硫糖铝和铝对两栖类动物胃十二指肠碳酸氢盐分泌的刺激作用：局部前列腺素代谢的作用
Stimulation of amphibian gastroduodenal bicarbonate secretion by sucralfate and aluminium: role of local prostaglandin metabolism.
作者信息
Crampton J R, Gibbons L C, Rees W D
机构信息
University of Department of Medicine Addenbrooke's Hospital, Cambridge.
出版信息
Gut. 1988 Jul;29(7):903-8. doi: 10.1136/gut.29.7.903.
The present studies were designed to explore the possible mode of protective and ulcer healing actions of sucralfate by examining its effect on gastroduodenal bicarbonate secretion by isolated amphibian mucosa. Luminal sucralfate (0.5 g/l) significantly increased bicarbonate secretion by fundic and antral mucosa without influencing transmucosal potential difference. Significant stimulation of duodenal bicarbonate secretion occurred only at 1.0 g/l without change in potential difference. Aluminium, a component of sucralfate, produced similar increases in bicarbonate secretion, while the sucrose and sulphate components were without effect. Pretreatment of mucosae with the cyclooxygenase inhibitor, indomethacin (10 5M) did not abolish the secretory response to sucralfate or aluminium. The results suggest that stimulation of gastroduodenal bicarbonate secretion, possibly by the aluminium moiety of sucralfate, may play a role in its protective and ulcer healing actions.
本研究旨在通过检测硫糖铝对离体两栖类动物黏膜胃十二指肠碳酸氢盐分泌的影响，探讨其可能的保护和促进溃疡愈合作用方式。腔内硫糖铝（0.5 g/l）显著增加了胃底和胃窦黏膜的碳酸氢盐分泌，而不影响跨黏膜电位差。仅在1.0 g/l时十二指肠碳酸氢盐分泌受到显著刺激，且电位差无变化。硫糖铝的成分铝也使碳酸氢盐分泌有类似增加，而蔗糖和硫酸盐成分则无作用。用环氧化酶抑制剂吲哚美辛（10⁻⁵M）预处理黏膜，并未消除对硫糖铝或铝的分泌反应。结果表明，可能由硫糖铝的铝部分刺激胃十二指肠碳酸氢盐分泌，这可能在其保护和促进溃疡愈合作用中发挥作用。
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