Nitrous oxide alters oxidative metabolic activities of rat neocortex in situ

Rosenthal, Myron; Adams, M. R.; LaManna, Joseph Charles

doi:10.1016/0006-8993(81)90245-6

Cited by 5 publications

(2 citation statements)

References 33 publications

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“…Rosenthal et al reported that in rats an increased oxidation of cytochrome a, as, occurs during N20 anaesthesia, suggesting an increased energy demand. 18 Pelligrino et al using a goat cerebrocortical mitochondrial preparation in vitro, observed that the increased 02 utilization during exposure to N20 may be due at least partly to a direct effect of N20 on mitochondrial respiration. 2 Under normal conditions, the brain is dependent upon a continuous supply of blood in order to obtain a continuous flow of 02 as well as glucose to the cells.…”

Section: N2/o2mentioning

confidence: 99%

Transcranial doppler sonography: nitrous oxide and cerebral blood flow velocity in children

Leon

Bissonnette

1991

Can J Anaesth

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Section: N2/o2mentioning

confidence: 99%

Transcranial doppler sonography: nitrous oxide and cerebral blood flow velocity in children

Leon

Bissonnette

1991

Can J Anaesth

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“…Also, N 2 O decreased the ratio of reduction/oxidation of cytochrome a , a 3 and it increased blood volume in rat brain, consistent with increased energy demand (Rosenthal et al . ). Similar cytochrome a , a 3 redox effects occur after cortical stimulation, and responses were attenuated by norepinephrine depletion by locus coeruleus lesion (Harik et al .…”

Section: Regulation Of Aerobic Glycolysis Via Adrenergic Receptorsmentioning

confidence: 97%

Aerobic glycolysis during brain activation: adrenergic regulation and influence of norepinephrine on astrocytic metabolism

Dienel

Cruz

2016

Journal of Neurochemistry

137

164

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Aerobic glycolysis occurs during brain activation and is characterized by preferential up-regulation of glucose utilization compared with oxygen consumption even though oxygen level and delivery are adequate. Aerobic glycolysis is a widespread phenomenon that underlies energetics of diverse brain activities, such as alerting, sensory processing, cognition, memory, and pathophysiological conditions, but specific cellular functions fulfilled by aerobic glycolysis are poorly understood. Evaluation of evidence derived from different disciplines reveals that aerobic glycolysis is a complex, regulated phenomenon that is prevented by propranolol, a non-specific b-adrenoceptor antagonist. The metabolic pathways that contribute to excess utilization of glucose compared with oxygen include glycolysis, the pentose phosphate shunt pathway, the malate-aspartate shuttle, and astrocytic glycogen turnover. Increased lactate production by unidentified cells, and lactate dispersal from activated cells and lactate release from the brain, both facilitated by astrocytes, are major factors underlying aerobic glycolysis in subjects with low blood lactate levels. Astrocyte-neuron lactate shuttling with local oxidation is minor. Blockade of aerobic glycolysis by propranolol implicates adrenergic regulatory processes including adrenal release of epinephrine, signaling to brain via the vagus nerve, and increased norepinephrine release from the locus coeruleus. Norepinephrine has a powerful influence on astrocytic metabolism and glycogen turnover that can stimulate carbohydrate utilization more than oxygen consumption, whereas breceptor blockade 're-balances' the stoichiometry of oxygenglucose or -carbohydrate metabolism by suppressing glucose and glycogen utilization more than oxygen consumption. This conceptual framework may be helpful for design of future studies to elucidate functional roles of preferential nonoxidative glucose utilization and glycogen turnover during brain activation. Keywords: aerobic glycolysis, astrocyte, epinephrine, glycogen, lactate, norepinephrine. J. Neurochem. (2016) 138, 14-52.This review first describes characteristics of aerobic glycolysis, and then identifies metabolic pathways that contribute to its becoming manifest with increases in their rates. Lactate release is recognized as a major, but not the only, factor in causing greater utilization of glucose than oxygen during brain activation. Astrocytes have a high impact on the phenomenon because of glycogen turnover, lactate dispersal through gap junctions, and lactate discharge from the brain. Aerobic glycolysis is prevented by propranolol, a non-specific b-adrenoceptor antagonist, implicating adrenergic signaling in regulation of the cellular activities that contribute to aerobic glycolysis. Analysis of studies in diverse fields ranging from metabolic assays of brain activation to memory consolidation led to a model describing adrenergic regulation of aerobic glycolysis. The model posits that stress-related Abbreviations used: AGC, aspartate-gl...

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Anesthetics

Cheng¹

1985

Alterations of Metabolites in the Nervous System

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Nitrous oxide alters oxidative metabolic activities of rat neocortex in situ

Cited by 5 publications

References 33 publications

Transcranial doppler sonography: nitrous oxide and cerebral blood flow velocity in children

Transcranial doppler sonography: nitrous oxide and cerebral blood flow velocity in children

Aerobic glycolysis during brain activation: adrenergic regulation and influence of norepinephrine on astrocytic metabolism

Anesthetics

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