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Summary: The effect of deep barbiturate anesthesia on brain glucose transport, TCA cycle flux, and aspartate, glutamate, and glutamine metabolism was assessed in the rat brain in vivo using 13C nuclear magnetic resonance spectroscopy at 9.4 T in conjunction with [1-13C] glucose infusions. Brain glucose con-centrations were elevated, consistent with a twofold reduced cerebral metabolic rate for glucose (CMRglc) compared with light -chloralose anesthesia. Using a mathematical model of neurotransmitter metabolism, several metabolic reaction rates were extracted from the rate of label incorporation. Total oxi-dative glucose metabolism, CMRglc(ox), was 0.33 ± 0.03 mol·g−1 · min−1. The neuronal TCA cycle rate was similar to that in the glia, 0.35 ± 0.03 mol · g−1 · min−1 and 0.26 ± 0.06 mol · g−1 · min−1, respectively, suggesting that neuronal en-ergy metabolism was mainly affected. The rate of pyruvate
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Choi et al. (2002) studied this question.
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