Objective—To investigate the effects of acepromazine maleate and morphine on aqueous tear production before, during, and after sevoflurane anesthesia in dogs. Animals—6 mixed-breed dogs. Procedures—In a Latin square study design, dogs underwent IM administration of morphine (1 mg/kg), acepromazine (0.05 mg/kg), or saline (0.9% NaCl) solution (0.05 mL/kg), followed by induction and maintenance of anesthesia with sevoflurane for 30 minutes. The protocol was repeated until all dogs had received all treatments, with a minimum of 7 days between anesthetic episodes. Aqueous tear production was measured via Schirmer tear test I before treatment (baseline); before anesthetic induction; 5, 10, 20, and 30 minutes after anesthetic induction; immediately once dogs recovered from anesthesia; and 2 and 10 hours after recovery. Results—Aqueous tear production for all treatments was significantly lower 10, 20, and 30 minutes (but not 5 minutes) after anesthetic induction than at baseline, before anesthetic induction, at recovery, and 2 and 10 hours after recovery. Aqueous tear production was significantly higher after saline solution administration than after morphine administration at the preinduction measurement point and 2 hours after recovery. No other differences were detected among the 3 treatments. Conclusions and Clinical Relevance—Aqueous tear production after anesthesia did not differ significantly from baseline values after any treatment following 30 minutes of sevoflurane anesthesia, suggesting premedication with morphine or acepromazine does not contribute to a decrease in lacrimation in these circumstances.

This study evaluated the analgesia effects of the epidural administration of 0.1 mg/kg bodyweight (BW) of morphine or 5 micrograms/kg BW of buprenorphine in ponies with radiocarpal joint synovitis. Six ponies were submitted to 3 epidural treatments: the control group (C) received 0.15 mL/kg BW of a 0.9% sodium chloride (NaCl) solution; group M was administered 0.1 mg/kg BW of morphine; and group B was administered 5 micrograms/kg BW of buprenorphine, both diluted in 0.9% NaCl to a total volume of 0.15 mL/kg BW administered epidurally at 10 s/mL. The synovitis model was induced by injecting 0.5 ng of lipopolysaccharide (LPS) in the left or right radiocarpal joint. An epidural catheter was later introduced in the lumbosacral space and advanced up to the thoracolumbar level. The treatment started 6 h after synovitis induction. Lameness, maximum angle of carpal flexion, heart rate, systolic arterial pressure, respiratory rate, temperature, and intestinal motility were evaluated before LPS injection (baseline), 6 h after LPS injection (time 0), and 0.5, 1, 2, 4, 6, 8, 10, 12, 16, 20, and 24 h after treatments. Although the model of synovitis produced clear clinical signs of inflammation, the lameness scores in group C were different from the baseline for only up to 12 h. Both morphine and buprenorphine showed a reduction in the degree of lameness starting at 0.5 and 6 h, respectively. Reduced intestinal motility was observed at 0.5 h in group M and at 0.5 to 1 h in group B. Epidural morphine was a more effective analgesic that lasted for more than 12 h and without side effects. It was concluded that morphine would be a valuable analgesic option to alleviate joint pain in the thoracic limbs in ponies.

Conventional methods of detecting Corynebacterium pseudotuberculosis, a bacterium that causes caseous lymphadenitis (CLA) in sheeps and goats focused on several serodiagnostic tests such as ELISA, Western blotting and various inhibition and precipitation techniques. This paper described a Surface Plasmon Resonance (SPR) protocol for the direct detection of polyclonal
antibodies against Corynebacterium pseudotuberculosis with immobilisation of the antigen on unmodified transducer surface. The lower limit of detection was determined to be 2 μg mL-1 of immobilised antigen (Ag). Sufficient binding interaction was monitored on unmodified transducer; and saturation of the binding interaction was observed at 80 μg mL-1 of interacted antibody.