title: Cerebral Glucose Metabolism and Sedation in Brain-injured Patients: A Microdialysis Study.
abstract: BACKGROUND
  Disturbed brain metabolism is a signature of primary damage and/or precipitates secondary injury processes after severe brain injury. Sedatives and analgesics target electrophysiological functioning and are as such well-known modulators of brain energy metabolism. Still unclear, however, is how sedatives impact glucose metabolism and whether they differentially influence brain metabolism in normally active, healthy brain and critically impaired, injured brain. We therefore examined and compared the effects of anesthetic drugs under both critical (<1 mmol/L) and noncritical (>1 mmol/L) extracellular brain glucose levels.
  
  
  METHODS
  We performed an explorative, retrospective analysis of anesthetic drug administration and brain glucose concentrations, obtained by bedside microdialysis, in 19 brain-injured patients.
  
  
  RESULTS
  Our investigations revealed an inverse linear correlation between brain glucose and both the concentration of extracellular glutamate (Pearson r=-0.58, P=0.01) and the lactate/glucose ratio (Pearson r=-0.55, P=0.01). For noncritical brain glucose levels, we observed a positive linear correlation between midazolam dose and brain glucose (P<0.05). For critical brain glucose levels, extracellular brain glucose was unaffected by any type of sedative.
  
  
  CONCLUSIONS
  These findings suggest that the use of anesthetic drugs may be of limited value in attempts to influence brain glucose metabolism in injured brain tissue.
authors.affiliation: *Department of Neurosurgery †Department of Neurobiology, Interdisciplinary Center for Neurosciences (IZN), Exzellenzcluster CellNetworks ‡The Bernstein Center for Computational Neuroscience, University of Heidelberg, Heidelberg, Germany.
authors.forename: Daniel N
authors.initials: DN
authors.lastname: Hertle
authors.forename: Edgar
authors.initials: E
authors.lastname: Santos
authors.forename: Anna M
authors.initials: AM
authors.lastname: Hagenston
authors.forename: Christine
authors.initials: C
authors.lastname: Jungk
authors.forename: Daniel
authors.initials: D
authors.lastname: Haux
authors.forename: Andreas W
authors.initials: AW
authors.lastname: Unterberg
authors.forename: Oliver W
authors.initials: OW
authors.lastname: Sakowitz
mesh_terms: D000328:Adult; D000368:Aged; D001921:Brain / Q000187:drug effects* / Q000378:metabolism*; D001930:Brain Injuries / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005947:Glucose / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D006993:Hypnotics and Sedatives / Q000494:pharmacology*; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D017551:Microdialysis / Q000379:methods*; D008874:Midazolam / Q000494:pharmacology; D008875:Middle Aged; D012189:Retrospective Studies
chemical_list: D006993:Hypnotics and Sedatives; D019344:Lactic Acid; D018698:Glutamic Acid; D005947:Glucose; D008874:Midazolam