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- Author or Editor: Clifford R. Swanson x
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Abstract
Objective—To compare the anesthetic efficacy and physiologic changes associated with exposure to tricaine methanesulfonate and clove oil (100% eugenol).
Animals—15 adult cultured red pacu (Piaractus brachypomus).
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)
Abstract
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.
