Lactate and excitatory amino acids measured by microdialysis are decreased by pentobarbital coma in head-injured patients.

Primary traumatic brain injury and secondary ischemic/hypoxic injury are being increasingly characterized at the neurochemical level. Neurochemical monitoring using microdialysis has shown that these forms of tissue damage share many common features. In particular, anaerobic glycolysis with increased lactate production and release of excitatory amino acids into the extracellular space are seen in both conditions. Clinical microdialysis studies have heretofore focused on methodological issues, establishment of basal analyte values, and clinico-neurochemical correlation. Here we report the neurochemical consequences of therapeutic intervention in head injury. Specifically, induction of thiopental coma to manage severe increased intracranial pressure in seven patients was associated with a 37% reduction of lactate, 59% reduction of glutamate, and 66% reduction in aspartate in the extracellular space of the brain.