The acute antiarrhythmic and toxic effects in mice and dogs of 2-ethylamino-2',6-'acetoxylidine (L-86), a metabolite of lidocaine.

L-86 is a major metabolite of lidocaine. In mice, the estimated LD5O and LDO.1 values for L-86 given orally were 234 and 151 mg/kg, respectively. The corresponding values for lidocaine hydrochloride monohydrate were 292 and 78 mg/kg. Oral doses of 190 mg/kg of L-86 or 78 mg/kg of lidocaine hydrochloride monohydrate given 20 minutes before exposure to chloroform vapors inhibited the ventricular fibrillation which accompanies chloroform-induced respiratory arrest in the mouse. In four unanesthetized dogs with ventricular arrhythmias produced by two-stage ligation of the anterior descending branch of the left coronary artery, progressively larger i.v. doses of L-86 were given at hourly intervals. Doses of 2.5 mg/kg produced only minimal effects upon the ventricular arrhythmias whereas doses of 5, 10 and 20 mg/kg produced distinct but transient antiarrhythmic effects. Emesis occurred in one dog after 5 mg/kg, in three dogs after 10 mg/kg and in two dogs after 20 mg/kg. Transient convulsions occurred in three dogs after 20 mg/kg. L-86 appears to be a more potent emetic than lidocaine in the dog, to be of similar potency with respect to lethality in mice and to be slightly less potent with respect to its antiarrhythmic actions in both mice and dogs. Thus, L-86 may contribute to the antiarrhythmic and toxic effects of lidocaine.