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investigated in the model for this study. The induction of acute inflammation and associated hyperalgesia with carrageenan is one of the most widely used and well-established rodent models for studying acute inflammation that persists for a limited period of

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in American Journal of Veterinary Research

T he induction of acute inflammation and associated hyperalgesia with carrageenan is one of the most widely used and well-established methods of studying acute inflammation in animal models, particularly mice and rats. 1 , 2 Carrageenan is a

Open access
in American Journal of Veterinary Research

designated chamber via infusion of 1 mL of a freshly prepared solution of 1% carrageenan. g Seven to 8 hours later, (−3 to −2 hours), 1 mL of fluid was collected from each chamber. Whole blood (200 mL) was collected aseptically via jugular venipuncture from

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine whether 1% diclofenac liposomal suspension (DLS) ointment would be absorbed transdermally and attenuate experimentally induced subcutaneous inflammation in horses.

Animals—7 healthy adult horses

Procedure—Inflammation was produced by injecting 1% sterile carrageenan into subcutaneously implanted tissue cages 8 hours before (time –8) and at the time of application of test ointment. A crossover design was used. Horses received 1 of 2 treatments (topically administered control or DLS ointments) during 48 hours of carrageenan-induced subcutaneous inflammation. A single application of test ointment (7.2 g) was applied over each tissue cage (time 0). Samples of transudate and blood were collected at –8, 0, 6, 12, 18, 24, 30, 36, and 48 hours. Plasma and transudate diclofenac concentrations were determined by use of high-performance liquid chromatography. Transudate concentrations of prostaglandin E2 (PGE2) were determined with a competitive enzyme immunoassay.

Results—DLS was absorbed transdermally. The highest concentration (mean ± SEM, 76.2 ± 29 ng/mL) was detectable in tissue-cage fluid within 18 hours after application. Minimal concentrations of diclofenac were detectable in plasma. Application of DLS significantly decreased transudate concentrations of PGE2 at 6 and 30 hours. Decreases in PGE2 concentration were observed in the DLS group at all collection times.

Conclusions and Clinical Relevance—A single topical application of DLS resulted in concentrations of diclofenac in transudate within 6 hours and significantly attenuated carrageenan-induced local production of PGE2. Results of this study suggest that DLS is readily absorbed transdermally and may be efficacious for reducing subcutaneous inflammation in horses. ( Am J Vet Res 2004;65:271–276)

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in American Journal of Veterinary Research

Abstract

Objective—To establish pharmacokinetic and pharmacodynamic properties of a racemic mixture and individual R(–) and S(+) enantiomeric forms of ketoprofen (KTP) in sheep and determine pharmacodynamic variables of KTP by pharmacokinetic-pharmacodynamic modeling.

Animals—8 female Dorset crossbred sheep.

Procedure—A tissue cage model of inflammation was used. Carrageenan was administered into tissue cages. Time course of cyclooxygenase (COX)-2 inhibition was determined in vivo by measurement of exudate prostaglandin E2 (PGE2) concentrations. Time course of COX-1 inhibition was determined ex vivo by measurement of serum thromboxane B2 (TXB2) concentrations. In addition, plasma concentration-time course and penetration of KTP enantiomers into inflammatory exudate and transudate (noninflamed tissue cage fluid) were investigated. Four treatments were compared: placebo, racemic mixture (rac-KTP [3 mg/kg of body weight, IV]), S(+) KTP (1.5 mg/kg, IV),and R(–) KTP (1.5 mg/kg, IV).

Results—Both KTP enantiomers had elimination halflife and mean residence time measurements that were short and volume of the central compartment and steady state volume of distribution that were low. Clearance was rapid, particularly for R(–) KTP. Elimination of both enantiomers from exudate was > 10 times slower than from plasma. Both rac-KTP and the individual enantiomers significantly inhibited serum TXB2 concentrations for 12 hours. Rac-KTP and S(+) KTP, but not R(–) KTP, also significantly inhibited PGE2 synthesis in exudate for 12 hours.

Conclusions and Clinical Relevance—Inhibition of serum TXB2 concentration and exudate PGE2 synthesis for similar time courses after S(+) KTP administration indicates that it is a nonselective inhibitor of COX in sheep. ( Am J Vet Res 2001;62:77–86)

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in American Journal of Veterinary Research

Abstract

Objective—To assess anti-inflammatory effects of carprofen (CPF), CPF enantiomers, and NG-nitro-L-arginine methyl ester (L-NAME) in sheep.

Animals—8 sheep.

Procedure—Sheep with SC tissue cages were used. After intracaveal injection of 1% carrageenan, sheep were given single doses of racemic (Rac; 50:50 mixture of S[+] and R[–] enantiomers)-CPF (4.0 mg/kg), R(–)CPF (2.0 mg/kg), S(+)CPF (2.0 mg/kg), L-NAME (25 mg/kg), and placebo (PLB) IV in a crossover design.

Results—Rac-CPF and S(+)CPF inhibited serum thromboxane2 (TXB2) and exudate prostaglandin (PG)E2 generation significantly for 32 hours. Maximal inhibitory effect for serum TXB2 was 79 ± 3% for Rac- CPF and 68 ± 6% for S(+)CPF. The Rac-CPF and S(+)CPF induced 50 to 98% reversible inhibitory effect for exudate PGE2 generation during a 4- to 32- hour period. The R(–)CPF and L-NAME attenuated serum TXB2 generation significantly. The R(–)CPF did not affect exudate PGE2 production, whereas L-NAME potentiated exudate, PGE2 generation by 30% during 4 to 32 hours. The S(+)CPF and L-NAME increased leukotriene B4 generation and WBC recruitment in exudate although significance was achieved only at a few time points. Increase in skin temperature over inflammatory cages was effectively inhibited by Rac- CPF and S(+)CPF but not by R(–)CPF.

