title: Lactate and the injured brain: friend or foe?
abstract: OBJECTIVE
  Energy metabolism is increasingly recognized as a key factor in the pathogenesis of acute brain injury (ABI). We review the role of cerebral lactate metabolism and summarize evidence showing that lactate may act as supplemental fuel after ABI.
  
  
  RESULTS
  The role of cerebral lactate has shifted from a waste product to a potentially preferential fuel and signaling molecule. According to the astrocyte-neuron lactate shuttle model, glycolytic lactate might act as glucose-sparing substrate. Lactate also is emerging as a key signal to regulate cerebral blood flow (CBF) and a neuroprotective agent after experimental ABI. Clinical investigation using cerebral microdialysis shows the existence of two main lactate patterns, ischemic - from anaerobic metabolism - and nonischemic, from activated glycolysis, whereby lactate can be used as supplemental energy fuel. Preliminary clinical data suggests hypertonic lactate solutions improve cerebral energy metabolism and are an effective treatment for elevated intracranial pressure (ICP) after ABI.
  
  
  CONCLUSIONS
  Lactate can be a supplemental fuel for the injured brain and is important to regulate glucose metabolism and CBF. Exogenous lactate supplementation may be neuroprotective after experimental ABI. Recent clinical data from ABI patients suggest hypertonic lactate solutions may be a valid therapeutic option for secondary energy dysfunction and elevated ICP.
authors.affiliation: aNeuroscience Critical Care Research Group, Department of Intensive Care Medicine, Faculty of Biology and Medicine, Centre Hospitalier Universitaire Vaudois (CHUV), University Hospital, Lausanne, Switzerland bJoseph Fourier University, Grenoble, France.
authors.forename: Pierre
authors.initials: P
authors.lastname: Bouzat
authors.forename: Mauro
authors.initials: M
authors.lastname: Oddo
mesh_terms: D001930:Brain Injuries / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy; D002540:Cerebral Cortex / Q000378:metabolism* / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D004734:Energy Metabolism; D005260:Female; D006019:Glycolysis; D006801:Humans; D006982:Hypertonic Solutions / Q000627:therapeutic use; D000860:Hypoxia / Q000378:metabolism* / Q000503:physiopathology; D019586:Intracranial Hypertension / Q000628:therapy*; D019344:Lactic Acid / Q000378:metabolism* / Q000627:therapeutic use*; D008297:Male; D018696:Neuroprotective Agents / Q000627:therapeutic use*
chemical_list: D006982:Hypertonic Solutions; D018696:Neuroprotective Agents; D019344:Lactic Acid