Regulation of gastroduodenal HCO-3 transport by luminal acid in the frog in vitro.
Regulation of gastroduodenal HCO-3 transport by luminal acid in the frog in vitro.
复制标题
体外青蛙中鲁米那酸对胃十二指肠 HCO-3 转运的调节。
DOI：
10.1152/ajpgi.1984.246.3.g235
复制
发表时间：
1984
期刊：
影响因子：
--
通讯作者：
G. Flemström
中科院分区：
文献类型：
--
作者：
J. Heylings;A. Garner;G. Flemström
鲁米诺酸（10 mM HCl）是哺乳动物胃和十二指肠内表面上皮HCO-3转运的体内刺激物。为了确定是否有体液机制参与调解这种反应，两栖动物胃底，胃窦，或近端十二指肠粘膜平行安装在一个体外室与他们的营养（serenum）表面面临一个共同的解决方案。将粘膜表面用单独的溶液浸泡，并在平行组织暴露于管腔酸期间滴定（pH 7.40）一个粘膜的HCO-3转运速率。在胃底HCO-3转运研究中，组胺H2-拮抗剂噻替丁（10（-4）M）可抑制H+分泌。胃底管腔酸刺激平行胃底（27 +/- 6%）或胃窦（53 +/- 27%）的HCO-3转运，但对平行十二指肠没有影响。胃窦腔酸对平行胃窦没有影响，表明胃兴奋剂是胃底起源。十二指肠腔酸增加平行十二指肠（21 +/- 5%）和胃底（109 +/- 32%）的HCO-3转运。HCO-3转运的刺激发生在十二指肠（约4.0）比胃底（约2.0）更高的管腔pH值。因此，暴露于管腔酸释放体液因子，能够刺激胃和十二指肠的表面上皮HCO-3转运。这些假定的刺激物的作用部分是组织特异性的，并且它们可能在介导粘膜保护对抗管腔酸中是重要的。
Luminal acid (10 mM HCl) is a stimulant of surface epithelial HCO-3 transport in mammalian stomach and duodenum in vivo. To determine whether a humoral mechanism is involved in mediation of this response, amphibian fundic, antral, or proximal duodenal mucosae were mounted in parallel in an in vitro chamber with their nutrient (serosal) surfaces facing a common solution. The mucosal surfaces were bathed by separate solutions and the rate of HCO-3 transport by one mucosa titrated (at pH 7.40) during exposure of the parallel tissue to luminal acid. In studies of fundic HCO-3 transport, H+ secretion was inhibited with the histamine H2-antagonist tiotidine (10(-4) M). Fundic luminal acid stimulated HCO-3 transport by a parallel fundus (27 +/- 6%) or antrum (53 +/- 27%) but had no effect on a parallel duodenum. Antral luminal acid had no effect on a parallel antrum, indicating that the gastric stimulant is of fundic origin. Duodenal luminal acid increased HCO-3 transport by both parallel duodenum (21 +/- 5%) and fundus (109 +/- 32%). Stimulation of HCO-3 transport occurred at higher luminal pH in duodenum (approximately 4.0) than in fundus (approximately 2.0). Thus, exposure to luminal acid releases humoral factor(s) capable of stimulating surface epithelial HCO-3 transport by both stomach and duodenum. The actions of these putative stimulants are in part tissue specific, and they may be important in mediation of mucosal protection against luminal acid.