Conclusion and Clinical Relevance—Carprofen is a potent cyclooxygenase inhibitor in vivo in sheep, and its anti-inflammatory effects are attributable only to S(+)CPF in Rac-CPF. Nitric oxide may enhance eicosanoid production and accelerate the acute inflammatory process. (Am J Vet Res 2002;63: 782–788)

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in American Journal of Veterinary Research

Abstract

Objective

To compare the analgesic and anti-inflammatory effects of the nonsteroidal anti-inflammatory drugs (NSAID), ketoprofen (2.20 and 3.63 mg/kg of body weight) and phenylbutazone (4.40 mg/kg), in an acute equine synovitis model.

Design

4 groups of 6 horses received NSAID or saline solution in a randomized design.

Animals

24 clinically normal mares and geldings.

Procedure

Left intercarpal joints were injected with sterile carrageenan to induce synovitis at the same time as IV administration of NSAID or saline solution. Clinical assessments were made and synovial fluid was withdrawn at 0, 1, 3, 6, 9, 12, 24, and 48 hours.

Results

The eicosanoids, prostaglandin E2 (PGE2) and leukotriene B4, increased in synovial fluid after synovitis induction in all horses then returned to near baseline by 48 hours. All NSAID-treated horses had decreased PGE2, compared with saline-treated horses. This effect lasted longer in phenylbutazone-treated horses than in ketoprofen-treated horses. There were no treatment effects on leukotriene B4. In saline-treated animals, lameness, joint temperature, and synovial fluid volume, protein concentration, and nucleated cells increased 3 to 12 hours after induction, with marked reduction by 48 hours. Only phenylbutazone treatment reduced lameness, joint temperature, and synovial fluid volume.

Conclusion

Phenylbutazone was more effective than ketoprofen in reducing lameness, joint temperature, synovial fluid volume, and synovial fluid PGE2. Results do not support lipoxygenase inhibition by either NSAID.

Clinical Relevance

This reversible model induced synovial fluid alterations similar to those observed in horses with septic arthritis. Results indicate that phenylbutazone may be more useful than ketoprofen in treating acute joint inflammation. (Am J Vet Res 1996;57:866–874)

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in American Journal of Veterinary Research

SUMMARY

Pharmacokinetic and pharmacodynamic variables of flunixin were studied in calves after IV administration of the drug at a dose rate of 2.2 mg/kg of body weight. The anti-inflammatory properties of flunixin were investigated, using a model of acute inflammation; this involved surgically implanting tissue cages at subcutaneous sites and stimulating the tissue cage granulation tissue by intracavitary injection of carrageenan. The actions of flunixin on exudate concentrations of several substances related to the inflammatory process, including proteases (metalloprotease [active and total] and cysteine and serine proteases), enzymes (lactate dehydrogenase, acid phosphatase, and β-glucuronidase [β-glu]), eicosanoid (prostaglandin E2 [pge 2], leukotriene B4, and serum thromboxane B2 [txb 2]) concentrations, and bradykinin (BK)-induced edema, were investigated.

Flunixin had a long elimination half-life—6.87 ± 0.49 hours—and volume of distribution was 2.11 ± 0.37 L/kg, indicating extensive distribution of the drug in the body. Body clearance was 0.20 ± 0.03 L/ kg/h.

Flunixin exerted inhibitory effects on serum txb 2 and exudate pge 2 concentrations, β-glu activity, and BK-induced swelling. Other enzymes and inflammatory mediators were not significantly affected. Pharmacokinetic/pharmacodynamic modeling of the data revealed similar mean concentration producing 50% of the maximal effect values for inhibition of exudate pge 2 and p-glu and of BK-induced swelling (0.070 ± 0.006, 0.064 ± 0.040, and 0.061 ± 0.030 μg/ml, respectively). A lower concentration producing 50% of the maximal effect value was obtained for inhibition of serum txb 2 concentration (0.023 ± 0.004 μg/ml). Differences also were observed in equilibration halflife for these actions, suggesting the existence of 3 distribution compartments correlating with 3 sites of action—a central compartment and shallow and deep peripheral compartments. Pharmacokinetic/pharma- codynamic modeling proved to be a useful analytical method, providing a quantitative description of in vivo drug pharmacodynamics and indicating possible mechanisms of action.

Free access
in American Journal of Veterinary Research

metacarpophalangeal joint of horses. doi: doi.org/10.2460/ajvr.82.1.39 AJVR Residents Nicole Alessia Mikoni, University of California-Davis. Evaluation of weight-bearing, locomotion, thermal antinociception, and footpad size in a carrageenan

Open access
in American Journal of Veterinary Research
Author:

metacarpophalangeal joint of horses. doi.org/10.2460/ajvr.82.1.39 AJVR Residents Nicole Alessia Mikoni, University of California-Davis. Evaluation of weight-bearing, locomotion, thermal antinociception, and footpad size in a carrageenan-induced inflammatory

Open access
in Journal of the American Veterinary Medical Association