Canadian Journal of Anesthesia, Vol 6, 251-262, Copyright © 1959 by Canadian Anesthesiologists' Society

The Effect of Perphenazine on Epinephrine-induced Cardiac Arrhythmias in Dogs: II, Anaesthesia with Cyclopropane, Chloroform, and Trichlorethylene

¹ Department of Anaesthesia, University of Saskatchewan College of Medicine and the Anaesthesia Laboratory, Medical Research Building, Saskatoon, Canada
² Medical Student Research Assistant from the University of Saskatchewan College of Medicine

The effect of 25 per cent cyclopropane, 0.5 per cent chloroform with 70 per cent nitrous oxide and 1 per cent trichlorethylene with 70 per cent nitrous oxide on the heart rate was observed during thirty-six acute experiments in dogs in which pulmonary ventilation was regulated, and the concentrations of the inhaled anaesthetics were accurately controlled. There was marked slowing of the heart rate with cyclopropane, slight slowing with chloroform, and little or no change with trichlorethylene. There was no significant difference in the heart rate in the animals that were premedicated with perphenazine 0.25 mg/kg, as compared to the unpremedicated animals.

Sensitization to epinephrine-provoked cardiac arrhythmias by a standard concentration and rate of injection (0.02 mg/ml/sec.) were observed, when the total dose was regulated according to the animals' weight. It was found that ventricular fibrillation was less likely to occur when epinephrine was injected during anaesthesia with 0.5 per cent chloroform than with 25 per cent cyclopropane, or with 1 per cent trichlorethylene. In a similar study with Fluothane and the azeotropic mixture of Fluothane and diethyl ether, the cardiac response to epinephrine with 0.5 per cent Fluothane was similar to that with 25 per cent cyclopropane, and the 1 per cent of the azeotropic mixture was similar to that with 0.5 per cent chloroform.

Premedication with perphenazine (0.25 mg./kg.) caused a significant reduction in the severity and duration of the cardiac arrhythmias provoked by epinephrine if pulmonary ventilation was adequate throughout the experiment, but did not cause reversal of the pressor response. It was suggested that the elimination of epinephrine-provoked cardiac arrhythmias by perphenazine would require such alteration in the depth of anaesthesia or dose of perphenazine as would reduce the validity of the results of these experiments for practical application.

Note:

Supported in part by a grant-in-aid from Schering Corporation, Montreal, Canada.