A R Cross1, S C Budsberg, T J Keefe. 1. Department of Small Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens 30602, USA.
Abstract
OBJECTIVE: To examine the ability of meloxicam, a cyclooxygenase inhibitor, to mediate the effects of sodium urate-induced acute stifle synovitis in dogs. ANIMALS: 12 clinically normal adult hound-type dogs. PROCEDURE: A blinded, randomized, controlled single crossover design study was performed to determine the efficacy of meloxicam, using 2 dosage groups. In 2 experimental phases, dogs, according to group, received meloxicam (0.1 or 0.5 mg/kg of body weight) or matched volume of meloxicam vehicle, with a washout period of 21 to 28 days between phases. Blood samples for hematologic and biochemical analysis, as well as synovial fluid or cytologic analysis, were collected immediately before and approximately 24 hours after articular challenge of dogs under propofol anesthesia. Ground reaction forces (GRF) and subjective clinical scores were determined before and at 4, 8, 12, and 24 hours after articular challenge. Vertical force data included peak force, impulse, limb loading, and unloading rates. Craniocaudal data were divided into braking and propulsion phases and consisted of peak force and associated impulses. RESULTS: Except for propulsion impulse at 24 hours, all GRF variables were significantly greater at all post-synovitis induction times in the group receiving the high meloxicam dose. Significant differences in all GRF variables were seen at various times between the low-dose meloxicam group and the corresponding control group, and between the low- and high-dose meloxicam groups. Similar significance was seen in the subjective clinical evaluations. Strong correlations existed between the subjective and objective data. CONCLUSIONS: Meloxicam was effective in attenuating the effects of sodium urate-induced acute synovitis in dogs. Kinetic gait data provided an objective measurement of lameness in an experimentally induced arthritis model and quantified lameness improvements in response to medication with a nonsteroidal anti-inflammatory drug.
OBJECTIVE: To examine the ability of meloxicam, a cyclooxygenase inhibitor, to mediate the effects of sodium urate-induced acute stifle synovitis in dogs. ANIMALS: 12 clinically normal adult hound-type dogs. PROCEDURE: A blinded, randomized, controlled single crossover design study was performed to determine the efficacy of meloxicam, using 2 dosage groups. In 2 experimental phases, dogs, according to group, received meloxicam (0.1 or 0.5 mg/kg of body weight) or matched volume of meloxicam vehicle, with a washout period of 21 to 28 days between phases. Blood samples for hematologic and biochemical analysis, as well as synovial fluid or cytologic analysis, were collected immediately before and approximately 24 hours after articular challenge of dogs under propofol anesthesia. Ground reaction forces (GRF) and subjective clinical scores were determined before and at 4, 8, 12, and 24 hours after articular challenge. Vertical force data included peak force, impulse, limb loading, and unloading rates. Craniocaudal data were divided into braking and propulsion phases and consisted of peak force and associated impulses. RESULTS: Except for propulsion impulse at 24 hours, all GRF variables were significantly greater at all post-synovitis induction times in the group receiving the high meloxicam dose. Significant differences in all GRF variables were seen at various times between the low-dose meloxicam group and the corresponding control group, and between the low- and high-dose meloxicam groups. Similar significance was seen in the subjective clinical evaluations. Strong correlations existed between the subjective and objective data. CONCLUSIONS:Meloxicam was effective in attenuating the effects of sodium urate-induced acute synovitis in dogs. Kinetic gait data provided an objective measurement of lameness in an experimentally induced arthritis model and quantified lameness improvements in response to medication with a nonsteroidal anti-inflammatory drug.