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Abstract

Objective—To develop a protocol to induce and maintain gastric ulceration in horses and to determine whether gastric ulceration affects physiologic indices of performance during high-speed treadmill exercise.

Animals—20 healthy Thoroughbreds.

Procedures—Each horse was acclimatized to treadmill exercise during a 2-week period. Subsequently, baseline data were collected (day 0) and each horse began an incrementally increasing exercise training program (days 1 through 56). Beginning on day 14, horses were administered omeprazole (4 mg/kg, PO, q 24 h until day 56) or no drug (10 horses/group) and underwent alternating 24-hour periods of feeding and feed withholding for 10 days to induce gastric ulceration. Extent of gastric ulceration was assessed weekly thereafter via gastroscopy. Physiologic indices of performance were measured at days 0 and 56. Gastric ulceration and exercise performance indices were compared within and between groups.

Results—In untreated horses, gastric ulcers were induced and maintained through day 56. Gastric ulcer formation was prevented in omeprazole-treated horses. There were significant interactions between time (pre- and post-training data) and treatment (nonulcer and ulcer groups) for mass-specific maximal O2 consumption ( O 2max/Mb) and mass-specific maximal CO2 production ( CO 2max/Mb). Post hoc analysis revealed a difference between groups for O 2max/Mb at day 56. Within-group differences for O 2max/Mb and CO 2max/Mb were detected for omeprazole-treated horses, but not for the horses with ulcers.

Conclusions and Clinical Relevance—In horses, gastric ulcers were induced and maintained by use of alternating periods of feeding and feed withholding in association with treadmill exercise (simulated racetrack training). Gastric ulcers adversely affected physiologic indices of performance in horses.

Full access
in American Journal of Veterinary Research

Abstract

Objective

To determine the role of nitric oxide and an apamin-sensitive nonadrenergic-noncholinergic inhibitory transmitter in in vitro contractile activity of the third compartment in llamas.

Sample Population

Isolated strips of third compartment of the stomach from 5 llamas.

Procedure

Strips were mounted in tissue baths containing oxygenated Kreb's buffer solution and connected to a polygraph chart recorder to measure contractile activity. Atropine, guanethidine, and indomethacin were added to tissue baths to inhibit muscarinic receptors, adrenoreceptors, and prostaglandin synthesis. Responses to electrical field stimulation following addition of the nitric oxide antagonist Νω-nitro-L-arginine methyl ester (L-NAME) and apamin were evaluated.

Results

Electrical field stimulation (EFS) resulted in a reduction in the amplitude and frequency of contractile activity, followed by rebound contraction when EFS was stopped. Addition of L-NAME resulted in a significant reduction in inhibition of contractile activity. Addition of apamin also resulted in a significant reduction in inhibitory contractile activity at most stimulation frequencies. The combination of L-NAME and apamin resulted in a significant reduction in inhibition at all frequencies.

Conclusion

Nitric oxide and a transmitter acting via an apamin-sensitive mechanism appear to be involved in inhibition of contractile activity of the third compartment in llamas.

Clinical Relevance

Results suggest that nitric oxide plays an important role in mediating contractile activity of the third compartment in llamas. Use of nitric oxide synthase inhibitors may have a role in the therapeutic management of llamas with lesions of the third compartment. (Am J Vet Res 1998;59:1166— 1169)

Free access
in American Journal of Veterinary Research

Abstract

Objectives

To evaluate the role of nitric oxide (NO), vasoactive intestinal peptide (VIP), and a transmitter acting through an apamin-sensitive mechanism in mediating inhibitory transmission in the equine jejunal circular muscle, and to determine the distribution of VIP-and NO-producing nerve fibers in the myenteric plexus and circular muscle.

Procedure

Circular muscle strips were suspended in tissue baths containing an oxygenated modified Krebs solution and attached to isometric force transducers. Responses to electrical field stimulation (EFS), tetrodotoxin, the NO antagonists l-N-nitro-arginine-methyl-ester (L-NAME) and N-nitro-l-arginine, apamin, VIP, authentic NO, and the NO donar sodium nitroprusside were tested. Immunostaining for VIP-like and NADPH diaphorase histochemical staining were performed on paraformaldehyde-fixed tissue.

