Effects of hydrochloric, acetic, butyric, and propionic acids on pathogenesis of ulcers in the nonglandular portion of the stomach of horses

Jenifer A. Nadeau Department of Large Animal Clinical Sciences, University of Tennessee, Knoxville, TN 37996.
Present address is the Department of Animal Science, College of Agriculture and Natural Resources, University of Connecticut, Storrs, CT 06269.

Search for other papers by Jenifer A. Nadeau in
Current site
Google Scholar
PubMed
Close
 PhD
,
Frank M. Andrews Department of Large Animal Clinical Sciences, University of Tennessee, Knoxville, TN 37996.

Search for other papers by Frank M. Andrews in
Current site
Google Scholar
PubMed
Close
 DVM, MS
,
Clark S. Patton Department of Pathology, University of Tennessee, Knoxville, TN 37996.

Search for other papers by Clark S. Patton in
Current site
Google Scholar
PubMed
Close
 DVM, MS
,
Robert A. Argenzio Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27606.

Search for other papers by Robert A. Argenzio in
Current site
Google Scholar
PubMed
Close
 PhD
,
Alan G. Mathew College of Veterinary Medicine, and the Department of Animal Sciences, College of Agricultural Sciences and Natural Resources, University of Tennessee, Knoxville, TN 37996.

Search for other papers by Alan G. Mathew in
Current site
Google Scholar
PubMed
Close
 PhD
, and
Arnold M. Saxton College of Veterinary Medicine, and the Department of Animal Sciences, College of Agricultural Sciences and Natural Resources, University of Tennessee, Knoxville, TN 37996.

Search for other papers by Arnold M. Saxton in
Current site
Google Scholar
PubMed
Close
 PhD

Click on author name to view affiliation information

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)

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)

All Time Past Year Past 30 Days
Abstract Views 126 0 0
Full Text Views 564 316 29
PDF Downloads 363 160 5
Advertisement