OBJECTIVE To investigate effects of body condition on permeability of intestinal mucosa in horses. ANIMALS 13 horses (7 obese and 6 lean) from 8 to 15 years of age. PROCEDURES Body condition score was assessed, and an oral sugar test (OST) was performed to evaluate glucose and insulin dynamics. Horses were allowed a 2-week diet acclimation period and were then euthanized. Tissue samples were collected from the jejunum, ileum, cecum, pelvic flexure, right dorsal colon, and rectum. Mucosal permeability was assessed by measuring transepithelial resistance and lipopolysaccharide (LPS) flux across tissue samples mounted in Ussing chambers. RESULTS 5 obese horses and 1 lean horse had evidence of insulin dysregulation, whereas 1 obese and 5 lean horses had no abnormalities in results of the OST. Results for the OST were not available for 1 obese horse. Mucosal transepithelial resistance did not differ in any intestinal segment between obese and lean horses. Obese horses had a significantly higher LPS flux across jejunal mucosa, compared with results for lean horses, but there were no significant differences between obese and lean horses for other intestinal segments. CONCLUSIONS AND CLINICAL RELEVANCE Obese horses may have had greater paracellular mucosal permeability of jejunal mucosa to LPS, compared with that for lean horses. This finding was consistent with data for the gastrointestinal mucosa of humans and mice and supported the hypothesis that obese horses may be at higher risk from chronic exposure to increased amounts of LPS, compared with the risk for lean horses.

OBJECTIVE To determine the plasma pharmacokinetics and safety of 1% diclofenac sodium cream applied topically to neonatal foals every 12 hours for 7 days. ANIMALS Twelve 2- to 14-day old healthy Arabian and Arabian-pony cross neonatal foals. PROCEDURES A 1.27-cm strip of cream containing 7.3 mg of diclofenac sodium (n = 6 foals) or an equivalent amount of placebo cream (6 foals) was applied topically to a 5-cm square of shaved skin over the anterolateral aspect of the left tarsometatarsal region every 12 hours for 7 days. Physical examination, CBC, serum biochemistry, urinalysis, gastric endoscopy, and ultrasonographic examination of the kidneys and right dorsal colon were performed before and after cream application. Venous blood samples were collected at predefined intervals following application of the diclofenac cream, and plasma diclofenac concentrations were determined by liquid chromatography–mass spectrometry. RESULTS No foal developed any adverse effects attributed to diclofenac application, and no significant differences in values of evaluated variables were identified between treatment groups. Plasma diclofenac concentrations peaked rapidly following application of the diclofenac cream, reaching a maximum of < 1 ng/mL within 2 hours, and declined rapidly after application ceased. CONCLUSIONS AND CLINICAL RELEVANCE Topical application of the 1% diclofenac sodium cream to foals as described appeared safe, and low plasma concentrations of diclofenac suggested minimal systemic absorption. Practitioners may consider use of this medication to treat focal areas of pain and inflammation in neonatal foals.

OBJECTIVE To characterize epithelial cells of the small intestine and colon in horses without clinical gastrointestinal abnormalities with an emphasis on the stem cell niche constituents. SAMPLE Mucosal biopsy specimens from small and large intestines obtained from 12 horses euthanized for reasons unrelated to gastrointestinal disease or systemic disease. PROCEDURES Intestinal biopsy specimens were collected by sharp dissection immediately following euthanasia. Specimens were prepared for immunohistochemical, immunofluorescence, and transmission electron microscopic imaging to detect and characterize each epithelial cell type. Antibodies against protein biomarkers for cellular identification were selected on the basis of expression in other mammalian species. RESULTS Intestinal epithelial cell types were identified by means of immunostaining and morphological characterization with transmission electron microscopy. Some differences in biomarker expression and antibody cross-reactivity were identified in equine tissue, compared with other species. However, each known type of mucosal epithelial cell was identified in equine tissue. CONCLUSIONS AND CLINICAL RELEVANCE The methodology used can enhance detection of stem cells and progenitor cells as well as postmitotic cell lineages in equine intestinal tissues. Results may have relevance to regenerative potential of intestinal mucosa and survival in horses with colic.

OBJECTIVE To analyze the transit time from various locations in the intestines of cows with cecal dilatation-dislocation (CDD), healthy control cows, and cows with left displacement of the abomasum (LDA). ANIMALS 15 cows with naturally occurring CDD (group 1), 14 healthy control cows (group 2), and 18 cows with LDA (group 3). PROCEDURES 5 electronic transmitters were encased in capsules and placed in the lumen of the ileum, cecum, proximal portion of the colon, and 2 locations in the spiral colon (colon 1 and colon 2) and used to measure the transit time (ie, time between placement in the lumen and excretion of the capsules from the rectum). Excretion time of the capsules from each intestinal segment was compared among groups. RESULTS Cows recovered well from surgery, except for 1 cow with relapse of CDD 4 days after surgery and 2 cows with incisional infection. High variability in capsule excretion times was observed for all examined intestinal segments in all groups. Significant differences were detected for the excretion time from the colon (greater in cows with CDD than in healthy control cows) and cecum (less in cows with LDA than in cows of the other 2 groups). CONCLUSIONS AND CLINICAL RELEVANCE The technique developed to measure excretion time of capsules from bovine intestines was safe and reliable; however, the large variability observed for all intestinal segments and all groups would appear to be a limitation for its use in assessment of intestinal transit time of cattle in future studies.

