Literature DB >> 21336786

Potential non-hypoxic/ischemic causes of increased cerebral interstitial fluid lactate/pyruvate ratio: a review of available literature.

Daniel B Larach1, W Andrew Kofke, Peter Le Roux.   

Abstract

Microdialysis, an in vivo technique that permits collection and analysis of small molecular weight substances from the interstitial space, was developed more than 30 years ago and introduced into the clinical neurosciences in the 1990s. Today cerebral microdialysis is an established, commercially available clinical tool that is focused primarily on markers of cerebral energy metabolism (glucose, lactate, and pyruvate) and cell damage (glycerol), and neurotransmitters (glutamate). Although the brain comprises only 2% of body weight, it consumes 20% of total body energy. Consequently, the ability to monitor cerebral metabolism can provide significant insights during clinical care. Measurements of lactate, pyruvate, and glucose give information about the comparative contributions of aerobic and anaerobic metabolisms to brain energy. The lactate/pyruvate ratio reflects cytoplasmic redox state and thus provides information about tissue oxygenation. An elevated lactate pyruvate ratio (>40) frequently is interpreted as a sign of cerebral hypoxia or ischemia. However, several other factors may contribute to an elevated LPR. This article reviews potential non-hypoxic/ischemic causes of an increased LPR.

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Year:  2011        PMID: 21336786     DOI: 10.1007/s12028-011-9517-8

Source DB:  PubMed          Journal:  Neurocrit Care        ISSN: 1541-6933            Impact factor:   3.210


  136 in total

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Journal:  J Cereb Blood Flow Metab       Date:  2005-06       Impact factor: 6.200

Review 2.  Cerebral energy metabolism and microdialysis in neurocritical care.

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Journal:  Crit Care Med       Date:  2006-03       Impact factor: 7.598

Review 4.  Metabolic intermediates in lactic acidosis: compounds, samples and interpretation.

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Journal:  Anesthesiology       Date:  1978-08       Impact factor: 7.892

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Journal:  J Neurochem       Date:  1978-11       Impact factor: 5.372

7.  In vivo measurements of brain glucose transport using the reversible Michaelis-Menten model and simultaneous measurements of cerebral blood flow changes during hypoglycemia.

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Journal:  J Cereb Blood Flow Metab       Date:  2001-06       Impact factor: 6.200

8.  Increased pentose phosphate pathway flux after clinical traumatic brain injury: a [1,2-13C2]glucose labeling study in humans.

Authors:  Joshua R Dusick; Thomas C Glenn; W N Paul Lee; Paul M Vespa; Daniel F Kelly; Stefan M Lee; David A Hovda; Neil A Martin
Journal:  J Cereb Blood Flow Metab       Date:  2007-02-07       Impact factor: 6.200

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Journal:  Diabetes Res Clin Pract       Date:  1998-05       Impact factor: 5.602

10.  Inhibition of hepatic gluconeogenesis by ethanol.

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Journal:  Biochem J       Date:  1969-03       Impact factor: 3.857

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4.  Lack of consistent intracranial pressure pulse morphological changes during episodes of microdialysis lactate/pyruvate ratio increase.

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Review 6.  Physiological monitoring of the severe traumatic brain injury patient in the intensive care unit.

Authors:  Peter Le Roux
Journal:  Curr Neurol Neurosci Rep       Date:  2013-03       Impact factor: 5.081

Review 7.  Brain tissue oxygenation, lactate-pyruvate ratio, and cerebrovascular pressure reactivity monitoring in severe traumatic brain injury: systematic review and viewpoint.

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