Hogan D L, Ainsworth M A, Isenberg J I
Department of Medicine, School of Medicine, University of California, San Diego Medical Center 92103-8413.
Aliment Pharmacol Ther. 1994 Oct;8(5):475-88. doi: 10.1111/j.1365-2036.1994.tb00319.x.
The gastroduodenal epithelium is covered by an adherent mucus layer into which bicarbonate is secreted by surface epithelial cells. This mucus-bicarbonate barrier is an important first line of defence against damage by gastric acid and pepsin, and has been demonstrated in all species including human. Similar to gastric acid secretion, regulation of gastric and duodenal bicarbonate secretion can be divided into three phases: cephalic, gastric and duodenal. In humans, sham-feeding increases bicarbonate secretion in both the stomach and duodenum which is mediated by cholinergic vagal fibres in the stomach, but seems to be noncholinergic in the duodenum. Gastric distention and luminal acidification increases gastric bicarbonate production. Whereas there are no data relating to the gastric phase of human duodenal bicarbonate secretion, in animals, food and acid in the stomach independently stimulate duodenal bicarbonate output. To date, the duodenal phase of human gastric bicarbonate secretion has not been studied, but data from animals reveal that duodenal acidification augments bicarbonate secretion in the stomach. In all species tested, direct acidification of the duodenum is a potent stimulant of local bicarbonate production. In humans, the pH threshold for bicarbonate secretion is pH 3.0. Mediation of gastroduodenal bicarbonate secretion is provided by a variety of agonists and antagonists, tested mainly in animals, but some have been evaluated in humans. Prostaglandins of the E class and VIP are major factors that control bicarbonate secretion. Bicarbonate secretion, and the mucus-bicarbonate layer in general, is adversely effected by ulcerogenic factors such as aspirin, NSAIDs, bile salts, and cigarette smoking. Furthermore, duodenal ulcer patients have an impairment in bicarbonate production within the duodenal bulb, at rest and in response to stimulation. These findings indicate that the mucus-bicarbonate barrier is an important first line of defence in the pathogenesis of peptic ulcer disease.
胃十二指肠上皮被一层附着的黏液层覆盖，表面上皮细胞向其中分泌碳酸氢盐。这种黏液 - 碳酸氢盐屏障是抵御胃酸和胃蛋白酶损伤的重要第一道防线，在包括人类在内的所有物种中均有体现。与胃酸分泌类似，胃和十二指肠碳酸氢盐分泌的调节可分为三个阶段：头期、胃期和十二指肠期。在人类中，假饲可增加胃和十二指肠的碳酸氢盐分泌，这是由胃内的胆碱能迷走神经纤维介导的，但在十二指肠中似乎是非胆碱能的。胃扩张和管腔内酸化会增加胃碳酸氢盐的产生。虽然尚无关于人类十二指肠碳酸氢盐分泌胃期的数据，但在动物中，胃内的食物和酸可独立刺激十二指肠碳酸氢盐的分泌。迄今为止，尚未对人类胃碳酸氢盐分泌的十二指肠期进行研究，但动物实验数据显示，十二指肠酸化可增强胃内碳酸氢盐的分泌。在所有测试物种中，十二指肠的直接酸化是局部碳酸氢盐产生的有效刺激因素。在人类中，碳酸氢盐分泌的pH阈值为pH 3.0。多种激动剂和拮抗剂参与了胃十二指肠碳酸氢盐分泌的调节，这些研究主要在动物中进行，但也有一些在人类中进行了评估。E类前列腺素和血管活性肠肽是控制碳酸氢盐分泌的主要因素。碳酸氢盐分泌以及一般的黏液 - 碳酸氢盐层会受到阿司匹林、非甾体抗炎药、胆盐和吸烟等致溃疡因素的不利影响。此外，十二指肠溃疡患者在十二指肠球部的碳酸氢盐产生存在障碍，无论是在静息状态还是受到刺激时。这些发现表明，黏液 - 碳酸氢盐屏障在消化性溃疡病的发病机制中是重要的第一道防线。
