Effects of acepromazine maleate on platelet function assessed by use of adenosine diphosphate activated- and arachidonic acid- activated modified thromboelastography in healthy dogs.

OBJECTIVE: To evaluate the effect of acepromazine maleate administered IV on platelet function assessed in healthy dogs by use of a modified thromboelastography assay. ANIMALS: 6 healthy adult mixed-breed dogs. PROCEDURES: Dogs received each of 3 treatments (saline [0.9% NaCl] solution [1 to 2 mL, IV] and acepromazine maleate [0.05 and 0.1 mg/kg, IV]) in a randomized crossover study with a minimum 3-day washout period between treatments. From each dog, blood samples were collected via jugular venipuncture immediately before and 30 and 240 minutes after administration of each treatment. A modified thromboelastography assay, consisting of citrated kaolin-activated (baseline assessment), reptilase-ADP-activated (ADP-activated), and reptilase-arachidonic acid (AA)-activated (AA-activated) thromboelastography, was performed for each sample. Platelet inhibition was evaluated by assessing the percentage change in maximum amplitude for ADP-activated or AA-activated samples, compared with baseline values. Percentage change in maximum amplitude was analyzed by use of Skillings-Mack tests with significance accepted at a family-wise error rate of P < 0.05 by use of Bonferroni corrections for multiple comparisons. RESULTS: No significant differences were found in the percentage change of maximum amplitude from baseline for ADP-activated or AA-activated samples among treatments at any time. CONCLUSIONS AND CLINICAL RELEVANCE: Platelet function in dogs, as assessed by use of a modified thromboelastography assay, was not inhibited by acepromazine at doses of 0.05 or 0.1 mg/kg, IV. This was in contrast to previous reports in which it was suggested that acepromazine may alter platelet function via inhibition of ADP and AA.

Behavioral and clinical pathology changes in koi carp (Cyprinus carpio) subjected to anesthesia and surgery with and without intra-operative analgesics.

Fish surgery is becoming increasingly common in laboratory and clinical settings. Behavioral and physiologic consequences of surgical procedures may affect experimental results, so these effects should be defined and, if possible, ameliorated. We document behavioral and clinical pathology changes in koi carp (Cyprinus carpio) undergoing surgery with tricaine methanesulphonate (MS-222) anesthesia, with and without intraoperative administration of the opiate butorphanol (0.4 mg/kg intramuscularly) or the nonsteroidal antiinflammatory analgesic ketoprofen (2 mg/kg intramuscularly). For all fish combined, surgery resulted in reduced activity, lower position in the water column, and decreased feeding intensity at multiple time points after surgery. The butorphanol-treated group was the only one not to experience significant (P < 0.05) alterations from presurgical behaviors. Clinical pathology changes at 48 h after anesthesia and surgery included decreased hematocrit, total solids, phosphorus, total protein, albumin, globulin, potassium, and chloride and increased plasma glucose, aspartate aminotransferase, creatine kinase, and bicarbonate. The only clinical pathology difference between treatment groups was a lower increase in creatine kinase in the ketoprofen-treated group. No adverse effects of butorphanol or ketoprofen at these doses were identified. These results suggest a mild behavioral sparing effect of butorphanol and reduced muscle damage from the antiinflammatory activity of ketoprofen.