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Halothane‐sparing effect of xylazine in dogs and subsequent reversal with tolazoline

1984; Wiley; Volume: 7; Issue: 1 Linguagem: Inglês

10.1111/j.1365-2885.1984.tb00874.x

1365-2885

William J. Tranquilli, J. C. Thurmon, J. E. Corbin, G. John Benson, Lloyd Davis,

Antibiotics Pharmacokinetics and Efficacy

Halothane MAC (the minimum alveolar concentration of halothane to produce anaesthesia in 50% of the animals tested) was determined to be 0.92 ± 0.16 volumes % in eight English Pointer dogs. Alterations in halothane MAC induced by an intravenous bolus of xylazine (1.1 mg/kg) and then tolazoline (5 mg/kg) was determined in each dog following control (halothane MAC) measurement. Following xylazine administration, MAC significantly decreased to 0.57 ± 0.023%. Immediately following determination of the xylazine‐halothane MAC value in each dog, tolazoline was administered and the halothane requirement (MAC) was again assessed. Halothane MAC significantly increased to 1.24 ± 0.036%. Tolazoline administration induced immediate arousal in the xylazine‐halothane anaesthetized dogs requiring a rapid increase in halothane concentration to maintain anaesthesia. Thus, the administration of tolazoline, an alpha adrenergic antagonist, following xylazine administration significantly increased the anaesthetic requirement (MAC) of halothane. Xylazine, an alpha 2 adrenergic agonist, decreased halothane anaesthetic requirement (MAC) in the eight dogs studied. These results are consistent with the hypotheses that stimulation of central alpha 2 receptors is the mechanism by which xylazine produces sedation and that inhibition of CNS excitatory neurotransmitter release decreases halothane anaesthetic requirement. In contrast, the increase in halothane requirement and arousal from xylazine‐halothane anaesthesia that occurred following i.v. tolazoline administration indicates an increase in CNS excitatory neurotransmitter activity.