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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-10670

Stover, J F; Pleines, U E; Morganti-Kossmann, M C; Stocker, R; Kempski, O S; Kossmann, T (1999). Thiopental and midazolam do not seem to impede metabolism of glutamate in brain-injured patients. Psychopharmacology, 141(1):66-70.

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Abstract

Increased extracellular glutamate levels are related to glial and neuronal damage. Glutamate-mediated toxicity is limited by glial uptake and metabolic transformation of glutamate to glutamine and the energetic compounds alanine and lactate which are utilized by surrounding neurons. Under in vitro conditions, barbiturates have been shown to reduce glutamate uptake and its further metabolism, possibly impeding metabolic coupling between astrocytes and neurons. The aims were to investigate if under clinical conditions, the barbiturate thiopental reduces important detoxification of glutamate, resulting in lower CSF glutamine, alanine and lactate levels as opposed to patients receiving midazolam. During long-term administration of thiopental and midazolam, pathologically elevated ventricular CSF glutamate levels were associated with significantly increased glutamine and alanine levels up to 14 days after trauma. CSF lactate, however, remained normal. These data suggest that long-term administration of thiopental and midazolam under clinical conditions does not impede enzymatic activities responsible for detoxification and metabolism of glutamate.

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Division of Surgical Intensive Care Medicine
DDC:610 Medicine & health
Language:English
Date:1999
Deposited On:13 Mar 2009 13:57
Last Modified:27 Nov 2013 20:17
Publisher:Springer
ISSN:0033-3158
Publisher DOI:10.1007/s002130050807
PubMed ID:9952066
Citations:Web of Science®. Times Cited: 2
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Scopus®. Citation Count: 2

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