Abstract
The electrophysiological basis of pharmacological actions of halothane on canine cardiac fibers was examined to elucidate the mechanism of the induction of the arrhythmia by the combination of anesthetic and epinephrine. The pacemaker activity of the right bundle branch (RBB) was compared with that of the sinus node under the influence of halothane and epinephrine. In the spontaneously active fiber of RBB, halothane (1.3% v/v) caused remarkable increase in the slope of pacemaker potential and in the rate of firing in most preparations. In contrast, halothane produced a profound depression in pacemaker activity of the sinus node in half number of preparations, but the remaining preparations were not affected significantly. The positive chronotropic action of epinephrine was augmented by halothane in RBB preparations, while the enhancement was not observed in atrial preparations. These effects might result in an enhanced liability to arrhythmia.
