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Abstract

Objectives

To determine effects of finely ground diet and food deprivation on pH and bile acid concentration in the proximal portion of the porcine stomach and effects of bile acids and pH on the pars esophageal mucosa in vitro.

Animals

Sixteen 15- to 30-kg pigs.

Procedures

Gastric content samples obtained from pigs fed a finely ground pelleted or coarsely ground meal diet were assayed for gastric pH and bile acids. Stratified squamous epithelium was studied in an Ussing chamber, and histologically. Electrical conductance and transmucosal mannitol fluxes (as indices of tissue permeability) were determined at pH 4.0, 2.0, and 1.5 and in response to treatment with 0, 1, 2, or 3 mM taurodeoxycholate or glycocholate.

Results

Pigs fed the finely ground feed had significantly (P = 0.01 ) lower proximal stomach pH than did pigs fed the coarse meal. Proximal stomach bile acids concentration was significantly (P = 0.04) higher in pigs fed the finely ground diet. The H+ and bile acids concentration increased with time after feeding. In vitro exposure of the stratified mucosa to high H+ (pH < 4.0) and bile salt concentration (≥ 1.0 mM) resulted in significant (P < 0.05) dose-dependent increase in tissue conductance and mannitol fluxes, whereas low pH or bile acids alone had little effect.

Conclusions

High H+ and bile acids concentration in the stomach of pigs fed finely ground diets or subjected to feed deprivation may contribute to ulceration of the pars esophageal tissue. Bile acids act synergistically and in dose-dependent manner, with low pH causing damage to the stratified squamous epithelium in vitro. (Am J Vet Res 1998;59:1170-1176)

Free access
in American Journal of Veterinary Research

Abstract

Objective—To identify expression and localization of cyclooxygenase (COX)-1 and COX-2 in healthy and ischemic-injured left dorsal colon of horses.

Sample Population—Left dorsal colon tissue samples from 40 horses.

Procedures—Tissue samples that were used in several related studies on ischemia and reperfusion were evaluated. Samples were collected during anesthesia, before induction of ischemia, and following 1 hour of ischemia, 1 hour of ischemia and 30 minutes of reperfusion, 2 hours of ischemia, 2 hours of ischemia and 30 minutes of reperfusion, and 2 hours of ischemia and 18 hours of reperfusion. Histomorphometric analyses were performed to characterize morphological injury. Immunohistochemical analyses were performed to characterize expression and localization of COX-1 and COX-2.

Results—COX-1 and COX-2 were expressed in control tissues before ischemia was induced, predominantly in cells in the lamina propria. Ischemic injury significantly increased expression of COX-2 in epithelial cells on the colonic surface and in crypts. A similar significant increase of COX-1 expression was seen in the epithelial cells.

Conclusions and Clinical Relevance—On the basis of information on the role of COX-2, upregulation of COX-2 in surface epithelium and crypt cells following ischemic injury in equine colon may represent an early step in the repair process.

Full access
in American Journal of Veterinary Research