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

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

In: Intensive Care Medicine, 2014, vol. 40, no. 3, p. 412-421

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    Titel
    • Cerebral metabolic effects of exogenous lactate supplementation on the injured human brain
    Autor
    • Bouzat, Pierre. Department of Intensive Care Medicine, Neuroscience Critical Care Research Group, Faculty of Biology and Medicine, University Hospital of Lausanne, Rue du Bugnon 46, 1011, Lausanne, Switzerland
    • Sala, Nathalie. Department of Intensive Care Medicine, Neuroscience Critical Care Research Group, Faculty of Biology and Medicine, University Hospital of Lausanne, Rue du Bugnon 46, 1011, Lausanne, Switzerland
    • Suys, Tamarah. Department of Intensive Care Medicine, Neuroscience Critical Care Research Group, Faculty of Biology and Medicine, University Hospital of Lausanne, Rue du Bugnon 46, 1011, Lausanne, Switzerland
    • Zerlauth, Jean-Baptiste. Department of Radiology, Faculty of Biology and Medicine, University Hospital of Lausanne, 1011, Lausanne, Switzerland
    • Marques-Vidal, Pedro. Faculty of Biology and Medicine, Institute of Social and Preventive Medicine, University Hospital of Lausanne, 1011, Lausanne, Switzerland
    • Feihl, François. Division of Clinical Pathophysiology, Department of Internal Medicine, Faculty of Biology and Medicine, University Hospital of Lausanne, 1011, Lausanne, Switzerland
    • Bloch, Jocelyne. Division of Neurosurgery, Department of Clinical Neurosciences, Faculty of Biology and Medicine, University Hospital of Lausanne, 1011, Lausanne, Switzerland
    • Messerer, Mahmoud. Division of Neurosurgery, Department of Clinical Neurosciences, Faculty of Biology and Medicine, University Hospital of Lausanne, 1011, Lausanne, Switzerland
    • Levivier, Marc. Division of Neurosurgery, Department of Clinical Neurosciences, Faculty of Biology and Medicine, University Hospital of Lausanne, 1011, Lausanne, Switzerland
    • Meuli, Reto. Department of Radiology, Faculty of Biology and Medicine, University Hospital of Lausanne, 1011, Lausanne, Switzerland
    • Magistretti, Pierre. Laboratory of Neuroenergetics and Cellular Dynamics, Faculty of Biology and Medicine, Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Centre de Neurosciences Psychiatriques, University Hospital of Lausanne, 1011, Lausanne, Switzerland
    • Oddo, Mauro. Department of Intensive Care Medicine, Neuroscience Critical Care Research Group, Faculty of Biology and Medicine, University Hospital of Lausanne, Rue du Bugnon 46, 1011, Lausanne, Switzerland
    Dokumententyp
    • Postprint
    Sprache
    • Englisch
    Veröffentlicht in
    • Intensive Care Medicine, 2014, vol. 40, no. 3, p. 412-421. Springer Berlin Heidelberg
    Andere elektronische Ausgabe
    OAI-PMH-ID
    • oai:doc.rero.ch:324811
    Summary
    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. 5mmol/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±16h 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 0.47mmol/L, 95% confidence interval (CI) 0.31-0.63mmol/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.