Paimela H, Kiviluoto T, Mustonen H, Sipponen P, Kivilaakso E
II Department of Surgery, Helsinki University, Central Hospital, Finland.
Dig Dis Sci. 1990 Oct;35(10):1244-8. doi: 10.1007/BF01536414.
The tolerance of the duodenal mucosa to luminal acid was investigated by measuring with a liquid sensor pH microelectrode technique the epithelial surface pH (pHs) and subepithelial tissue pH (pHt) in rat proximal (duodenal bulb, Brunner gland area) and distal duodenum exposed to luminal acid. Under basal conditions, pHs was roughly equal in both parts of the duodenum; proximal duodenum, 7.40 +/- 0.14 (mean +/- SEM) at the villus tip and 7.54 +/- 0.16 at the depth of crypt; distal duodenum, 7.46 +/- 0.19 and 7.55 +/- 0.09, respectively. Yet, exposure of the mucosa to luminal acid (10 mM HCl) provoked a significantly lesser decrease of pHs (0.25 +/- 0.13 vs 0.42 +/- 0.12 pH units) in the proximal duodenum, suggesting that the response of epithelial HCO3 secretion to luminal acid is stronger in that part of the duodenum. Further, the initial acidification of pHs was followed in the proximal duodenum by a secondary alkalinization of pHs, leading to normalization of pHs, which may suggest activation of compensatory protective mechanisms. pHt at the villus tip was likewise roughly equal in both parts of duodenum (7.29 +/- 0.05 vs 7.17 +/- 0.04), but, again, acidification of the luminal perfusate progressively from 10 to 100 mM HCl induced a much earlier and significantly more profound acidification in the distal than in the proximal duodenum. The possible contribution of Brunner glands to the greater mucosal tolerance to acid in the proximal duodenum was assessed by investigating whether stimulation or inhibition of Brunner gland secretion modulates the response of the duodenal mucosa to acid.(ABSTRACT TRUNCATED AT 250 WORDS)
通过使用液体传感器pH微电极技术测量暴露于腔内酸的大鼠近端（十二指肠球部、Brunner腺区）和远端十二指肠的上皮表面pH（pHs）和上皮下组织pH（pHt），研究十二指肠黏膜对腔内酸的耐受性。在基础条件下，十二指肠两部分的pHs大致相等；近端十二指肠，绒毛顶端为7.40±0.14（平均值±标准误），隐窝深度为7.54±0.16；远端十二指肠分别为7.46±0.19和7.55±0.09。然而，黏膜暴露于腔内酸（10 mM HCl）时，近端十二指肠的pHs下降明显较小（0.25±0.13对0.42±0.12 pH单位），这表明十二指肠该部位上皮HCO3分泌对腔内酸的反应更强。此外，近端十二指肠pHs最初酸化后接着是二次碱化，导致pHs恢复正常，这可能表明激活了代偿性保护机制。绒毛顶端的pHt在十二指肠两部分同样大致相等（7.29±0.05对7.17±0.04），但是，同样地，腔内灌注液从10 mM HCl逐渐增加到100 mM HCl时，远端十二指肠比近端十二指肠更早且酸化程度明显更深。通过研究刺激或抑制Brunner腺分泌是否调节十二指肠黏膜对酸的反应，评估了Brunner腺对近端十二指肠黏膜对酸的更大耐受性的可能作用。（摘要截断于250字）