Objective—To ultrasonographically measure the thickness of the individual wall layers of the duodenum, jejunum, and colon of dogs. Animals—85 dogs with no clinical signs or ultrasonographic evidence of gastrointestinal tract disease. Procedures—Total wall thickness and thickness of the mucosa, submucosa, muscularis, and serosa were measured ultrasonographically in the duodenum, jejunum, and colon of each dog. Results—The mucosal layer was the thickest layer of the duodenum and jejunum. There was a significant difference in thickness of the mucosal layer between small and large dogs. Mean ± SD thickness of the mucosal layer of the duodenum for small, medium, and large dogs was 2.4 ± 0.5 mm, 2.6 ± 0.6 mm, and 2.8 ± 0.5 mm, respectively. Mean ± SD thickness of the mucosal layer of the jejunum for small, medium, and large dogs was 1.8 ± 0.4 mm, 2.0 ± 0.4 mm, and 2.2 ± 0.5 mm, respectively. The remaining wall layers of the duodenum and jejunum were similar in thickness, and there were no significant differences among small, medium, and large dogs. All layers contributed equally to the total colonic wall thickness. Mean ± SD thickness of the colonic wall for small, medium, and large dogs was 1.5 ± 0.3 mm, 1.4 ± 0.5 mm, and 1.6 ± 0.4 mm, respectively. Conclusions and Clinical Relevance—Values for thickness of the wall layers of the duodenum, jejunum, and colon of dogs reported here may be useful for assessing gastrointestinal tract diseases primarily targeting a specific wall layer.

The purpose of the study was to compare the conductance and mannitol permeability of canine colonic mucosa in response to carprofen or 2,4-dinitrophenol (DNP) with or without tempol pretreatment. Ten colonic mucosa sections per dog were mounted in Ussing chambers. Treatments were done in duplicate. Mucosa was exposed to carprofen (200 μg/mL) or DNP (0.25 mM), both with and without tempol (1 mM) pretreatment. Conductance was calculated every 15 min for 240 min. Mannitol flux was calculated over 3 consecutive 60-minute periods. Histology or electron microscopy was done after exposure. Conductance over time, mannitol flux, frequency of histologic categories, and electron microscopic changes were analyzed for treatment effects. The mean ± standard deviation (SD) conductance over time for carprofen or DNP-treated colons was not significantly different from control regardless of tempol pretreatment. Period 3 mannitol fluxes for carprofen and DNP-treated colon were not significantly different, but were greater than control. Period 3 mannitol flux for tempol + carprofen was significantly less than tempol + DNP-treated colon. Sloughing of cells and erosions were seen in the mucosa of carprofen-treated colon. Mitochondrial damage was seen more often in carprofen-treated than DNP-treated or control colon. Tempol pretreatment resulted in more ruptured mitochondria in the carprofen-treated colon; however, other mitochondrial changes were not significantly affected by tempol pretreatment in either carprofen or DNP treated colon. Treatment with carprofen or DNP increased the mannitol flux, but pretreatment with tempol mitigated the carprofen effect. It is apparent that structural mitochondrial damage occurs in the canine colonic mucosa after carprofen and DNP exposure.

Objective—To determine the effect of large colon ischemia and reperfusion on concentrations of the inflammatory neutrophilic protein calprotectin and other clinicopathologic variables in jugular and colonic venous blood in horses. Animals—6 healthy horses. Procedures—Horses were anesthetized, and ischemia was induced for 1 hour followed by 4 hours of reperfusion in a segment of the pelvic flexure of the large colon. Blood samples were obtained before anesthesia, before induction of ischemia, 1 hour after the start of ischemia, and 1, 2, and 4 hours after the start of reperfusion from jugular veins and veins of the segment of the large colon that underwent ischemia and reperfusion. A sandwich ELISA was developed for detection of equine calprotectin. Serum calprotectin concentrations and values of blood gas, hematologic, and biochemical analysis variables were determined. Results—Large colon ischemia caused metabolic acidosis, a significant increase in lactate and potassium concentrations and creatine kinase activities, and a nonsignificant decrease in glucose concentrations in colonic venous blood samples. Values of these variables after reperfusion were similar to values before ischemia. Ischemia and reperfusion induced activation of an inflammatory response characterized by an increase in neutrophil cell turnover rate in jugular and colonic venous blood samples and calprotectin concentrations in colonic venous blood samples. Conclusions and Clinical Relevance—Results of this study suggested that large colon ischemia and reperfusion caused local and systemic inflammation in horses. Serum calprotectin concentration may be useful as a marker of this inflammatory response.