Vattay P, Feil W, Klimesch S, Wenzl E, Starlinger M, Schiessel R
University Clinic of Surgery I, Vienna General Hospital, Austria.
Gut. 1988 Mar;29(3):284-90. doi: 10.1136/gut.29.3.284.
Low luminal acid concentrations stimulate alkaline secretion (AS) by the duodenal mucosa. We investigated acid stimulated alkaline secretion by proximal rabbit duodenal mucosa in an Ussing-chamber under different luminal acid concentrations and its relation to mucosal damage. Luminal alkalinisation and potential difference (PD) were measured and mucosal damage was investigated histologically. Luminal acid caused an increase of alkaline secretion over baseline (0.95 +/- 0.19 mu Eq/cm2/10 min; n = 55): 0.1 mmol: 7%, 1 mmol/l: 17%, 5 mmol/l: 22%, 10 mmol/l: 33%, 20 mmol/l: 34%, 50 mmol: 39%, 100 mmol/l: 27%. At acid concentrations of 10 mmol/l and above the PD fell from 2.0 +/- 1.0 mV to zero. Histology showed [H+]-dependent mucosal damage ranging from villus tip lesions to deep mucosal injury. Stimulation of alkaline secretion was not specific for acid. Ethanol (14%) stimulated alkaline secretion by 26%, and 28% ethanol by 40% over baseline. Ouabain and/or anoxia sensitive (active) alkaline secretion constituted 80% and 100% respectively of basal alkaline secretion. After exposure to various luminal acid concentrations passive diffusion (sensitive only to removal of nutrient HCO3-) was solely responsible for the rise in alkaline secretion. Only after 14% ethanol a small rise in ouabain and/or anoxia sensitive HCO3- transport was observed. Under the conditions of this study stimulation of duodenal alkaline secretion is not specific for luminal acid, but occurs also with luminal ethanol; both agents stimulate alkaline secretion depending on their concentration. In this model passive diffusion of HCO3- associated with increasing mucosal damage is the major component of the rise in alkaline secretion.
低管腔酸浓度刺激十二指肠黏膜分泌碱性物质（AS）。我们在不同管腔酸浓度下，利用尤斯灌流小室研究了兔十二指肠近端黏膜酸刺激的碱性分泌及其与黏膜损伤的关系。测量了管腔碱化和电位差（PD），并通过组织学研究了黏膜损伤情况。管腔酸使碱性分泌比基线水平增加（0.95±0.19微当量/平方厘米/10分钟；n = 55）：0.1毫摩尔/升时增加7%，1毫摩尔/升时增加17%，5毫摩尔/升时增加22%，10毫摩尔/升时增加33%，20毫摩尔/升时增加34%，50毫摩尔/升时增加39%，100毫摩尔/升时增加27%。在酸浓度为10毫摩尔/升及以上时，PD从2.0±1.0毫伏降至零。组织学显示存在[H⁺]依赖性黏膜损伤，从绒毛尖端病变到深层黏膜损伤不等。碱性分泌的刺激并非酸所特有。乙醇（14%）使碱性分泌比基线水平增加26%，28%乙醇使其增加40%。哇巴因和/或缺氧敏感（活性）碱性分泌分别占基础碱性分泌的80%和100%。暴露于各种管腔酸浓度后，被动扩散（仅对去除营养性HCO₃⁻敏感）是碱性分泌增加的唯一原因。仅在14%乙醇作用后，观察到哇巴因和/或缺氧敏感的HCO₃⁻转运略有增加。在本研究条件下，十二指肠碱性分泌的刺激并非管腔酸所特有，乙醇也可引起；两种物质均根据其浓度刺激碱性分泌。在该模型中，与黏膜损伤增加相关的HCO₃⁻被动扩散是碱性分泌增加的主要成分。
