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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