Thiopental and midazolam do not seem to impede metabolism of glutamate in brain-injured patients

increased extracellular glutamate levels are related to glial and neuronal damage. Glutamate-mediated toxicity is limited by glial uptake and metaboli c transformation of glutamate to glutamine and the energetic compounds alan ine and lactate which are utilized by surrounding neurons. Under in vitro c onditions, 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, th e barbiturate thiopental reduces important detoxification of glutamate, res ulting in lower CSF glutamine, alanine and lactate levels as opposed to pat ients receiving midazolam, During long-term administration of thiopental an d 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 sug gest that long-term administration of thiopental and midazolam under clinic al conditions does not impede enzymatic activities responsible for detoxifi cation and metabolism of glutamate.