ALTERATIONS IN THE ARRHYTHMOGENIC DOSE OF EPINEPHRINE AFTER XYLAZINE OR MEDETOMIDINE ADMINISTRATION IN ISOFLURANE-ANESTHETIZED DOGS

Eight dogs (body weight, 12.5 to 21.5 kg) were assigned at random to e ach of 3 treatment groups (IS, IX, IM) that were not given glycopyrrol ate and to each of 3 groups that were given glycopyrrolate (IGS, IGX, IGM). Dogs were anesthetized with isoflurane (1.95% end-tidal concentr ation), and ventilation was controlled (P-CO2, 35 to 40 mm of Hg end-t idal concentration). Glycopyrrolate was administered IV and IM at a do sage of 11 mu g/kg of body weight, each. Saline solution, xylazine (1. 1 mg/kg, IM), or medetomidine (15 mu g/kg, IM) was administered 10 min utes after baseline ADE determination. Redetermination of the ADE at t he same infusion rate was started 10 minutes after drug administration . Arrhythmogenic dose was determined by constant infusion of epinephri ne at rates of 1.0, 2.5, and 5.0 mu g/kg/min. The ADE was defined as t he total dose of epinephrine that induced at least 4 ectopic ventricul ar depolarizations within 15 seconds during a 3-minute infusion, or wi thin 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical a nalysis of the differences between baseline and treatment ADE values w as performed by use of one-way ANOVA. Mean +/- SEM baseline ADE values for groups IS, IX, and IM were 1.55 +/- 0.23, 1.61 +/- 0.28, and 1.95 +/- 0.65 mu g/kg, respectively. Differences for groups IS, IX, and IM were -0.12 +/- 0.05, -0.31 +/- 0.40, and -0.17 +/- 0.26, respectively . Differences for groups IGS, IGX, and IGM could not be calculated bec ause arrhythmias satisfying the ADE criteria were not observed at the maximal infusion rate of 5.0 mu g/kg/min, Differences among groups IS, IX, and IM were not significant. We conclude that in isoflurane-anest hetized dogs: preanesthetic dosages of xylazine (1.1 mg/kg, IM) or med etomidine (15 mu g/kg, IM) do not enhance arrhythmogenicity, and at th ese dosages, there is no difference in the arrhythmogenic potential of either alpha(2)-adrenergic receptor agonist.