title: Lactate administration attenuates cognitive deficits following traumatic brain injury.
abstract: Moderately head injured patients often suffer long term neurological sequelae. There is no therapy for brain trauma and current treatments aim only to minimize secondary damage. These secondary effects are often triggered by the inability to re-establish ionic homeostasis after injury, due to large energy demands. Recent reports have demonstrated that neurons are capable of utilizing lactate as an energy source, thus this report examines the usefulness of lactate administration in the attenuation of behavioural deficits following a moderate brain injury. Lactate infusion (i.v.) was started 30 min after lateral fluid percussion injury and continued for 3 h. Cognitive deficits were determined using the Morris water maze. Lactate infused injured animals demonstrated significantly less cognitive deficits than saline infused injured animals. Thus, lactate infusion attenuated the cognitive deficits normally observed in this model, and therefore may provide moderately head injured patients with a treatment to help ameliorate the sequelae.
authors.affiliation: Departments of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0631, USA. acrice@hsc.vcu.edu
authors.forename: Ann C
authors.initials: AC
authors.lastname: Rice
authors.forename: Robert
authors.initials: R
authors.lastname: Zsoldos
authors.forename: Tao
authors.initials: T
authors.lastname: Chen
authors.forename: Margaret S
authors.initials: MS
authors.lastname: Wilson
authors.forename: B
authors.initials: B
authors.lastname: Alessandri
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Hamm
authors.forename: M Ross
authors.initials: MR
authors.lastname: Bullock
mesh_terms: D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects / Q000502:physiology; D001930:Brain Injuries / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D003072:Cognition Disorders / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D019344:Lactic Acid / Q000378:metabolism / Q000494:pharmacology*; D008297:Male; D018782:Maze Learning / Q000187:drug effects* / Q000502:physiology; D009410:Nerve Degeneration / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000378:metabolism / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D018696:Neuroprotective Agents; D019344:Lactic Acid