Takeuchi K
Department of Applied Pharmacology, Kyoto Pharmaceutical University, Japan.
Yakugaku Zasshi. 1990 Feb;110(2):85-104. doi: 10.1248/yakushi1947.110.2_85.
Bicarbonate secretion from the surface epithelial cells in the duodenum is an active process depending on tissue metabolism and blood flow, and regulated by humoral and neuronal factors as well as endogenous prostaglandins (PGs). The duodenal mucosa has been also able to respond luminal acid by a significant rise in alkaline secretion, mediated mainly by PGs, and the impairment of this process is involved in the pathogenic mechanism of various duodenal ulcer models. The mechanism of mucosal protection by HCO3- secretion is two ways: one is neutralization of luminal acid, and the other the establishment of pH gradient in the mucus gel with the aid of the physicochemical property of mucus. Although the majority of H+ is neutralized by secreted HCO3- in the lumen and mucus gel, the ultimate mucosal protection is ensured by removal of back-diffused H+ through intramucosal neutralization with HCO3- and translocation by blood flow. Thus, HCO3- secretion in collaboration with mucus plays an important role as the first line of defense (pre-epithelial barrier) in the duodenal mucosal protection.
十二指肠表面上皮细胞的碳酸氢盐分泌是一个依赖于组织代谢和血流的主动过程，受体液、神经因素以及内源性前列腺素（PGs）的调节。十二指肠黏膜也能够通过显著增加碱性分泌来对腔内酸作出反应，这主要由PGs介导，而这一过程的受损参与了各种十二指肠溃疡模型的发病机制。通过HCO₃⁻分泌实现黏膜保护的机制有两种：一种是中和腔内酸，另一种是借助黏液的物理化学性质在黏液凝胶中建立pH梯度。尽管大多数H⁺在管腔和黏液凝胶中被分泌的HCO₃⁻中和，但最终的黏膜保护是通过与HCO₃⁻进行黏膜内中和以及通过血流转运来清除反向扩散的H⁺来确保的。因此，HCO₃⁻分泌与黏液协同作用，在十二指肠黏膜保护中作为第一道防线（上皮前屏障）发挥重要作用。
