Objective—To determine effects of reactive oxygen metabolites (ROMs), with and without flunixin meglumine, on equine right ventral colon (RVC) in vitro.
Animals—18 healthy horses and ponies.
Procedures—In 3 groups of 6 animals each, short-circuit current and conductance were measured in RVC mucosa in Ussing chambers. The 3 groups received physiologic saline (0.9% NaCl) solution, IV, 10 minutes before euthanasia and tissue incubation in Krebs-Ringer-bicarbonate (KRB) solution; flunixin meglumine (1.1 mg/kg, IV) 10 minutes before euthanasia and tissue incubation in KRB solution; or physiologic saline solution, IV, 10 minutes before euthanasia and incubation in KRB solution with 2.7 × 10−5M flunixin meglumine. Incubation conditions included control (no addition) and ROM systems, including addition of 1mM xanthine and 80 mU of xanthine oxidase (to produce the superoxide radical), 1mM H2O2, and 1mM H2O2 and 0.5mM ferrous sulfate (to produce the hydroxyl radical).
Results—All ROMs that were added or generated significantly increased the short-circuit current except in tissues coincubated with flunixin meglumine, and they induced mild epithelial vacuolation and apoptosis, but did not disrupt the epithelium nor change conductance, lactate dehydrogenase release, or [3H]mannitol flux.
Conclusions and Clinical Relevance—Responses to ROMs could be attributed to increased chloride secretion and inhibited neutral NaCl absorption in equine RVC, possibly by stimulating prostaglandin production. The ROMs examined under conditions of this study could play a role in prostaglandin-mediated colonic secretion in horses with enterocolitis without causing direct mucosal injury.
Objective—To study the effects of phenylbutazone,
indomethacin, prostaglandin E2 (PGE2), glutamine,
and butyrate on restitution of oxidant-injured right dorsal
colon of horses in vitro.
Sample Population—Right dorsal colon from 9 adult
horses euthanatized for reasons other than gastrointestinal
Procedure—Mucosal segments from the right dorsal
colon were injured via exposure to HOCl and incubated
in Ussing chambers in solutions containing
phenylbutazone, indomethacin, indomethacin and
PGE2, glutamine, and butyrate. Transepithelial resistance
and mucosal permeability to mannitol were
measured, and all mucosal segments were examined
Results—The HOCl-injured mucosa had lower resistance
and higher permeability to mannitol, compared
with control tissue. Histologic changes were also evident.
Resistance of HOCl-injured mucosa recovered
partially during the incubation period, and glutamine
improved recovery. Phenylbutazone and
indomethacin increased resistance, but these
increases were not significant. Butyrate and PGE2
had no effects, compared with nontreated HOCl-injured
tissues. Mucosal permeability to mannitol was
lower in glutamine-treated tissue, compared with
nontreated tissue. Histologic changes reflected the
resistance and permeability changes.
Conclusions and Clinical Relevance—According to
our findings, phenylbutazone and indomethacin do
not seem to interfere with restitution of oxidant-injured
mucosa of equine colon in vitro, and glutamine
could facilitate mucosal restitution. (Am J Vet Res 2004;65:1589–1595)
Objectives—To establish reference values for the range of the number of eosinophils found in equine gastrointestinal mucosa and to describe the distribution of this cell within the equine gastrointestinal mucosa.
Sample Population—Gastrointestinal mucosal specimens from 14 adult horses euthanatized for reasons other than gastrointestinal disease.
Procedures—Gastrointestinal mucosal specimens were collected and grouped according to their anatomic regions. For histologic examination slides were stained with Luna's eosinophil stain to determine eosinophil accumulation and distribution. The mucosa was divided into 5 sections for each anatomic location, and the percentage of eosinophils in each of the 5 sections relative to the total eosinophil count in all sections was determined. Additionally, the number of eosinophils per square millimeter of mucosa was calculated as a measure of the degree of eosinophil accumulation.
Results—Lowest numbers of eosinophils were found in the stomach, and numbers increased from there to the cecum, then decreased from the ascending colon (right ventral colon, left ventral colon, pelvic flexure, left dorsal colon, and right dorsal colon) to small colon. In all gastrointestinal sections, most eosinophils were located near the muscularis mucosae and were rarely found near or on the luminal surface of the mucosa.
Conclusions and Clinical Relevance—The distribution of eosinophils in the gastrointestinal tract of horses followed a pattern within the mucosa and between different sections of the gastrointestinal tract. The derived reference values and distribution data could be used to detect changes in eosinophil response in the equine gastrointestinal mucosa caused by diseases states.