Search Results

You are looking at 1 - 3 of 3 items for :

  • Author or Editor: Faye Harmon x
  • Refine by Access: All Content x
Clear All Modify Search

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

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