Cerebral blood flow and oxygen uptake, and cerebrospinal fluid biochemistry in severe coma

Brodersen, P; Jørgensen, Erik

doi:10.1136/jnnp.37.4.384

Cited by 65 publications

(6 citation statements)

References 29 publications

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“…According to these authors, the reason may be extracerebral contamination of the blood in the jugular bulb or maldistribution of the cerebral blood flow with the presence of non-nutritional flow. High jugular venous oxygen tension or saturation has also been observed in comatose patients after cardiac arrest (BRODERSEN & I n this study we also found high jugular venous tension and low cerebral oxygen uptake, which were both unrelated to cerebral blood flow, time after the acute injury, localization of the cerebral injury, and the clinical outcome, These results are in agreement with other clinical studies ( GORDON & BERGVALL 1973, BRODERSEN & J0RGENSEN 1974, FIESCHI et al 1974) and provide further evidence in favour of the assumption that a critical, low CMR,, cannot be defined. JBRGENSEN 1974, SIEMKOWICZ 1977.…”

Section: Discussionsupporting

confidence: 92%

Cerebral Metabolic Rate of Oxygen (CMR_O2) in the Acute Phase of Brain Injury

Cold¹

1978

Acta Anaesthesiol Scand

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In 22 comatose patients with acute brain injury, the cerebral metabolic rate of oxygen (CMRO2) was calculated as the product of the hemispheric cerebral blood flow (CBF) and the arteriovenous oxygen content difference. All patients were subjected to moderate sedation without barbiturates, normothermia and respiratory treatment. The CBF was calculated by the 133xenon washout method as the average of 16 regions. The results indicate high jugular venous oxygen tension and, in some studies, very low oxygen consumption. A critical, low CMRO2 was not found, and values of about 0.4 ml/100 g/min were compatible with restitution of intellectual function. The CMRO2 was unrelated to the clinical outcome and to the time after the trauma. In bilateral studies, the lowest values were measured in the most severely injured hemisphere.

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Section: Discussionsupporting

confidence: 92%

Cerebral Metabolic Rate of Oxygen (CMR_O2) in the Acute Phase of Brain Injury

Cold¹

1978

Acta Anaesthesiol Scand

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“…However, in TBM cases there are typically low levels of glucose in the CSF [ 22 ], corresponding to a CSF to serum glucose ratio less than 0.5 or an absolute CSF glucose concentration of less than 2.2 mM. Furthermore, several studies have shown no correlation between CSF lactic acid levels and cerebral blood flow (i.e., they are unrelated to ischemia) [ 23 – 25 ]. Thus, elevated lactic acid in CSF of TBM cases is unlikely to be due to anaerobic respiration but instead is possibly a product of temporarily increased flux in the glycolysis pathway.…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal fluid in tuberculous meningitis exhibits only the L-enantiomer of lactic acid

et al. 2016

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BackgroundThe defining feature of the cerebrospinal fluid (CSF) collected from infants and children with tuberculous meningitis (TBM), derived from an earlier untargeted nuclear magnetic resonance (NMR) metabolomics study, was highly elevated lactic acid. Undetermined was the contribution from host response (L-lactic acid) or of microbial origin (D-lactic acid), which was set out to be determined in this study.MethodsIn this follow-up study, we used targeted ultra-performance liquid chromatography–electrospray ionization–tandem mass spectrometry (UPLC–ESI–MS/MS) to determine the ratio of the L and D enantiomers of lactic acid in these CSF samples.ResultsHere we report for the first time that the lactic acid observed in the CSF of confirmed TBM cases was in the L-form and solely a response from the host to the infection, with no contribution from any bacteria. The significance of elevated lactic acid in TBM appears to be that it is a crucial energy substrate, used preferentially over glucose by microglia, and exhibits neuroprotective capabilities.ConclusionThese results provide experimental evidence to support our conceptual astrocyte–microglia lactate shuttle model formulated from our previous NMR-based metabolomics study — highlighting the fact that lactic acid plays an important role in neuroinflammatory diseases such as TBM. Furthermore, this study reinforces our belief that the determination of enantiomers of metabolites corresponding to infectious diseases is of critical importance in substantiating the clinical significance of disease markers.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-016-1597-9) contains supplementary material, which is available to authorized users.

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“…CSF lactate has been shown to reflect changes in parenchymal rather than blood lactate concentrations (Prockop, 1968). CSF lactate has been reported to rise in stroke, seizure, meningitis, hypoxic and posthypoglycemic coma, head trauma, and brain death (Brodersen and Jorgensen, 1974;Fishman, 1980;Wood, 1980;Busse and Hoffman, 1983). The slightly elevated levels in patients B and C might have been caused by the seizures and coma they suffered.…”

Section: Discussionmentioning

confidence: 99%

High‐Resolution Proton Magnetic Resonance Analysis of Human Cerebrospinal Fluid

Petroff¹,

Yu²,

Ogino³

1986

Journal of Neurochemistry

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High‐resolution proton magnetic resonance spectroscopy was used to analyze human cerebrospinal fluid obtained from patients with several neurological problems. The major metabolites measured included glucose, lactate, glutamine, citrate, inositol, acetate, creatine, creatinine, β‐hydroxybutyrate, alanine, and pyruvate. A drug vehicle, propylene glycol, was also measured. Alterations in the cerebrospinal fluid of these metabolites provided information concerning metabolism of the brain. Magnetic resonance spectroscopy offered a simple and rapid means of assessing these and other exogenous and endogenous compounds in diseases affecting the nervous system.

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Cerebral blood flow and oxygen uptake, and cerebrospinal fluid biochemistry in severe coma

Cited by 65 publications

References 29 publications

Cerebral Metabolic Rate of Oxygen (CMR_O2) in the Acute Phase of Brain Injury

Cerebral Metabolic Rate of Oxygen (CMR_O2) in the Acute Phase of Brain Injury

Cerebrospinal fluid in tuberculous meningitis exhibits only the L-enantiomer of lactic acid

High‐Resolution Proton Magnetic Resonance Analysis of Human Cerebrospinal Fluid

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Cerebral blood flow and oxygen uptake, and cerebrospinal fluid biochemistry in severe coma

Cited by 65 publications

References 29 publications

Cerebral Metabolic Rate of Oxygen (CMRO2) in the Acute Phase of Brain Injury

Cerebral Metabolic Rate of Oxygen (CMRO2) in the Acute Phase of Brain Injury

Cerebrospinal fluid in tuberculous meningitis exhibits only the L-enantiomer of lactic acid

High‐Resolution Proton Magnetic Resonance Analysis of Human Cerebrospinal Fluid

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Product

Resources

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Cerebral Metabolic Rate of Oxygen (CMR_O2) in the Acute Phase of Brain Injury

Cerebral Metabolic Rate of Oxygen (CMR_O2) in the Acute Phase of Brain Injury