Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Observational Study
. 2013 Nov;33(11):1815-22.
doi: 10.1038/jcbfm.2013.142. Epub 2013 Aug 21.

Cerebral extracellular lactate increase is predominantly nonischemic in patients with severe traumatic brain injury

Nathalie Sala  1 , Tamarah Suys, Jean-Baptiste Zerlauth, Pierre Bouzat, Mahmoud Messerer, Jocelyne Bloch, Marc Levivier, Pierre J Magistretti, Reto Meuli, Mauro Oddo
Affiliations
Observational Study

Cerebral extracellular lactate increase is predominantly nonischemic in patients with severe traumatic brain injury

Nathalie Sala et al. J Cereb Blood Flow Metab. 2013 Nov.

Abstract

Growing 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 (PbtO2) was studied. Brain lactate metabolism was assessed by quantification of elevated CMD lactate samples (>4 mmol/L); these were matched to CMD pyruvate and PbtO2 values and dichotomized as glycolytic (CMD pyruvate >119 μmol/L vs. low pyruvate) and hypoxic (PbtO2 <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 PbtO2 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 PbtO2 (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.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Schematic illustration to show the position and shape of the region of interests (ROIs) on perfusion computed tomography (CT), in relation to the brain anatomy. The left side of the panel shows how ROIs were selected for the measurement of cerebral blood flow in predominant white matter tissue on a contrast-enhanced CT. The right side of the panel is a three-dimensional representation of ROIs in relation to the brain anatomy.
Figure 2
Figure 2
Cerebral lactate metabolic patterns in patients with traumatic brain injury (TBI) during the total duration of monitoring. Histograms represent individual cerebral metabolic lactate patterns (hypoxic vs. glycolytic) during the entire monitoring duration (average 5 days; n=24 patients). Hypoxic lactate=cerebral microdialysis (CMD) lactate >4 mmol/L with PbtO2 <20 mm Hg; glycolytic lactate=CMD lactate >4 mmol/L with pyruvate >119 μmol/L. Data are mean±s.e.m.
Figure 3
Figure 3
Cerebral lactate metabolic patterns in patients with traumatic brain injury (TBI) over the first 5 days of monitoring. Histograms represent individual cerebral metabolic lactate patterns (hypoxic vs. glycolytic) during the first 5 days after TBI. Hypoxic lactate=cerebral microdialysis (CMD) lactate >4 mmol/L with PbtO2 <20 mm Hg; glycolytic lactate=CMD lactate >4 mmol/L with pyruvate >119 μmol/L. Data are mean±s.e.m.
Figure 4
Figure 4
The relationship between regional cerebral lactate metabolic patterns and global brain perfusion. Illustrative examples of the relationship between brain perfusion (measured by perfusion computed tomography (CT)) and cerebral lactate metabolism, showing cerebral glycolytic lactate with normal (A) or supranormal (B) brain perfusion vs. cerebral hypoxic lactate and oligemic brain perfusion (C). Frame 1, unenhanced brain CT showing placement of intracranial monitoring; Frames 2, 3, and 4: perfusion CT maps depicting cerebral blood flow (CBF) (mL/100 g/min), cerebral blood volume (CBV) (mL/100 g), and mean transit time (MTT) (s), respectively.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Pellerin L, Magistretti PJ. Glutamate uptake into astrocytes stimulates aerobic glycolysis—a mechanism coupling neuronal activity to glucose utilization. Proc Natl Acad Sci USA. 1994;91:10625–10629. - PMC - PubMed
    1. Pellerin L, Pellegri G, Bittar PG, Charnay Y, Bouras C, Martin JL, et al. Evidence supporting the existence of an activity-dependent astrocyte–neuron lactate shuttle. Dev Neurosci. 1998;20:291–299. - PubMed
    1. Schurr A, Miller JJ, Payne RS, Rigor BM. An increase in lactate output by brain tissue serves to meet the energy needs of glutamate-activated neurons. J Neurosci. 1999;19:34–39. - PMC - PubMed
    1. Bouzier-Sore AK, Voisin P, Canioni P, Magistretti PJ, Pellerin L. Lactate is a preferential oxidative energy substrate over glucose for neurons in culture. J Cereb Blood Flow Metab. 2003;23:1298–1306. - PubMed
    1. Schurr A, Payne RS, Miller JJ, Rigor BM. Brain lactate, not glucose, fuels the recovery of synaptic function from hypoxia upon reoxygenation—an in vitro study. Brain Res. 1997;744:105–111. - PubMed

Publication types

MeSH terms