期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 22, 期 11, 页码 1343-1351出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/01.WCB.0000040945.89393.46
关键词
NMR; glutamate neurotransmission; pentobarbital; energy metabolism; glucose transport
资金
- NCRR NIH HHS [P41RR08079] Funding Source: Medline
- NIDDK NIH HHS [R21DK58004] Funding Source: Medline
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 13 C nuclear magnetic resonance spectroscopy at 9.4 T in conjunction with [1-C-13] glucose infusions. Brain glucose concentrations were elevated, consistent with a twofold reduced cerebral metabolic rate for glucose (CMRglc) compared with light a-chloralose anesthesia. Using a mathematical model of neurotransmitter metabolism, several metabolic reaction rates were extracted from the rate of label incorporation. Total oxidative glucose metabolism, CMRglc(ox), was 0.33 +/- 0.03 mumol.g(-1).min(-1). The neuronal TCA cycle rate was similar to that in the glia, 0.35 +/- 0.03 mumol.g(-1).min(-1) and 0.26 +/- 0.06 mumol.g(-1).min(-1), respectively, suggesting that neuronal energy metabolism was mainly affected. The rate of pyruvate carboxylation was 0.03 +/- 0.01 mumol.g(-1).min(-1). The exchange rate between cytosolic glutamate and mitochondrial 2-oxoglutarate, V., was equal to the rate of neuronal pyruvate dehydrogenase flux. This indicates that V-x is coupled to CMRglc(ox), implying that the malate-aspartate shuttle is the major mechanism that facilitates label exchange across the inner mitochondrial membrane. The apparent rate of glutamatergic neurotransmission, V-NT, was 0.04 +/- 0.01 mumol.g(-1).min(-1), consistent with strong reductions in electrical activity. However, the rates of cerebral oxidative glucose metabolism and glutamatergic neurotransmission, CMRglc(ox)/v(NT), did not correlate with a 1: 1 stoichiometry.
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