Sodium sulfate significantly inhibited the decline in epithelial electrical resistance (R) produced by mucosal acidification (pH 1.4) of rabbit esophagus mounted in the Ussing chamber. This protective effect was not due to the cation, to sodium loading, hyperosmolality, or pH change of the mucosal solution. Protection was specific for sulfate ions (SO42-), since other divalent (HPO42-) or impermeant anions (gluconate-) failed to prevent the acid-induced decline in R. In vivo studies in HCl-perfused rabbit esophagi confirmed protection by SO42-. Tissues exposed to SO42- and HCl had higher R, lower permeability to H+ and mannitol, and less morphologic damage than controls exposed to HCl. These results suggest that SO42- have a unique protective action against acid injury to esophageal epithelia, and this action appears to explain the cytoprotective properties of sucralfate, a clinically effective agent for treating acid-peptic disease in humans.
|Original language||English (US)|
|Journal||American Journal of Physiology - Gastrointestinal and Liver Physiology|
|State||Published - Dec 1 1986|
ASJC Scopus subject areas
- Physiology (medical)