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in Journal of the American Veterinary Medical Association

SUMMARY

The role of platelet-activating factor in mediating the cardiovascular and peripheral cellular responses to large-colon ischemia and reperfusion, was explored in anesthetized ponies. A specific platelet-activating factor (PAF) antagonist (WEB 2086) was administered to a group of 6 ponies, and another 6 ponies (controls) were given an equivalent volume of saline solution, prior to 1 hour of large-colon torsion. After correction of the torsion, ponies were monitored during the reperfusion period. Significant (P < 0.05) hypotension and metabolic acidosis developed in all ponies after correction of colonic torsion, cardiac index increased initially, but then decreased significantly (P < 0.05) over the study period. Mean times between correction of torsion and onset of cardiac failure and death were not different between groups. Significant (P < 0.05) thrombocytopenia developed during the reperfusion period in control ponies, but not in WEB-treated ponies. Blood leukocyte concentration in control ponies was more variable and significantly (P < 0.05) decreased immediately upon reperfusion, compared with that in WEB-treated ponies. We conclude that although the cardiovascular responses to colonic ischemia and reperfusion are not prevented by use of a specific paf-antagonist, specific peripheral cellular responses are mediated by paf.

Free access
in American Journal of Veterinary Research

Summary

Positive end-expiratory pressure (peep) was applied in 74 anesthetized, ventilated horses during colic surgery, to attempt to increase arterial oxygen tensions. In 28 horses with an initial P a O 2 < 70 mm of Hg, peep increased P a O 2 values to a mean of 173 ± 24 mm of Hg. Arterial oxygen content increased from 14.1 ± 0.05 ml/dl to 17.2 ± 0.05 ml/dl. In the remaining 46 horses, peep increased P a O 2 from a mean value of 101 ± 6 mm of Hg to 194 ± 15 mm of Hg, and arterial oxygen content increased from 14.9 ± 0.09 ml/dl to 16.9 ± 0.07 ml/dl.

Cardiovascular depression and decrease in arterial blood pressure was observed after the application of peep in 54 horses. These 54 horses required use of pressors (n = 8), inotropes (n = 32), or both (n = 14) to keep the mean arterial blood pressure > 60 mm of Hg. Combined with pharmacologic support of blood pressure, peep could be a useful clinical treatment of arterial hypoxemia in horses.

Free access
in Journal of the American Veterinary Medical Association
Authors and

Summary

To investigate the cardiopulmonary effects of positive end-expiratory pressure (peep), values of 10, 20, and 30 cm of H2O, were applied to anesthetized, dorsally recumbent, ventilated ponies. After iv induction of general anesthesia, peep was superimposed on controlled ventilation with 100% oxygen, and changes in gas exchange and cardiac function were measured. Increasing values of peep in these ponies caused a linear increase in the mean (± SEM) functional residual capacity, from a control value (zero end-expiratory pressure) of 1.7 ± 0.24 L to 2.2 ± 0.31, 2.9 ± 0.32 and 3.4 ± 0.3 L at peep of 10, 20, and 30 cm of H2O, respectively (P < 0.05). Paralleling these changes, intrapulmonary shunt fraction decreased significantly (P < 0.05) from a control value of 12.9 ± 0.5%, to 7.5 ± 1.1 and 2.1 ± 0.6%, at peep of 20 and 30 cm of H2O, respectively. Cardiac output was decreased by increasing values of peep, from control value of 11.7 ± 1.56 L/min to 9.9 ± 1.51, 8.8 ± 1.33 and 5.62 ± 0.56 L/min at peep of 10, 20, and 30 cm of H20, respectively. Related to decreasing cardiac output, tissue oxygen delivery also decreased as peep was increased, from control value of 2.0 ± 0.09 L/min to 1.8 ± 0.07, 1.6 ± 0.06, and 1.03 ± 0.04 L/min at peep of 10, 20, and 30 cm of H2O, respectively.

