖类动物黏膜研究了硫糖铝对胃十二指肠碳酸氢盐分泌的影响。向管腔溶液中添加0.5毫克硫糖铝后，观察到胃碳酸氢盐分泌速率显著增加。仅在较高浓度1毫克时，十二指肠碱分泌才受到刺激。用吲哚美辛预处理可阻止硫糖铝后观察到的胃和十二指肠碳酸氢盐分泌增加。其他实验表明，硫糖铝可刺激黏膜匀浆中前列腺素E2的形成。这些研究表明，硫糖铝是胃十二指肠碳酸氢盐分泌的强效刺激剂，且该作用依赖于黏膜前列腺素的形成。这些效应可能在该药物的作用方式中起重要作用。
