To compare the ability of acetaminophen-codeine (AC; 15.5 to 18.5 mg/kg and 1.6 to 2.0 mg/kg, respectively) or carprofen (4.2 to 4.5 mg/kg) administered PO to attenuate experimentally induced lameness in dogs.
7 purpose-bred dogs.
A blinded crossover study was performed. Dogs were randomly assigned to receive AC or carprofen treatment first and then the alternate treatment a minimum of 21 days later. Synovitis was induced in 1 stifle joint during each treatment by intra-articular injection of sodium urate (SU). Ground reaction forces were assessed, and clinical lameness was scored at baseline (before lameness induction) and 3, 6, 9, 12, 24, 36, and 48 hours after SU injection. Plasma concentrations of acetaminophen, carprofen, codeine, and morphine were measured at various points. Data were compared between and within treatments by repeated-measures ANOVA.
During AC treatment, dogs had significantly higher lameness scores than during carprofen treatment at 3, 6, and 9 hours after SU injection. Peak vertical force and vertical impulse during AC treatment were significantly lower than values during carprofen treatment at 3, 6, and 9 hours. Plasma concentrations of carprofen (R)- and (S)-enantiomers ranged from 2.5 to 19.2 μg/mL and 4.6 to 25.0 μg/mL, respectively, over a 24-hour period. Plasma acetaminophen concentrations ranged from 0.14 to 4.6 μg/mL and codeine concentrations from 7.0 to 26.8 ng/mL, whereas plasma morphine concentrations ranged from 4.0 to 58.6 ng/mL.
CONCLUSIONS AND CLINICAL RELEVANCE
Carprofen as administered was more effective than AC at attenuating SU-induced lameness in dogs.
Objective—To investigate the ability of ABT-116 (a proprietary antagonist of transient receptor potential vanilloid type 1) administered at 2 doses to attenuate lameness in dogs with experimentally induced urate synovitis.
Animals—8 purpose-bred mixed-breed dogs.
Procedures—In a 4-way crossover study, dogs orally received each of low-dose ABT-116 treatment (LDA; 10 mg/kg), high-dose ABT-116 treatment (HDA; 30 mg/kg), firocoxib (5 mg/kg), and no treatment (nontreatment) once a day for 2 days, in a randomly assigned order. Synovitis was induced on the second day of each treatment period by intra-articular injection of either stifle joint with sodium urate, alternating between joints for each treatment period, beginning with the left stifle joint. Ground reaction forces, clinical lameness scores, and rectal temperature were assessed before the injection (baseline) and at various points afterward.
Results—Lameness scores at the 2-, 6-, and 12-hour assessment points were higher than baseline scores for HDA and nontreatment, whereas scores at the 2- and 6-hour points were higher than baseline scores for LDA. For firocoxib, there was no difference from baseline scores in lameness scores at any point. Compared with baseline values, peak vertical force and vertical impulse were lower at 2 and 6 hours for HDA and nontreatment and at 2 hours for LDA. No changes in these values were evident for firocoxib. The HDA or LDA resulted in higher rectal temperatures than did treatment with firocoxib or nothing, but those temperatures did not differ among treatments.
Conclusions and Clinical Relevance—HDA had no apparent effect on sodium urate–induced lameness; LDA did attenuate the lameness but not as completely as firocoxib treatment. High rectal temperature is an adverse effect of oral ABT-116 administration that may be of clinical concern.
Objective—To compare ground reaction forces (GRFs) measured by use of a pressure-sensitive walk-way (PSW) and a force plate (FP) and evaluate weekly variation in the GRFs and static vertical forces in dogs.
Animals—34 clinically normal dogs and 5 research dogs with lameness.
Procedure—GRF data were collected from 5 lame and 14 clinically normal dogs by use of an FP and a PSW. Peak vertical force (PVF), vertical impulse (VI), and velocity measurements (determined by use of photocells and PSW data) were compared between groups. Peak vertical force, VI, stride length, ground phase time (ie, contact time), and static body weight distribution data were collected on 2 occasions, 1 week apart, in 20 different clinically normal dogs by use of a PSW; week-to-week variation in values was evaluated.
Results—Measurements of velocity derived by use of the photocells were not different from those derived by use of the PSW. For any 1 limb, values derived by use of the PSW were significantly lower than values derived with the FP. For values obtained by use of either technique, there were no differences between left and right limbs except for values of PVF measured via PSW in forelimbs. Values of PVF, VI, contact time, stride length, and static weight distribution generated by the PSW did not vary from week to week.
Conclusions and Clinical Relevance—Values for GRFs varied between the FP and PSW. However, data derived by use of PSW were consistent and could be used to evaluate kinetic variables over time in the same dog.
Objective—To investigate the ability of perzinfotel (an N-methyl-d-aspartate receptor antagonist) and a proprietary phospholipase A2 (PLA2) inhibitor to attenuate lameness in dogs with sodium urate (SU)–induced synovitis.
Animals—8 adult dogs.
Procedures—A blinded 4-way crossover study was performed. Dogs received perzinfotel (10 mg/kg), a proprietary PLA2 inhibitor (10 mg/kg), carprofen (4.4 mg/kg; positive control treatment), or no treatment (negative control treatment). On the fourth day after initiation of treatment, synovitis was induced via intra-articular injection of SU 1 hour before administration of the last treatment dose. Ground reaction forces were measured and clinical lameness evaluations were performed before (baseline [time 0]) and 2, 4, 6, 8, 12, and 25 hours after SU injection. There was a 21-day washout period between subsequent treatments. Data were analyzed via repeated-measures ANOVAs.
