Knutson L, Flemström G, Gustavsson S, Jedstedt G, Lönnerholm G
Scand J Gastroenterol. 1987 Jan;22(1):87-90. doi: 10.3109/00365528708991862.
The bicarbonate secretion by the duodenal mucosa, which is stimulated by luminal acid, is very probably important in mucosal protection against the acid. It was of interest to investigate whether long-term deprivation of the mucosa of this acid stimulus affected the alkali secretion. Sprague-Dawley rats were treated for 4-6 weeks with either omeprazole, 14 mg/kg body weight twice daily, or ranitidine, 300 mg/kg twice daily, by means of gastric intubation. The rate of bicarbonate secretion by the duodenal mucosa was determined in situ by continuous titration. Neither the basal secretion nor the increase in secretion in response to stimulation by prostaglandin E2 or luminal acid (pH 2.0 for 5 or 60 min) differed in treated animals from that in controls that had received placebo (p greater than 0.05). Thus, 4-6 weeks of treatment with omeprazole or ranitidine did not reduce duodenal mucosal bicarbonate secretion in the rat, nor did these drugs diminish the ability of this mucosa to respond to prolonged luminal acidification or luminally administered prostaglandin E2.
十二指肠黏膜分泌的碳酸氢盐受腔内酸刺激，很可能在黏膜抵御酸的过程中发挥重要作用。研究长期剥夺黏膜的这种酸刺激是否会影响碱分泌，这很有意思。通过胃插管，将体重为14mg/kg的奥美拉唑每日两次或300mg/kg的雷尼替丁每日两次给斯普拉格-道利大鼠治疗4至6周。通过连续滴定原位测定十二指肠黏膜碳酸氢盐的分泌速率。与接受安慰剂的对照组相比，治疗组动物的基础分泌以及对前列腺素E2或腔内酸（pH 2.0，持续5或60分钟）刺激的分泌增加均无差异（p大于0.05）。因此，用奥美拉唑或雷尼替丁治疗4至6周并未降低大鼠十二指肠黏膜碳酸氢盐的分泌，这些药物也未削弱该黏膜对长时间腔内酸化或腔内给予前列腺素E2的反应能力。
