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The effects of halothane on canine ventricular automaticity and contractility were studied in intact and isolated heart preparations in which the right anterior papillary muscle and sinoatrial node of a recipient dog were separately perfused with arterial blood from a donor animal. One percent halothane inhaled by the donor dog decreased blood pressure and heart rate in the donor animal and sensitized the ventricle of the donor dog to the arrythmic effects of norepinephrine. One per cent halothane inhaled by donor dogs also produced negative inotropic and chronotropic responses in the isolated, perfused sinoatrial and ventricular oprparations, but had no effect on positive chronotropic or inotropic responses to norepinephrine or perivascular nerve stimulation. Norepinephrine administered to donor dogs produced no arrhythmia in either spontaneously beating or electrically paced recipient hearts even though producing ventricular fibrillation in the donor. The results suggest that re-entry mechanisms play an important role in halothane-catecholamine-induced arrhythmias.
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