Abstract

Equine gastric ulcers are common in the nonglandular (NG) region and volatile fatty acids (VFAs), byproducts of carbohydrate fermentation by resident gastric bacteria, have been implicated. Lactic acid (LA), also produced by bacteria, may cause ulcers.Our objective was to investigate the in vitro effects of LA on NG mucosal bioelectric properties. Equine gastric tissues (n=13) were studied in Ussing chambers to measure short‐circuit current (Isc) and potential difference (PD). Electrical resistance (R) and conductance (G) were calculated after addition of HCl and LA (5, 10, 20, or 40 mM) in normal Ringer's Solution. Tissues were examined for histopathology.Mucosa exposed to HCl in NRS at pH 1.5 and 4.0 had a significant decrease in Isc and PD; whereas tissues exposed to LA (5, 10, and 20 mM) did not demonstrate significant decreases in Isc and PD. However, mucosa exposed to LA (40 mM), at pH 1.5 demonstrated increased G and decreased R. Histologic changes were consistent with HCl‐induced damage.HCl induced alterations in bioelectric properties of equine NG mucosa, whereas addition of LA (5, 10, 20 mM) did not. However, 40 mM LA at pH 1.5 increased tissue permeability. Lactic acid, produced by resident gastric bacteria, may increase equine NG mucosal permeability by a different mechanism than VFAs which may be important in gastric ulcer pathogenesis.Funded by the Comparative Gastroenterology Society.

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