Effect of Mild Hypothermia on Active and Basal Cerebral Oxygen Metabolism and Blood Flow

Abstract

The compartmentation of CMRO₂ began with Kety’s hypothesis that because anesthetics produce anesthesia through the reversible inhibition of synaptic transmission, they should affect CMRO₂ only to the extent associated with synaptic transmission (Kety, 1965). Michenfelder (1975) tested this hypothesis and showed that, indeed, massive doses of thiopental infused into dogs on cardiopulmonary bypass attenuated CMRO₂ only to the point of cortical electroencephalographic (EEG) silence and about 50% of normal. Continued infusion at doses several fold higher than required to abolish the cortical EEG did not further reduce CMRO₂ below 50% of normal. Thus, the concept of active CMRO₂ (ACMRO₂), i.e., associated with an active EEG, and basal CMRO₂ (BCMRO₂), i.e., associated with some basal level of cerebral metabolic activity was formulated, each representing about 50% of total CMRO₂ (TCMRO₂). Astrup and associates (Astrup, Skovsted, et al., 1981; Astrup, Sorensen, et al., 1981) extended this concept and divided the BCMRO₂ compartment into that associated with Ne⁺-K⁺ leak flux representing about 40% of BCMRO₂, and the other 60% of BCMRO₂ attributed to unidentified metabolic processes. Thus, thiopental allows the differentiation of the active and basal compartments by abolishing the active compartment.