[Hemodynamic and metabolic effects of barbiturates on the human central nervous system]

Anoxic cerebral ischemia results in an almost instantaneous stoppage of the EEG, and a depletion of the cerebral energy reserves with anaerobic orientation. The experimental work, especially of Safar and Michenfelder, have proven the significant cerebral protection under barbituric hypometabolism. The cerebral impacts of barbiturates in the animal, in vitro and in vivo, are multiple: decrease in glycolysis, energetic stabilisation, a blocking of the adenylcyclase activity, membrane stabilisation by trapping of the free radicals or by an increase of the cerebral osmolarity, ect... In man, the metabolic and the hemodynamic data, of which there is little, have only confirmed the reports of metabolic and circulatory depression made by Himwich as early as 1947. The use of barbiturates in postischemic protection poses a problem of their specificity. For an equivalent cerebral metabolic depression a protective effect could not be proven with the tilisation of halogens nor with the morphines... Other narcotics (Alfatésine, Gamma OE) also depress the CNS, but their protective effects are unknown. MICHENFELDER attributes the barbituric protection to the "functional neuron" block without interference at the metabolic level of cellular life. The specificity of barbiturates in this block has yet to be proven. In the post-ischemic resuscitation, Safar insists, and rightly so, on the urgency to correct the cerebral hypoperfusion with a parallel barbituric induction. If there is no "specificity" in the narcotic hypometabolism, it would be logically imperative to use that which provides the best protection, in the shortest, delay, and with the least systemic depression.