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  • Author or Editor: Clark S. Patton x
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Abstract

Objective—To identify the pathogenesis of gastric ulcers by comparing injury to the nonglandular gastric mucosa of horses caused by hydrochloric acid (HCl) or volatile fatty acids (VFAs).

Sample Population—Gastric tissues from 30 horses.

Procedure—Nonglandular gastric mucosa was studied by use of Ussing chambers. Short-circuit current (Isc) and potential difference were measured and electrical resistance calculated for tissues after addition of HCl and VFAs to normal Ringer's solution (NRS). Tissues were examined histologically.

Results—Mucosa exposed to HCl in NRS (pH, 1.5) had a significant decrease in Isc, compared with Isc for mucosa exposed to NRS at pH 4.0 or 7.0. Also, exposure to 60mM acetic, propionic, and butyric acids (pH, 4.0 or 1.5) caused an immediate significant decrease in Isc. Recovery of sodium transport was detected only in samples exposed to acetic acid at pH 4.0. Recovery of sodium transport was not seen in other mucosal samples exposed to VFAs at pH ≤ 4.0.

Conclusions and Clinical Relevance—Acetic, butyric, and propionic acids and, to a lesser extent, HCl caused decreases in mucosal barrier function of the nonglandular portion of the equine stomach. Because of their lipid solubility at pH ≤ 4.0, undissociated VFAs penetrate cells in the nonglandular gastric mucosa, which causes acidification of cellular contents, inhibition of sodium transport, and cellular swelling. Results indicate that HCl alone or in combination with VFAs at gastric pH ≤ 4.0 may be important in the pathogenesis of gastric ulcers in the nonglandular portion of the stomach of horses. (Am J Vet Res 2003;64:404–412)

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in American Journal of Veterinary Research

Abstract

Objective—To identify in vitro effects of hydrochloric acid, valeric acid, and other volatile fatty acids (VFAs) on the pathogenesis of ulcers in the nonglandular portion of the equine stomach.

Sample Population—Gastric tissues from 13 adult horses.

Procedure—Nonglandular gastric mucosa was studied by use of Ussing chambers. Short-circuit current (Isc) and potential difference were measured and electrical resistance and conductance calculated after tissues were bathed in normal Ringer's solution (NRS) or NRS and hydrochloric, valeric, acetic, propionic, and butyric acids. Treated tissues were examined histologically.

Results—Incubation in 60mM valeric acid at pH ≤ 7.0 abruptly and irreversibly abolished Isc, which was followed by a slower decrease in resistance and an increase in conductance. Incubation in 60mM acetic, propionic, and butyric acids and, to a lesser extent, hydrochloric acid at pH ≤ 7.0 significantly decreased Isc, which was followed by an increase in resistance and a decrease in conductance.

Conclusions and Clinical Relevance—Incubation in valeric acid at pH ≤ 7.0 caused a dramatic decrease in mucosal barrier function in the nonglandular portion of the stomach. Changes in barrier function attributable to exposure to valeric acid were associated with histopathologic evidence of cellular swelling in all layers of the nonglandular mucosa. Because of its high lipid solubility, valeric acid penetrates the nonglandular gastric mucosa, resulting in inhibition of sodium transport and cellular swelling. Valeric acid and other VFAs in gastric contents may contribute to the pathogenesis of ulcers in the nonglandular portion of the stomach of horses. (Am J Vet Res 2003;64:413–417)

Full access
in American Journal of Veterinary Research