Local cerebral glucose consumption in the artificially ventilated rat: influence of nitrous oxide analgesia and of phenobarbital anesthesia

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Abstract
The objectives of the present study, which concerns local glucose consumption (1‐CMRg1) in the rat brain as measured with the 14C‐deoxyglucose technique of Sokoloff et al. (1977), were (1) to provide data for l‐CMRg1 in nitrous oxide analgesia and in phenobarbital anesthesia, allowing a comparison with previous results on oxygen consumption, and (2) to test a recent proposal that 70% N2O markedly reduces 1‐CMRg1 in (mainly) cortical structures. Under 70% N2O, 1‐CMRg1 in frontal and parietal cortex was close to 0.7 μmol·g‐1·min‐1. This value is in excellent agreement with previous values for “cortical” oxygen consumption. In phenobarbital anesthesia, 1‐CMRg1 was lower than that expected from oxygen consumption, probably reflecting the fact that barbiturate anesthesia is accompanied by consumption of endogenous substrates. Experiments on adrenalectomized animals that were given local anesthesia and protected from external stimuli failed to demonstrate that 70% N2O depresses 1‐CMRg1. In fact, N2O was found to increase 1‐CMRg1 in many structures. It is concluded that if I‐CMRg1 is lower in ventilated animals than in spontaneously breathing, conscious controls, the depression is more likely to be due to the neuromuscular blockade.