The chief hazard in the use of hypothermic anesthesia continues to be the occurrence of ventricular fibrillation. In order to avoid this complication, the level of hypothermia induced during surgical procedures is usually restricted to rectal temperatures above 28 C (82.4 F). The advantages of hypothermia in surgery increase, however, in proportion to the lowering of temperature. In an effort to control fibrillation at low temperatures, the antiarrhythmic effects of many pharmacological agents have been investigated,1,2 but few have been found wholly satisfactory.
Aminoacetic acid U. S. P. (Glycine), an amino acid, has been reported to suppress cyclopropane-epinephrine-induced arrhythmias.3 In a previous study,4 intravenous aminoacetic acid was shown to be easily administered, safe, and well tolerated by hypothermic animals. The present investigation was initiated, therefore, to evaluate the use of intravenous aminoacetic acid as a means of preventing ventricular fibrillation during hypothermia, with and without the added