Influence of cholinergic blockade on the development of epinephrine-induced ventricular arrhythmias in halothane- and isoflurane-anesthetized dogs.

The arrhythmogenic effects of anesthetic drugs are assessed using the arrhythmogenic dose of epinephrine (ADE) model. The purpose of this study was to determine the influence of cholinergic blockade (CB) produced by glycopyrrolate (G) on ADE in 1.5 minimum alveolar concentration (MAC) halothane (H)- and isoflurane (I)-anesthetized dogs. Eight dogs (weighing between 12.5 and 21.5 kg) were randomly assigned to four treatment groups (H, HG, I, and IG) and each treatment was replicated three times. Anesthesia was induced and maintained with H (1.31%, end-tidal [ET]) or I (1.95%, ET) in oxygen. Ventilation was controlled (carbon dioxide [PCO2] 35 to 40 mmHg, ET). G was administered 10 minutes before ADE determination at a dose of 22 microgram/kg (11 microgram/kg, intravenous [IV] and 11 micrograms/kg, intramuscular [IM]). The ADE was determined by IV infusion of epinephrine at sequentially increasing rates of 1.0, 2.5, and 5.0 micrograms/kg/min; and defined as the total dose of epinephrine producing at least four ectopic ventricular contractions (EVCs) within 15 seconds during a 3-minute infusion and up to 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Data were analyzed using a randomized complete block analysis of variance. When significant (P < .05) F values were found a least significant difference test was used to compare group means. Values are reported as means +/- standard error. The ADE (micrograms/kg) for H, HG, I, and IG were 1.53 +/- 0.08, 3.37 +/- 0.46, 1.61 +/- 0.21, and > 15.00, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)