Thus, the effects of increasing values of peep in these ponies included increased functional residual capacity and arterial oxygenation, but marked reduction in cardiac output, resulting in no improvement or decrease in total oxygen delivery. Although peep is useful for improving arterial oxygenation, the deleterious cardiovascular effects should be anticipated or ameliorated by use of volume loading and/or inotrope administration.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To define relationships between hoofacceleration patterns of galloping horses and dynamic properties of the track.

Animals—8 Thoroughbred horses without lameness.

Procedure—Acceleration-time curves were recorded by use of accelerometers attached to each hoof as each horse galloped over the track straightaway. Four sessions were conducted for each horse, with the track surface modified by sequentially adding water before each session. These acceleration-time curves were analyzed to determine peak accelerations during the support phase of the stride. Track dynamic properties (hardness, rebound, deceleration rate, rebound rate, and penetration) were recorded with a track-testing device. Moisture content and dry density were measured from soil samples. Stepwise multiple regression was used to identify relationships between hoof-acceleration variables and track dynamic properties.

Results—Track rebound rate was most consistently related to hoof variables, especially through an inverse relationship with negative acceleration peaks for all hooves. Also, rebound rate was related to initial acceleration peak during propulsion of the hooves of the forelimb and the nonlead hind limb as well as to the second acceleration peak during propulsion of the lead hooves of the hind limb and nonlead forelimb.

Conclusions and Clinical Relevance—The inverse relationship between track rebound rate and negative acceleration peaks for all hooves reflects the most important dynamic property of a track. Any factor that reduces negative acceleration of the hooves will increase stride efficiency by allowing smoother transition from retardation to propulsion and therefore may be important in determining the safety of racing surfaces. (Am J Vet Res 2005;66:589–595)

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in American Journal of Veterinary Research

Summary

The role of platelet-activating factor (paf) in mediating the colonic damage that develops after large-colon torsion was studied in 14 ponies. Morphologic changes in areas of the ascending colon and selected abdominal and thoracic viscera after 1 hour of large-colon torsion and 3 to 5 hours of reperfusion were determined, as well as the protective effects of systemic administration of a specific paf antagonist (WEB 2086). Ponies were selected then allocated at random and in equal numbers to 2 groups that received 1 of 2 treatments prior to induction of large-colon torsion: group 1 —control (saline solution), and group 2 — WEB 2086 (3 mg/kg of body weight loading dose and 3 mg/kg/h for the remainder of the study). In each pony, full-thickness tissue specimens from the gastrointestinal tract —cecum, pelvic flexure, left and right ventral colon, and right dorsal colon —heart, left lung, liver, left adrenal gland, spleen, and right kidney were collected and histologically evaluated. Edema, mucosal necrosis, and neutrophil infiltration in colonic sections were graded from 0 (normal) to 3 (most severe changes). Sections of liver and lung from 3 ponies in each group, and colon from 1 pony in each group, also were examined by transmission electron microscopy to determine the presence of ultrastructural alterations.

Ischemia and reperfusion induced marked changes in all sections of colon in all ponies: moderate to severe submucosal edema, moderate necrosis of the superficial epithelium and lamina propria, and necrosis of the mucosal crypt epithelium. Extra-vascular neutrophil accumulation was evident in all sections of colon and cecum, but not in other tissues. Ultrastructural lesions were not present in hepato-cytes or pneumocytes, or in the endothelial cells of liver, lung, and colon. Bacteria were observed by electron microscopy in 5% of hepatic sinusoids. Administration of a specific paf antagonist, WEB 2086, failed to reduce severity of the observed lesions, indicating that it was not cytoprotective at the dosage used in this model of ischemia-reperfusion injury.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate cyclooxygenase isozyme distribution in tissues from dogs and determine the differential sensitivity of canine cyclooxygenase (COX)-1 and -2 isozymes to nonsteroidal anti-inflammatory drugs (NSAIDs).

