Gastroenterology

Gastroenterology

Volume 96, Issue 6, June 1989, Pages 1466-1477
Gastroenterology

Alimentary tract
Serosal bicarbonate protects against acid injury to rabbit esophagus

https://doi.org/10.1016/0016-5085(89)90514-3Get rights and content

Abstract

The role of serosal bicarbonate ions (HCO3) in protection against acid injury was investigated in rabbit esophageal mucosa mounted in Ussing chambers. Luminal acidification reduced potential difference and resistance in tissues exposed serosally to HCO3 or (unbuffered) HCO3-free solution. Whereas resistance declined similarly in both groups, potential difference declined less in HCO3 solution. After washout, HCO3-bathed tissues also had a greater increase in resistance, lower permeability to mannitol, and less histologic damage. Furthermore, as protection by HCO3 was not blocked by pretreatment with either the anion exchange blocker, 4 acetamido-4′-isothiocyanatostilbene 2-2′-disulfonic acid, or the carbonic anhydrase inhibitor, acetazolamide, and replacement of HCO3 with N-2-hydroxy-ethylpiperazine-N′-2-ethane sulfonic acid, a buffer impermeant to cells, was protective, an extracellular site for protection by HCO3 was likely. Where in the extracellular space HCO3 buffers H+ is unclear, but the absence of change in luminal pH and the inability to prevent the acid-induced increase in permeability in HCO3-bathed tissues argue against a luminal (preepithelial) site. Also, rapid repair was not demonstrated, indicating that a luminal site for protection after surface cell damage was unlikely. We conclude that serosal HCO3 is important in esophageal protection against acid damage by buffering H+ within the intercellular compartment of the extracellular space.

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    This study was supported by the National Institutes of Health (grants 5-R01-DK36013, R01-DK-1535017) and by the National Institute of Diabetes and Digestive and Kidney Diseases (grant 5-P30-DK-34987).

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