Evidence for barbiturate protection in focal cerebral ischemia: A hypothesis for mechanism and clinical utility

Abstract

Recent reports by several groups of investigators have documented an anatomic and clinical protective effect afforded by barbiturate drugs in a variety of animal models of both global and focal cerebral ischemia. (2,9,12,14) Additional pharmacologic and physiologic data support the fact that barbiturate anesthesia lowers cerebral blood flow and depresses cerebral metabolic rates of oxygen and glucose.(10,13) The potential application of hypometabolic therapy to man has been the subject of speculation and, indeed, some preliminary clinical investigation.(11) Before subjecting patients with cerebral lesions to the additional risks of hypotension and depressed respiration inherent in barbiturate therapy, it is imperative to establish a firm data base demonstrating efficacy as well as safety in large numbers of laboratory animals. Moreover, the goals of such radical treatment must be attainable and a tenable working hypothesis must be developed which is consistent with both the therapeutic objectives and the experimental data.