Objective—To compare the anesthetic efficacy and
physiologic changes associated with exposure to tricaine
methanesulfonate and clove oil (100%
Animals—15 adult cultured red pacu (Piaractus
Procedure—Fish were exposed to each of 6 anesthetic
concentrations in a within-subjects complete
crossover design. Stages of anesthesia and recovery
were measured, and physiologic data were collected
before and during anesthesia.
Results—Interval to induction was more rapid and
recovery more prolonged in fish exposed to eugenol,
compared with those exposed to tricaine methanesulfonate.
The margin of safety for eugenol was narrow,
because at the highest concentration, most fish
required resuscitation. Mixed venous-arterial PO2 consistently
decreased with anesthesia, while PCO2 consistently
increased with anesthesia in all fish regardless
of anesthetic agent. The increase in PCO2 was
accompanied by a decrease in pH, presumably secondary
to respiratory acidosis. Anesthesia was associated
with increased blood glucose, potassium, and
sodium concentrations as well as Hct and hemoglobin.
Fish anesthetized with eugenol were more likely
to react to a hypodermic needle puncture than fish
anesthetized with tricaine methanesulfonate.
Conclusions and Clinical Relevance—Anesthesia
induced with tricaine methanesulfonate or eugenol
contributes to hypoxemia, hypercapnia, respiratory
acidosis, and hyperglycemia in red pacu. Similar to tricaine
methanesulfonate, eugenol appears to be an
effective immobilization compound, but eugenol is
characterized by more rapid induction, prolonged
recovery, and a narrow margin of safety. Care must
be taken when using high concentrations of eugenol
for induction, because ventilatory failure may occur
rapidly. In addition, analgesic properties of eugenol
are unknown. (Am J Vet Res 2001;62:337–342)
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.