GASTRIC BICARBONATE SECRETION IN HUMANS - EFFECT OF PENTAGASTRIN, BETHANECHOL, AND 11,16,16-TRIMETHYL PROSTAGLANDIN-E2
GASTRIC BICARBONATE SECRETION IN HUMANS - EFFECT OF PENTAGASTRIN, BETHANECHOL, AND 11,16,16-TRIMETHYL PROSTAGLANDIN-E2
复制标题
DOI：
10.1172/jci110969
复制
发表时间：
1983-01-01
影响因子：
15.9
通讯作者：
FELDMAN, M
中科院分区：
文献类型：
--
作者：
FELDMAN, M
虽然胃主要以其分泌HCl的能力而闻名，但越来越多的证据表明，胃粘膜也分泌碳酸氢盐。从胃分泌的二组分模型出发，建立了一种同时测量胃HCO3-分泌和H+分泌的简便方法。该方法基于胃液量、H+浓度和渗透压，在体外和体内都得到了验证。14例健康人基础胃液HCO3分泌量为0.7~8.7 mmol/h，平均2.6 mmol/h。基础HCO3分泌量为.apprx。基础H+分泌量的50%，个体基础HCO3-与H+分泌量呈显著正相关(r=0.79)。HCO3-在基础非顶叶分泌物中以.apprx的浓度分泌。静脉注射90 mmol/L的五肽胃泌素可明显刺激H+的分泌，但不增加HCO3-的分泌。在五肽胃泌素输注过程中，胆碱能激动剂苯乙酚显著增加H+的分泌(从20.2~24.7 mmol/h)和HCO3-的分泌(从2.2~4.2 mmol/h)。前列腺素[PG]E2类似物[11，16，16-三甲基PGE2，RO21-6937]在五肽胃泌素输注过程中显著减少H+的分泌，增加HCO3的分泌。PGE2后胃液H+净排出量减少更多是由于H+分泌抑制，而不是HCO3分泌刺激。健康人胃明显活跃地分泌HCO3-，胃HCO3-分泌受胆碱能刺激和前列腺素E_2的影响。
Although the stomach is mainly known for its ability to secrete HCl, there is increasing evidence that the gastric mucosa also secretes bicarbonate. A simple method for simultaneous measurement of gastric HCO3- secretion and H+ secretion was developed from a 2-component model of gastric secretion. The method, which is based upon gastric juice volume, H+ concentration and osmolality, was validated both in vitro and in vivo. In 14 healthy human beings, basal gastric HCO3- secretion averaged 2.6 mmol/h (range, 0.7-8.7 mmol/h). Basal HCO3- secretion was .apprx. 50% of basal H+ secretion and there was a significant correlation between basal HCO3- and H+ secretion in individual subjects (r = 0.79). HCO3- was secreted in basal nonparietal secretion at a concentration of .apprx. 90 mmol/l. I.V. pentagastrin infusion markedly stimulated H+ secretion but did not increase HCO3- secretion. During pentagastrin infusion, the cholinergic agonist, bethanechol, significantly augmented H+ secretion (from 20.2 to 24.7 mmol/h) and increased HCO3- secretion (from 2.2 to 4.2 mmol/h). A prostaglandin[PG]E2 analog [11,16,16-trimethyl PGE2, RO21-6937] significantly reduced H+ secretion and increased HCO3 secretion during pentagastrin infusion. The reduction in net gastric juice H+ output following PGE2 was due more to H+ secretory inhibition than to HCO3- secretory stimulation. The healthy human stomach apparently actively secretes HCO3-, and gastric HCO3- secretion can be influenced by cholinergic stimulation and by PGE2.