Brain Protection after Anoxic Brain Injury: Is Lactate Supplementation Helpful?

Filippo Annoni, Lorenzo Peluso, Elisa Gouvêa Bogossian, Jacques Creteur, Elisa R Zanier, Fabio Silvio Taccone

Research output: Contribution to journalReview articlepeer-review


While sudden loss of perfusion is responsible for ischemia, failure to supply the required amount of oxygen to the tissues is defined as hypoxia. Among several pathological conditions that can impair brain perfusion and oxygenation, cardiocirculatory arrest is characterized by a complete loss of perfusion to the brain, determining a whole brain ischemic-anoxic injury. Differently from other threatening situations of reduced cerebral perfusion, i.e., caused by increased intracranial pressure or circulatory shock, resuscitated patients after a cardiac arrest experience a sudden restoration of cerebral blood flow and are exposed to a massive reperfusion injury, which could significantly alter cellular metabolism. Current evidence suggests that cell populations in the central nervous system might use alternative metabolic pathways to glucose and that neurons may rely on a lactate-centered metabolism. Indeed, lactate does not require adenosine triphosphate (ATP) to be oxidated and it could therefore serve as an alternative substrate in condition of depleted energy reserves, i.e., reperfusion injury, even in presence of adequate tissue oxygen delivery. Lactate enriched solutions were studied in recent years in healthy subjects, acute heart failure, and severe traumatic brain injured patients, showing possible benefits that extend beyond the role as alternative energetic substrates. In this manuscript, we addressed some key aspects of the cellular metabolic derangements occurring after cerebral ischemia-reperfusion injury and examined the possible rationale for the administration of lactate enriched solutions in resuscitated patients after cardiac arrest.

Original languageEnglish
Pages (from-to)1714
Issue number7
Publication statusPublished - Jul 6 2021


  • Acidosis/etiology
  • Animals
  • Brain Injuries, Traumatic/etiology
  • Cell Death/drug effects
  • Cerebrovascular Circulation/drug effects
  • Energy Metabolism/drug effects
  • Heart Arrest/complications
  • Humans
  • Hypertonic Solutions
  • Hypoxia-Ischemia, Brain/etiology
  • Lactic Acid/therapeutic use
  • Neurons/drug effects
  • Neuroprotective Agents/therapeutic use
  • Oxidative Stress/drug effects
  • Reperfusion Injury/etiology
  • Resuscitation/methods


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