Format

Send to

Choose Destination
See comment in PubMed Commons below
Dig Dis Sci. 1990 Oct;35(10):1244-8.

Tolerance of rat duodenum to luminal acid.

Author information

1
II Department of Surgery, Helsinki University, Central Hospital, Finland.

Abstract

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)

PMID:
1976495
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center