THE most recent edition of ‘Lumb and Jones’ is full of relevant and accessible information about anaesthesia and analgesia. Although it features over 80 contributing authors, there is an overriding clarity to the text, which makes it an ideal practice reference text, for answering specific questions, as well as being an effortless, informative read.
The book presents clinically relevant information very well. An evidence-based approach is used in the presentation of the content, which informs …
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.
Summary Eight dogs (body weight, 12.5 to 21.5 kg) were assigned at random to each of 3 treatment groups ( is , ix , im ) that were not given glycopyrrolate and to each of 3 groups that were given glycopyrrolate ( igs , igx , igm ). Dogs were anesthetized with isoflurane (1.95% end-tidal concentration), and ventilation was controlled (P CO 2 , 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered iv and im at a dosage of 11 μg/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, im ), or medetomidine (15 μg/kg, im ) was administered 10 minutes after baseline ade determination. Redetermination of the ade at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0, 2.5, and 5.0 μg/kg/min. The ade was defined as the total dose of epinephrine that induced at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion, or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline and treatment ade values was performed by use of one-way anova. Mean ± sem baseline ade values for groups is , ix , and im were 1.55 ± 0.23, 161 ± 0.28, and 1.95 ± 0.65 μg/kg, respectively. Differences for groups is , ix , and im were – 0.12 ± 0.05, – O.31 ± 0.40, and – 0.17 ± 0.26, respectively. Differences for groups igs , igx , and igm could not be calculated because arrhythmias satisfying the ade criteria were not observed at the maximal infusion rate of 5.0 μg/kg/min. Differences among groups is , ix , and im were not significant. We conclude that in isoflurane-anesthetized dogs: preanesthetic dosages of xylazine (1.1 mg/kg, im ) or medetomidine (15 μg/kg, im ) do not enhance arrhythmogenicity, and at these dosages, there is no difference in the arrhythmogenic potential of either α 2 -adrenergic receptor agonist.
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