Alterations in the arrhythmogenic dose of ...
|Title||Alterations in the arrhythmogenic dose of epinephrine after xylazine or medetomidine administration in halothane-anesthetized dogs|
|Author(s)||Kip A. Lemke, W. J. Tranquilli, J. C. Thurmon, G. J. Benson, W. A. Olson|
|Journal||American Journal of Veterinary Research|
|Abstract||In a series of trials at least 3 days apart, dogs (12.5 to 21.5 kg) were assigned at random to each of 6 groups: halothane-saline (HS), halothane-xylazine (HX), halothane-medetomidine (HM) and the corresponding groups with glycopyrrolate (HGS, HGX, HGM). Dogs were anaesthetized with halothane (1.31% end-tidal concentration), and ventilation was controlled (PCO2 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered i.v. and i.m. at a dosage of 11 micro g/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, i.m.), or medetomidine (15 micro g/kg, i.m.) was administered 10 min after baseline arrhythmogenic dose of epinephrine (ADE) determination. Redetermination of the ADE at the same infusion rate was started 10 min after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0 and 2.5 micro g/kg min-1. The ADE was defined as the total dose of epinephrine inducing at least 4 ectopic ventricular depolarizations within 15 sec during a 3-min infusion or within 1 min after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Use of one-way ANOVA showed that differences between baseline and posttreatment ADE among groups HS, HX, and HM, or among groups HGS, HGX, and HGM were not significant. It was concluded that with and without cholinergic blockade in halothane-anaesthetized dogs, preanaesthetic dosages of xylazine or medetomidine used in this study do not enhance arrhythmogenicity, and at these dosages, there is no difference in the arrhythmogenic potential of either alpha 2-adrenoceptor agonist..|
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