Cerebral metabolic effects of exogenous lactate supplementation on the injured human brain

Pierre Bouzat, Nathalie Sala, Tamarah Suys, Jean Baptiste Zerlauth, Pedro Marques-Vidal, François Feihl, Jocelyne Bloch, Mahmoud Messerer, Marc Levivier, Reto Meuli, Pierre J. Magistretti, Mauro Oddo*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

137 Scopus citations


Purpose: Experimental evidence suggests that lactate is neuroprotective after acute brain injury; however, data in humans are lacking. We examined whether exogenous lactate supplementation improves cerebral energy metabolism in humans with traumatic brain injury (TBI). Methods: We prospectively studied 15 consecutive patients with severe TBI monitored with cerebral microdialysis (CMD), brain tissue PO2 (PbtO2), and intracranial pressure (ICP). Intervention consisted of a 3-h intravenous infusion of hypertonic sodium lactate (aiming to increase systemic lactate to ca. 5 mmol/L), administered in the early phase following TBI. We examined the effect of sodium lactate on neurochemistry (CMD lactate, pyruvate, glucose, and glutamate), PbtO2, and ICP. Results: Treatment was started on average 33 ± 16 h after TBI. A mixed-effects multilevel regression model revealed that sodium lactate therapy was associated with a significant increase in CMD concentrations of lactate [coefficient 0.47 mmol/L, 95 % confidence interval (CI) 0.31-0.63 mmol/L], pyruvate [13.1 (8.78-17.4) μmol/L], and glucose [0.1 (0.04-0.16) mmol/L; all p < 0.01]. A concomitant reduction of CMD glutamate [-0.95 (-1.94 to 0.06) mmol/L, p = 0.06] and ICP [-0.86 (-1.47 to -0.24) mmHg, p < 0.01] was also observed. Conclusions: Exogenous supplemental lactate can be utilized aerobically as a preferential energy substrate by the injured human brain, with sparing of cerebral glucose. Increased availability of cerebral extracellular pyruvate and glucose, coupled with a reduction of brain glutamate and ICP, suggests that hypertonic lactate therapy has beneficial cerebral metabolic and hemodynamic effects after TBI.

Original languageEnglish (US)
Pages (from-to)412-421
Number of pages10
JournalIntensive Care Medicine
Issue number3
StatePublished - Mar 2014

Bibliographical note

Funding Information:
Acknowledgments The authors thank Béatrice Pellet, from the Division of Pharmacy, for the preparation of sodium lactate, as well as all neurosurgical fellows, ICU physicians, and ICU nurses for their help and support. This work was supported by grants from the Swiss National Science Foundation (Grant Nr. 320030_138191, to M.O.), the European Critical Care Research Network, European Society of Intensive Care Medicine (to M.O.), and the Gueules Cassées Foundation (to P.B.). This work received the best abstract award at the European Society of Intensive Care Medicine congress in Paris, 2013.


  • Brain metabolism
  • Cerebral microdialysis
  • Hypertonic
  • Lactate
  • Traumatic brain injury

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine


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