The effects of atropine and methotrimeprazine on the epinephrine-induced arrhythmias in halothane-anesthetized dogs

The effects of atropine and methotrimeprazine on epinephrine-induced ventri cular arrhythmias were evaluated in halothane-anesthetized dogs. Ten mixed- breed dogs were assigned to 3 treatments (saline, atropine, and methotrimep razine) in a randomized complete block design. Anesthesia was induced and m aintained with halothane (1.5 minimum alveolar concentration) in oxygen. Co ntrolled ventilation was used throughout to maintain eucapnia. Saline, atro pine (0.05 mg/kg, IV) or methotrimeprazine (0.5 mg/kg, IV) were administere d and, 5 minutes later the arrhythmogenic dose of epinephrine (ADE) was mea sured by IV infusion of progressively increasing infusion rates of epinephr ine, until the ventricular arrhythmia criterion was met (at least 4 ectopic ventricular contractions (EVCs) during a 15-second period). Data were anal yzed using a student's t-test for ADE values and multivariate profile analy sis for heart rate (HR), arterial blood pressure (ABP), and rate pressure p roduct (RPP). The ADE increased in atropine- and methotrimeprazine-treated groups, whereas 1 and 4 animals from these groups did not develop any ventr icular arrhythmia, respectively. Epinephrine induced multiform premature ve ntricular contractions (PVCs) in the atropine group, whereas ventricular es cape beats were observed in the control and methotrimeprazine groups. Heart rate and RPP decreased, and ABP increased at the time of ADE observation i n the control group. Epinephrine infusion in the atropine group caused mark ed increases in HR, ABP, and RPP, which were associated with pulsus alterna ns in 2 animals. It was concluded that 1) the presence of cholinergic block ade influences the type of ventricular arrhythmia induced by epinephrine; 2 ) increased ADE values recorded following atropine administration must be c autiously interpreted, since in this situation the PVCs were associated wit h signs of increased myocardial work and ventricular failure; and 3) the us e of a broader arrhythmia criterion (EVCs instead of PVCs) may not allow a direct comparison between ADE values, since it includes ventricular arrhyth mias mediated by different mechanisms.