Results—Peak vertical force (PVF) and vertical impulse (VI) values for negative control and perzinfotel treatments were significantly lower at 2 and 4 hours, compared with baseline values. Values for PVF and VI for the PLA2 inhibitor and positive control treatments did not differ from baseline values at any time points. Between-treatment comparisons revealed significantly higher PVF and VI values for the positive control treatment than for the negative control and perzinfotel treatments at 2 and 4 hours. Values for VI were higher for PLA2 inhibitor treatment than for negative control treatment at 2 hours.
Conclusions and Clinical Relevance—Perzinfotel did not significantly alter SU–induced lameness. The proprietary PLA2 inhibitor attenuated lameness but not as completely as did carprofen.
Objective—To evaluate the quality of information
regarding osteoarthritis (OA) in dogs currently available
on the World Wide Web.
Procedure—5 search engines were searched with
the keywords "dog," "degenerative joint disease,"
"canine," and "osteoarthritis," and the first 50 sites
listed by each search engine were analyzed. Unique
Web site addresses were distributed to 3 diplomates
of the American College of Veterinary Surgeons, who
provided a standardized evaluation of each site.
Results—30 unique Web sites were evaluated.
Twenty (66%) provided information consistent with
conventional knowledge as outlined in textbooks and
peer-reviewed literature, 8 (27%) provided experimental
or anecdotal information in addition to conventional
knowledge, and 2 (7%) provided misleading information.
Mean scores for overall usefulness of the information
provided in regard to clinical features of and
treatment for OA were 1.3 and 1.5, respectively (1 =
information of minimal use; 5 = very useful information).
Twenty-three (77%) sites encouraged pet owners
to seek the advice of a veterinarian. Twenty-three
(77%) sites were given overall quality scores < 2, and
7 (23%) were given scores between 2 and 3 (1 = site
was counterproductive; 5 = site was very valuable).
Conclusions and Clinical Relevance—Results suggest
that the quality of information currently available
on the Web that addresses OA in dogs is questionable.
Although most of the sites conveyed some conventional
information with reasonable accuracy, the
information was incomplete, of minimal use, and
often considered counterproductive. (J Am Vet Med
Objective—To determine the effects of nonsteroidal anti-inflammatory drugs of various cyclooxygenase selectivities on hemostasis and prostaglandin expression in dogs.
Animals—8 client-owned dogs with clinical signs of osteoarthritis.
Procedures—Dogs received aspirin (5 mg/kg, PO, q 12 h), carprofen (4 mg/kg, PO, q 24 h), deracoxib (2 mg/kg, PO, q 24 h), and meloxicam (0.1 mg/kg, PO, q 24 h) for 10 days each, with an interval of at least 14 days between treatments. On days 0 and 10, blood was collected for platelet aggregation assays, thrombelastography, and measurement of lipopolysaccharide-stimulated prostaglandin E2, platelet thromboxane B2 (TXB2), and free serum TXB2 and 6-keto-prostaglandin F (PGF)-1α concentrations.
Results—Platelet aggregation decreased after treatment with aspirin and carprofen, whereas significant changes from baseline were not detected for the other drugs tested. Thrombelastograms obtained after treatment with carprofen revealed decreased maximum amplitude and α-angle, suggesting hypocoagulability. Maximum amplitude and coagulation index increased after treatment with deracoxib. Plasma concentrations of prostaglandin E2 decreased after treatment with carprofen or deracoxib, and platelet TXB2 production increased after treatment with aspirin. Serum concentrations of the prostacyclin metabolite 6-keto-PGF-1α did not change significantly after treatment with any of the drugs, although the ratio of free TXB2 to 6-keto-PGF-1α decreased slightly after treatment with carprofen and increased slightly after treatment with deracoxib.
Conclusions and Clinical Relevance—At the dosages tested, treatment with meloxicam affected platelet function minimally in dogs with osteoarthritis. Treatment with carprofen decreased clot strength and platelet aggregation. Clot strength was increased after treatment with deracoxib.
Objective—To determine pharmacokinetics of meloxicam in healthy green iguanas following PO and IV administration and assess potential toxicity.
Animals—21 healthy green iguanas (Iguana iguana).
Procedures—To assess pharmacokinetics, 13 iguanas were administered a single dose (0.2 mg/kg) of meloxicam PO and, 14 days later, the same dose IV. To assess potential toxicity, 4 iguanas were given meloxicam at a dosage of 1 or 5 mg/kg, PO, every 24 hours for 12 days, and results of histologic examination were compared with results for another 4 iguanas given a single dose of meloxicam (0.2 mg/kg).
Results—There were no significant differences between PO and IV administration with regard to terminal half-life (mean ± SD, 12.96 ± 8.05 hours and 9.93 ± 4.92 hours, respectively), mean area under the curve to the last measured concentration (5.08 ± 1.62 μg•h/mL and 5.83 ± 2.49 μg•h/mL), volume of distribution (745 ± 475 mL/kg and 487 ± 266 mL/kg), or clearance (40.17 ± 10.35 mL/kg/h and 37.17 ± 16.08 mL/kg/h). Maximum plasma concentration was significantly greater following IV (0.63 ± 0.17 μg/mL) versus PO (0.19 ± 0.07 μg/mL) administration. Time from administration to maximum plasma concentration and mean residence time were significantly longer following PO versus IV administration. Daily administration of high doses (1 or 5 mg/kg) for 12 days did not induce any histologic changes in gastric, hepatic, or renal tissues.
Conclusions and Clinical Relevance—Results suggested that administration of meloxicam at a dose of 0.2 mg/kg IV or PO in green iguanas would result in plasma concentrations > 0.1 μg/mL for approximately 24 hours. (Am J Vet Res 2010;71:1277–1283)