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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- 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.