Kinetic gait analysis assessment of meloxicam efficacy in a sodium urate-induced synovitis model in dogs.

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.

Toxicity and growth-promoting potential of spermine when fed to chicks.

Previous studies have shown that the feeding of putrescine, a biogenic amine and the precursor of the mammalian polyamines, can promote whole-body growth of chicks. The current study was undertaken to determine the effect of spermine, also a biogenic amine and the most cationic of the polyamines, under similar conditions. In Exp. 1, 120 week-old chicks were fed purified crystalline amino acid-based diets containing 0, .2, .4, .6, .8, or 1.0% spermine for 14 d. Spermine proved highly toxic and growth rates were reduced compared with controls when even .2% was fed. In Exp. 2, chicks were fed 0, .0375, .0750, or .1000% spermine. These concentrations proved less toxic than those used in Exp. 1. Supplemental dietary cysteine was then provided at 0, .3, .6, and .9% together with 0, .025, .050, or .400% spermine (Exp. 3) because depletion of cellular glutathione has been suggested as contributing to spermine's toxicity. Even high levels of cysteine supplementation did not overcome spermine's toxicity. Subsequent dietary provision of L-2-oxothiazolidine-4-carboxylic acid (OTC, Exp. 4), a cysteine prodrug, showed that depletion of cellular glutathione was not likely a cause of spermine toxicosis. A trend toward increased weight gain and feed efficiency was observed when low concentrations of spermine were fed. It was concluded, however, that dietary spermine was more toxic to chicks than was previously seen for putrescine, that any growth-promoting effects of dietary spermine are small, and that supplements of dietary cysteine or OTC are unlikely to increase these effects by overcoming spermine toxicosis.