Sample Population—Canine tissue samples (stomach, duodenum, ileum, jejunum, colon, spleen, cerebral cortex, lung, ovary, kidney, and liver) were obtained from 2 dogs for northern and western blot analyses, and blood for whole blood COX assays was obtained from 15 dogs.

Procedure—11 NSAIDs were evaluated to determine their COX-2 selectivity in whole blood assays. The concentrations of the drug needed to inhibit 50% of enzyme activity (IC50) were then calculated for comparison. Expression and tissue distribution of COX isozymes were determined by northern and western blot analysis.

Results—Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas NS398, carprofen, tolfenamic acid, nimesulide, and etodolac had more than 5 times greater preference for inhibiting COX-2 than COX-1. All canine tissues examined, including those from the gastrointestinal tract, coexpressed COX-1 and -2 mRNA, although protein expression was observed only for COX-1.

Conclusions and Clinical Relevance—Canine COX-2 was selectively inhibited by etodolac, nimesulide, and NS398; tolfenamic acid and carprofen also appeared to be preferential COX-2 inhibitors in dogs. The roles of COX-1 as a constitutive housekeeping enzyme and COX-2 as a proinflammatory inducible enzyme (as determined in humans) appear to apply to dogs; therefore, COX-2-selective inhibitors should prove useful in reducing the adverse effects associated with nonselective NSAIDs. (Am J Vet Res 2004;65:810–818)

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in American Journal of Veterinary Research

Abstract

Case Description—9 first-lactation dairy cows in a closed dairy herd had swelling in the forelimbs and forelimb lameness. Mycoplasmal arthritis and mastitis were diagnosed.

Clinical Findings—Swelling of the carpal joint, diffuse subcutaneous edema from the carpal to metacarpophalangeal joints, and forelimb lameness were evident in 9 first-lactation cows 7 to 21 days after parturition. Diagnostic testing revealed that 3 of 3 bulk-tank milk samples, 3 milk samples from cows with clinical mastitis, 2 fluid samples obtained from arthritic joints, and samples from the lungs and spleen of a cow that had died yielded positive results for Mycoplasma spp. Nucleic acid sequence analysis performed by use of a PCR assay on the joint fluid and lung tissues confirmed infection with Mycoplasma bovis.

Treatment and Outcome—Affected cows were treated by IM administration of flunixin meglumine and dexamethasone for 3 days. All cows were nonresponsive to treatment (3 cows died, and the other 6 were culled). Follow-up culture for Mycoplasma spp of milk samples from the bulk tank and from all lactating cows was recommended to screen for chronic subclinical carriers.

Clinical Relevance—Mycoplasmal infections may cause unusual initial clinical signs or an atypical history. When dairy cattle, including those residing in closed herds, have lameness, swelling of the carpal or metacarpophalangeal joints, edema of the distal portions of the forelimbs, or polyarthritis, infection with Mycoplasma spp should be investigated. Delay in diagnosis of mycoplasmal infections in dairy herds can result in substantial financial loss and the establishment of chronic subclinical carriers.

Full access
in Journal of the American Veterinary Medical Association

SUMMARY

The effects of exogenous platelet-activating factor (paf) were determined in anesthetized ponies. Administration of paf induced a decrease in cardiac index that resulted in systemic hypotension. This was followed by tachycardia, hypertension, and a return of cardiac index to baseline. Pulmonary aterial pressure increased markedly because of pulmonary vasoconstriction. Exogenous paf also caused leukopenia and thrombocytopenia. The specific PAP receptor antagonist (WEB 2086) blocked all paf-induced changes. Flunixin meglumine, a cyclooxygenase inhibitor, abolished the pulmonary hypertension and tachycardia, and attenuated the systemic hypotension but did not change the paf-induced peripheral cellular changes. The paf antagonist also inhibited platelet aggregation induced by paf in vitro. The paf-induced changes are similar to those reported after endotoxin exposure in horses.

Free access
in American Journal of Veterinary Research