Microdialysate concentration changes do not provide sufficient information to evaluate metabolic effects of lactate supplementation in brain-injured patients
(2016) In Journal of Cerebral Blood Flow and Metabolism 36(11). p.1844-1864- Abstract
Cerebral microdialysis is a widely used clinical tool for monitoring extracellular concentrations of selected metabolites after brain injury and to guide neurocritical care. Extracellular glucose levels and lactate/pyruvate ratios have high diagnostic value because they can detect hypoglycemia and deficits in oxidative metabolism, respectively. In addition, patterns of metabolite concentrations can distinguish between ischemia and mitochondrial dysfunction, and are helpful to choose and evaluate therapy. Increased intracranial pressure can be life-threatening after brain injury, and hypertonic solutions are commonly used for pressure reduction. Recent reports have advocated use of hypertonic sodium lactate, based on claims that it is... (More)
Cerebral microdialysis is a widely used clinical tool for monitoring extracellular concentrations of selected metabolites after brain injury and to guide neurocritical care. Extracellular glucose levels and lactate/pyruvate ratios have high diagnostic value because they can detect hypoglycemia and deficits in oxidative metabolism, respectively. In addition, patterns of metabolite concentrations can distinguish between ischemia and mitochondrial dysfunction, and are helpful to choose and evaluate therapy. Increased intracranial pressure can be life-threatening after brain injury, and hypertonic solutions are commonly used for pressure reduction. Recent reports have advocated use of hypertonic sodium lactate, based on claims that it is glucose sparing and provides an oxidative fuel for injured brain. However, changes in extracellular concentrations in microdialysate are not evidence that a rise in extracellular glucose level is beneficial or that lactate is metabolized and improves neuroenergetics. The increase in glucose concentration may reflect inhibition of glycolysis, glycogenolysis, and pentose phosphate shunt pathway fluxes by lactate flooding in patients with mitochondrial dysfunction. In such cases, lactate will not be metabolizable and lactate flooding may be harmful. More rigorous approaches are required to evaluate metabolic and physiological effects of administration of hypertonic sodium lactate to brain-injured patients.
(Less)
- author
- Dienel, Gerald A. ; Rothman, Douglas L. and Nordström, Carl Henrik LU
- organization
- publishing date
- 2016-11-01
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- brain metabolism, Cerebral microdialysis, glucose, lactate supplementation, traumatic brain injury
- in
- Journal of Cerebral Blood Flow and Metabolism
- volume
- 36
- issue
- 11
- pages
- 21 pages
- publisher
- Nature Publishing Group
- external identifiers
-
- pmid:27604313
- wos:000387263300002
- scopus:84994160290
- ISSN
- 0271-678X
- DOI
- 10.1177/0271678X16666552
- language
- English
- LU publication?
- yes
- id
- 7d0f9ce1-a91f-4f60-a92a-22a135b1340a
- date added to LUP
- 2016-11-21 12:21:41
- date last changed
- 2024-04-19 12:59:02
@article{7d0f9ce1-a91f-4f60-a92a-22a135b1340a,
abstract = {{<p>Cerebral microdialysis is a widely used clinical tool for monitoring extracellular concentrations of selected metabolites after brain injury and to guide neurocritical care. Extracellular glucose levels and lactate/pyruvate ratios have high diagnostic value because they can detect hypoglycemia and deficits in oxidative metabolism, respectively. In addition, patterns of metabolite concentrations can distinguish between ischemia and mitochondrial dysfunction, and are helpful to choose and evaluate therapy. Increased intracranial pressure can be life-threatening after brain injury, and hypertonic solutions are commonly used for pressure reduction. Recent reports have advocated use of hypertonic sodium lactate, based on claims that it is glucose sparing and provides an oxidative fuel for injured brain. However, changes in extracellular concentrations in microdialysate are not evidence that a rise in extracellular glucose level is beneficial or that lactate is metabolized and improves neuroenergetics. The increase in glucose concentration may reflect inhibition of glycolysis, glycogenolysis, and pentose phosphate shunt pathway fluxes by lactate flooding in patients with mitochondrial dysfunction. In such cases, lactate will not be metabolizable and lactate flooding may be harmful. More rigorous approaches are required to evaluate metabolic and physiological effects of administration of hypertonic sodium lactate to brain-injured patients.</p>}},
author = {{Dienel, Gerald A. and Rothman, Douglas L. and Nordström, Carl Henrik}},
issn = {{0271-678X}},
keywords = {{brain metabolism; Cerebral microdialysis; glucose; lactate supplementation; traumatic brain injury}},
language = {{eng}},
month = {{11}},
number = {{11}},
pages = {{1844--1864}},
publisher = {{Nature Publishing Group}},
series = {{Journal of Cerebral Blood Flow and Metabolism}},
title = {{Microdialysate concentration changes do not provide sufficient information to evaluate metabolic effects of lactate supplementation in brain-injured patients}},
url = {{http://dx.doi.org/10.1177/0271678X16666552}},
doi = {{10.1177/0271678X16666552}},
volume = {{36}},
year = {{2016}},
}