Alterations in the arrhythmogenic dose of epinephrine after xylazine or medetomidine administration in halothane-anesthetized dogs

Kip A. Lemke From the Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana-Champaign, IL 61801.

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William J. Tranquilli From the Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana-Champaign, IL 61801.

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John C. Thurmon From the Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana-Champaign, IL 61801.

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G. John Benson From the Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana-Champaign, IL 61801.

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William A. Olson From the Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana-Champaign, IL 61801.

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Summary

Eight dogs (12.5 to 21.5 kg) were assigned at random to each of 3 groups that were not given glycopyrrolate (hs, hx, hm) and to each of 3 groups that were given glycopyrrolate (hgs, hgx, hgm). Dogs were anesthetized with halothane (1.31% end-tidal concentration), and ventilation was controlled (PCO2 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 arrhythmogenic dose of epinephrine (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 and 2.5 μg/kg/min. The ade was defined as the total dose of epinephrine inducing 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 ade and posttreatment ade for groups hs, hx, and hm was performed by use of one-way anova. Mean ± sem baseline ade values for groups hs, hx, and hm were 1.50 ± 0.11, 1.49 ± 0.10, and 1.57 ± 0.22 pg/kg, respectively, and for groups hgs, hgx, and hgm were 3.37 ± 0.61, 3.10 ± 0.75, and 3.04 ± 0.94 pg/kg, respectively. Differences for groups hs, hx, and hm were – 0.02 ± 0.15, – 0.00 ± 0.14, and – 0.21 ± 0.17 μg/kg, respectively, and for groups hgs, hgx, and hgm, were – 0.59 ± 0.26, – 0.41 ± 0.15, and – 0.58 ± 0.20 μg/kg, respectively. Differences among groups hs, hx, and hm, or among groups hgs, hgx, and hgm were not significant. We conclude that without and with cholinergic blockade in halothane-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 α2-adrenoceptor agonist.

Summary

Eight dogs (12.5 to 21.5 kg) were assigned at random to each of 3 groups that were not given glycopyrrolate (hs, hx, hm) and to each of 3 groups that were given glycopyrrolate (hgs, hgx, hgm). Dogs were anesthetized with halothane (1.31% end-tidal concentration), and ventilation was controlled (PCO2 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 arrhythmogenic dose of epinephrine (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 and 2.5 μg/kg/min. The ade was defined as the total dose of epinephrine inducing 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 ade and posttreatment ade for groups hs, hx, and hm was performed by use of one-way anova. Mean ± sem baseline ade values for groups hs, hx, and hm were 1.50 ± 0.11, 1.49 ± 0.10, and 1.57 ± 0.22 pg/kg, respectively, and for groups hgs, hgx, and hgm were 3.37 ± 0.61, 3.10 ± 0.75, and 3.04 ± 0.94 pg/kg, respectively. Differences for groups hs, hx, and hm were – 0.02 ± 0.15, – 0.00 ± 0.14, and – 0.21 ± 0.17 μg/kg, respectively, and for groups hgs, hgx, and hgm, were – 0.59 ± 0.26, – 0.41 ± 0.15, and – 0.58 ± 0.20 μg/kg, respectively. Differences among groups hs, hx, and hm, or among groups hgs, hgx, and hgm were not significant. We conclude that without and with cholinergic blockade in halothane-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 α2-adrenoceptor agonist.

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