No abstract

Osteochondrosis is a disorder of growth cartilage in which a focal failure of blood supply has been proposed as an important initiating factor. In the present study we investigated the effect on epiphyseal growth cartilage of experimentally interrupting the blood supply to a limited area of the distal femur of growing pigs.In 12 pigs, a thin full-thickness cartilage slab was removed from the abaxial margin of the medial condyle, thereby transecting a limited number of cartilage canals. The pigs were culled 1, 2, 3, 7, 14, 21 and 29 days post-surgery. The condylar cartilage was studied histologically, immunohistologically and by use of the TUNEL method.The transection induced cellular death of cartilage canal elements followed by cellular death of chondrocytes within the deep layers of the resting zone of the epiphyseal growth cartilage. However, in the superficial layers of the resting zone, chondrocytes appeared to proliferate into and subsequently chondrify some of the necrotic cartilage canals. The dying and dead cells were TUNEL-positive, but active caspase 3-negative. The loss of vascular supply induced increased VEGF-immunostaining in chondrocytes surrounding the affected area.We conclude that transection of cartilage canals produces chondronecrosis in the deep resting zone of the epiphyseal growth cartilage similar to that observed in spontaneously occurring osteochondrosis.

BIS is not a precise indicator of degree of CNS depression in isoflurane-anesthetized horses. Thus, determination of BIS may not be a useful technique for monitoring anesthetic depth in isoflurane-anesthetized horses.

The pharmacokinetics and pharmacodynamics of meloxicam in piglets (16-23 days old) were studied using a stratified parallel group design. One group (n = 13) received 0.4 mg/kg meloxicam intravenously, while the other group (n = 12) received physiological saline solution. A carrageenan-sponge model of acute inflammation was used to evaluate the effects of meloxicam. The plasma clearance was low (0.061 L/kg/h), the volume of distribution was low (0.19 L/kg) and the elimination half-life was short (2.7 h). At most time points, the mean concentration of meloxicam in plasma exceeded the concentrations in exudate indicating a limited accumulation of the drug at the site of the inflammation. There were significant differences between the groups in the exudate prostaglandin E2 (PGE2) concentration, but the inhibition of PGE2 in the meloxicam group was limited. The inhibition of thromboxane B(2) (TXB2) production in serum in the meloxicam group was extensive, but of shorter duration than the PGE2 inhibition in exudate.

The chiral pharmacokinetics and pharmacodynamics of ketoprofen were investigated in a placebo-controlled study in piglets after intramuscular administration of 6 mg/kg racemic ketoprofen. The absorption half-lives of both enantiomers were short, and S-ketoprofen predominated over R-ketoprofen in plasma. A kaolin-induced inflammation model was used to evaluate the anti-inflammatory, antipyretic and analgesic effects of ketoprofen. Skin temperatures increased after the kaolin injection, but the effect of ketoprofen was small. No significant antipyretic effects could be detected, but body temperatures tended to be lower in the ketoprofen-treated piglets. Mechanical nociceptive threshold testing was used to evaluate the analgesic effects. The piglets in the ketoprofen-treated group had significantly higher mechanical nociceptive thresholds compared to the piglets in the placebo group for 12-24 h following the treatment. Pharmacokinetic/pharmacodynamic modelling of the results from the mechanical nociceptive threshold testing gave a median IC(50) for S-ketoprofen of 26.7 μg/mL and an IC(50) for R-ketoprofen of 1.6 μg/mL. This indicates that R-ketoprofen is a more potent analgesic than S-ketoprofen in piglets. Estimated ED(50) for racemic ketoprofen was 2.5 mg/kg.