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  • Author or Editor: Albert E. Jergens x
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The effects of hypertonic saline solution (htss) combined with colloids on hemostatic analytes were studied in 15 dogs. The analytes evaluated included platelet counts, one-stage prothrombin time, activated partial thromboplastin time, von Willebrand's factor antigen (vWf:Ag), and buccal mucosa bleeding times. The dogs were anesthetized, and jugular phlebotomy was used to induce hypovolemia (mean arterial blood pressure = 50 mm of Hg). Treatment dogs (n = 12) were resuscitated by infusion (6 ml/kg of body weight) of 1 of 3 solutions: htss combined with 6% dextran 70, 6% hetastarch, or 10% pentastarch. The control dogs (n = 3) were autotransfused. Hemostatic analytes were evaluated prior to induction of hypovolemia (baseline) and then after resuscitation (after 30 minutes of sustained hypovolemia) at 0.25, 0.5, 1, 6 and 24 hours.

All treatment dogs responded rapidly and dramatically to resuscitation with hypertonic solutions. Clinically apparent hemostatic defects (epistaxis, petechiae, hematoma were not observed in any dog. All coagulation variables evaluated, with the exception of vWf:Ag, remained within reference ranges over the 24-hour period. The vWf:Ag values were not statistically different than values from control dogs, and actual values were only slightly lower than reference ranges. Significant (P ≤ 0.04) differences were detected for one-stage prothrombin time, but did not exceed reference ranges. The results of this study suggested that small volume htss/colloid solutions do not cause significant alterations in hemostatic analytes and should be considered for initial treatment of hypovolemic or hemorrhagic shock.

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in American Journal of Veterinary Research


Objective—To characterize mucosal gene expression in dogs with chronic enteropathy (CE).

Animals—18 dogs with CE and 6 healthy control dogs.

Procedures—Small intestinal mucosal biopsy specimens were endoscopically obtained from dogs. Disease severity in dogs with CE was determined via inflammatory bowel index scores and histologic grading of biopsy specimens. Total RNA was extracted from biopsy specimens and microchip array analysis (approx 43,000 probe sets) and quantitative reverse transcriptase PCR assays were performed.

Results—1,875 genes were differentially expressed between dogs with CE and healthy control dogs; 1,582 (85%) genes were downregulated in dogs with CE, including neurotensin, fatty acid–binding protein 6, fatty acid synthase, aldehyde dehydrogenase 1 family member B1, metallothionein, and claudin 8, whereas few genes were upregulated in dogs with CE, including genes encoding products involved in extracellular matrix degradation (matrix metallopeptidases 1, 3, and 13), inflammation (tumor necrosis factor, interleukin-8, peroxisome proliferator–activated receptor γ, and S100 calcium-binding protein G), iron transport (solute carrier family 40 member 1), and immunity (CD96 and carcinoembryonic antigen–related cell adhesion molecule [CEACAM] 18). Dogs with CE and protein-losing enteropathy had the greatest number of differentially expressed genes. Results of quantitative reverse transcriptase PCR assay for select genes were similar to those for microchip array analysis.

Conclusions and Clinical Relevance—Expression of genes encoding products regulating mucosal inflammation was altered in dogs with CE and varied with disease severity.

Impact for Human Medicine—Molecular pathogenesis of CE in dogs may be similar to that in humans with inflammatory bowel disease.

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in American Journal of Veterinary Research


Objective—To determine whether substantial interobserver variation exists among diagnostic pathologists for descriptions of intestinal mucosal cell populations and whether histopathologic descriptions accurately predict when a patient does not have clinically evident intestinal disease.

Design—Comparative survey.

Sample Population—14 histologic slides of duodenal, ileal, or colonic tissue from 10 dogs and 3 cats.

Procedure—Each histologic slide was evaluated independently by 5 pathologists at 4 institutions. Pathologists, who had no knowledge of the tissues' origin, indicated whether slides were adequate for histologic evaluation and whether the tissue was normal or abnormal. They also identified the main infiltrating cell type in specimens that were considered abnormal, and whether infiltrates were mild, moderate, severe, or neoplastic.

Results—Quality of all slides was considered adequate or superior by at least 4 of the 5 pathologists. For intensity of mucosal cellular infiltrates, there was uniformity of opinion for 1 slide, near-uniformity for 6 slides, and nonuniformity for 7 slides. Five dogs did not have clinical evidence of intestinal disease, yet the pathologists' descriptions indicated that their intestinal tissue specimens were abnormal.

Conclusions and Clinical Relevance—Substantial interobserver variation was detected. Standardization of pathologic descriptions of intestinal tissue is necessary for meaningful comparisons with published articles. Clinicians must be cautious about correlating clinical signs and histopathologic descriptions of intestinal biopsy specimens. (J Am Vet Med Assoc 2002;220:1177–1182)

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in Journal of the American Veterinary Medical Association