Results

Subpopulations of myenteric neurons and nerve fibers in the circular muscle were positive for NADPH diaphorase and VIP-like staining. EFS caused a frequency-dependent inhibition of contractile activity. Tetrodotoxin prevented the EFS-induced inhibition of contractions. L-NAME (200 μM) and apamin 0.3 μM) significantly (P < 0.01) reduced EFS-stimulated inhibition of contractile activity at most frequencies tested. The effects of L-NAME and apamin were additive. In their combined presence, EFS induced excitation instead of inhibition (196.7% increase at 5 Hz, n = 28, P < 0.01). Inhibition of contractile activity by EFS was mimicked by sodium nitroprusside. Authentic NO (3-6 μM) abolished contractile activity. VIP induced a dose-dependent inhibition of contractile activity (89.1 ± 6.3% reduction at approximately 0.3 μM, n = 16). Antagonism of NO synthesis did not alter the response to VIP.

Conclusion

NO, VIP, and a substance acting through an apamin-sensitive mechanism appear to comediate inhibitory transmission in the equine jejunal circular muscle.

Clinical Relevance

These findings may suggest new therapeutic targets for motility disorders, such as agents that inhibit the synthesis or actions of NO. (Am J Vet Res 1996;57:1206-1213)

Free access
in American Journal of Veterinary Research

SUMMARY

Microvascular permeability of the jejunum of clinically normal equids and microvascular permeability associated with 60 minutes of ischemia (25% baseline blood flow) and subsequent reperfusion were investigated. Eight adult horses were randomly allotted to 2 equal groups: normal and ischemic/reperfusion injury. Lymphatic flow rates, mesenteric blood flow, and lymph and plasma protein concentrations were determined at 15-minute intervals throughout the study. Microvascular permeability was determined by estimates of the osmotic reflection coefficient, which was determined when the ratio of lymphatic protein to plasma protein concentration reached a constant minimal value as lymph flow rate increased (filtration-independent lymph flow rate), which occurred at venous pressure of 30 mm of Hg. Full-thickness jejunal biopsy specimens were obtained at the beginning and end of each experiment, and were prepared for light microscopy to estimate tissue volume (edema) and for transmission electron microscopy to evaluate capillary endothelial cell morphology.

The osmotic reflection coefficient for normal equine jejunum was 0.19 ± 0.06, and increased significantly (P < 0.0001) to 0.48 ± 0.05 after the ische- mia/reperfusion period. Microscopic evaluation revealed a significant increase (P < 0.0001) in submucosal and serosal volume and capillary endothelial cell damage in horses that underwent ischemia/reperfusion injury. Results indicate that ischemia/re-perfusion of the equine jejunum caused a significant increase in microvascular permeability.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To determine whether xanthine oxidase and dehydrogenase activities are altered during low flow ischemia and reperfusion of the small intestine of horses.

Animals

5 clinically normal horses without histories of abdominal problems.

Procedure

With the horse under general anesthesia, a laparotomy was performed and blood flow to a segment of the distal jejunum was reduced to 20% of baseline for 120 minutes and was then reperfused for 120 minutes. Biopsy specimens were obtained before, during, and after ischemia for determination of xanthine oxidase and dehydrogenase activities, and for histologic and morphometric analyses.

Results

Percentage of xanthine oxidase activity (as a percentage of xanthine oxidase and dehydrogenase activity) was not altered during ischemia and reperfusion. An inflammatory response developed and progressed during ischemia and reperfusion. Mucosal lesions increased in severity after ischemia and reperfusion. Mucosal surface area and volume decreased during ischemia and continued to decrease during reperfusion. Submucosal volume increased slightly during ischemia, and continued to increase during reperfusion.

Conclusions and Clinical Relevance

Evidence for conversion of xanthine dehydrogenase to xanthine oxidase during ischemia was not found. Factors other than production of reactive oxygen metabolites may be responsible for progressive epithelial loss, decrease in mucosal surface area and volume, and increase in submucosal volume observed in this study. Other methods of determining xanthine oxidase activity that detect the enzyme in sloughed epithelial cells should be used to better define the importance of this pathway in jejunal reperfusion injury in horses. (Am J Vet Res 1998;59:772-776)

Free access
in American Journal of Veterinary Research