000191016 001__ 191016
000191016 005__ 20181228151108.0
000191016 0247_ $$2doi$$a10.1038/jcbfm.2013.142
000191016 022__ $$a0271-678X
000191016 02470 $$2ISI$$a000326559300019
000191016 037__ $$aARTICLE
000191016 245__ $$aCerebral extracellular lactate increase is predominantly nonischemic in patients with severe traumatic brain injury
000191016 260__ $$bNature Publishing Group$$c2013$$aNew York
000191016 269__ $$a2013
000191016 300__ $$a8
000191016 336__ $$aJournal Articles
000191016 520__ $$aGrowing evidence suggests that endogenous lactate is an important substrate for neurons. This study aimed to examine cerebral lactate metabolism and its relationship with brain perfusion in patients with severe traumatic brain injury (TBI). A prospective cohort of 24 patients with severe TBI monitored with cerebral microdialysis (CMD) and brain tissue oxygen tension (PbtO(2)) was studied. Brain lactate metabolism was assessed by quantification of elevated CMD lactate samples (>4 mmol/L); these were matched to CMD pyruvate and PbtO(2) values and dichotomized as glycolytic (CMD pyruvate >119 mu mol/L vs. low pyruvate) and hypoxic (PbtO(2) <20 mm Hg vs. nonhypoxic). Using perfusion computed tomography (CT), brain perfusion was categorized as oligemic, normal, or hyperemic, and was compared with CMD and PbtO(2) data. Samples with elevated CMD lactate were frequently observed (41 +/- 8%), and we found that brain lactate elevations were predominantly associated with glycolysis and normal PbtO(2) (73 8%) rather than brain hypoxia (14 +/- 6%). Furthermore, glycolytic lactate was always associated with normal or hyperemic brain perfusion, whereas all episodes with hypoxic lactate were associated with diffuse oligemia. Our findings suggest predominant nonischemic cerebral extracellular lactate release after TBI and support the concept that lactate may be used as an energy substrate by the injured human brain.
000191016 6531_ $$acerebral blood flow
000191016 6531_ $$acerebral metabolism
000191016 6531_ $$acerebral microdialysis
000191016 6531_ $$alactate
000191016 6531_ $$atraumatic brain injury
000191016 700__ $$uCHUV Lausanne Univ Hosp, Neurosci Crit Care Res Unit, Dept Intens Care Med, CH-1011 Lausanne, Switzerland$$aSala, Nathalie
000191016 700__ $$uCHUV Lausanne Univ Hosp, Neurosci Crit Care Res Unit, Dept Intens Care Med, CH-1011 Lausanne, Switzerland$$aSuys, Tamarah
000191016 700__ $$uCHUV Lausanne Univ Hosp, Dept Radiol, CH-1011 Lausanne, Switzerland$$aZerlauth, Jean-Baptiste
000191016 700__ $$uCHUV Lausanne Univ Hosp, Neurosci Crit Care Res Unit, Dept Intens Care Med, CH-1011 Lausanne, Switzerland$$aBouzat, Pierre
000191016 700__ $$uCHUV Lausanne Univ Hosp, Serv Neurosurg, Dept Clin Neurosci, CH-1011 Lausanne, Switzerland$$aMesserer, Mahmoud
000191016 700__ $$uCHUV Lausanne Univ Hosp, Serv Neurosurg, Dept Clin Neurosci, CH-1011 Lausanne, Switzerland$$aBloch, Jocelyne
000191016 700__ $$uCHUV Lausanne Univ Hosp, Serv Neurosurg, Dept Clin Neurosci, CH-1011 Lausanne, Switzerland$$aLevivier, Marc
000191016 700__ $$0243698$$g134990$$uEcole Polytech Fed Lausanne, Brain Mind Inst, Lab Neuroenerget & Cellular Dynam, CH-1015 Lausanne, Switzerland$$aMagistretti, Pierre J.
000191016 700__ $$uCHUV Lausanne Univ Hosp, Dept Radiol, CH-1011 Lausanne, Switzerland$$aMeuli, Reto
000191016 700__ $$aOddo, Mauro$$uCHUV Lausanne Univ Hosp, Neurosci Crit Care Res Unit, Dept Intens Care Med, CH-1011 Lausanne, Switzerland
000191016 773__ $$j33$$tJournal Of Cerebral Blood Flow And Metabolism$$k11$$q1815-1822
000191016 909C0 $$xU11150$$0252265$$pLNDC
000191016 909CO $$qSV$$particle$$ooai:infoscience.tind.io:191016
000191016 917Z8 $$x219572
000191016 937__ $$aEPFL-ARTICLE-191016
000191016 973__ $$rREVIEWED$$sPUBLISHED$$aEPFL
000191016 980__ $$aARTICLE