• Daniel N Hertle, Edgar Santos, Anna M Hagenston, Christine Jungk, Daniel Haux, Andreas W Unterberg, and Oliver W Sakowitz.
• *Department of Neurosurgery †Department of Neurobiology, Interdisciplinary Center for Neurosciences (IZN), Exzellenzcluster CellNetworks ‡The Bernstein Center for Computational Neuroscience, University of Heidelberg, Heidelberg, Germany.
• J Neurosurg Anesthesiol. 2015 Jul 1;27(3):187-93.

BackgroundDisturbed 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.MethodsWe performed an explorative, retrospective analysis of anesthetic drug administration and brain glucose concentrations, obtained by bedside microdialysis, in 19 brain-injured patients.ResultOur 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.ConclusionsThese findings suggest that the use of anesthetic drugs may be of limited value in attempts to influence brain glucose metabolism in injured brain tissue.

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