Brain lactate metabolism in humans with subarachnoid hemorrhage

Lactate is central for the regulation of brain metabolism and is an alternative substrate to glucose after injury. Brain lactate metabolism in patients with subarachnoid hemorrhage has not been fully elucidated. Thirty-one subarachnoid hemorrhage patients monitored with cerebral microdialysis (CMD)...

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Vydáno v:Stroke (1970) Ročník 43; číslo 5; s. 1418
Hlavní autoři: Oddo, Mauro, Levine, Joshua M, Frangos, Suzanne, Maloney-Wilensky, Eileen, Carrera, Emmanuel, Daniel, Roy T, Levivier, Marc, Magistretti, Pierre J, LeRoux, Peter D
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 01.05.2012
Témata:
Adult
Brain - metabolism
Female
Humans
Lactates - metabolism
Male
Middle Aged
Oxygen - metabolism
Prognosis
Retrospective Studies
Subarachnoid Hemorrhage - diagnosis
Subarachnoid Hemorrhage - metabolism
Subarachnoid Hemorrhage - mortality
Survival Rate
ISSN:1524-4628, 1524-4628
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Shrnutí:Lactate is central for the regulation of brain metabolism and is an alternative substrate to glucose after injury. Brain lactate metabolism in patients with subarachnoid hemorrhage has not been fully elucidated. Thirty-one subarachnoid hemorrhage patients monitored with cerebral microdialysis (CMD) and brain oxygen (PbtO(2)) were studied. Samples with elevated CMD lactate (>4 mmol/L) were matched to PbtO(2) and CMD pyruvate and categorized as hypoxic (PbtO(2) <20 mm Hg) versus nonhypoxic and hyperglycolytic (CMD pyruvate >119 μmol/L) versus nonhyperglycolytic. Median per patient samples with elevated CMD lactate was 54% (interquartile range, 11%-80%). Lactate elevations were more often attributable to cerebral hyperglycolysis (78%; interquartile range, 5%-98%) than brain hypoxia (11%; interquartile range, 4%-75%). Mortality was associated with increased percentage of samples with elevated lactate and brain hypoxia (28% [interquartile range 9%-95%] in nonsurvivors versus 9% [interquartile range 3%-17%] in survivors; P=0.02) and lower percentage of elevated lactate and cerebral hyperglycolysis (13% [interquartile range, 1%-87%] versus 88% [interquartile range, 27%-99%]; P=0.07). Cerebral hyperglycolytic lactate production predicted good 6-month outcome (odds ratio for modified Rankin Scale score, 0-3 1.49; CI, 1.08-2.05; P=0.016), whereas increased lactate with brain hypoxia was associated with a reduced likelihood of good outcome (OR, 0.78; CI, 0.59-1.03; P=0.08). Brain lactate is frequently elevated in subarachnoid hemorrhage patients, predominantly because of hyperglycolysis rather than hypoxia. A pattern of increased cerebral hyperglycolytic lactate was associated with good long-term recovery. Our data suggest that lactate may be used as an aerobic substrate by the injured human brain.
Bibliografie:ObjectType-Article-1
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content type line 23
ISSN:1524-4628
1524-4628
DOI:10.1161/STROKEAHA.111.648568