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Brain metabolism is significantly impaired at blood glucose below 6 mM and brain glucose below 1 mM in patients with severe traumatic brain injury.

Meierhans R, Béchir M, Ludwig S, Sommerfeld J, Brandi G, Haberthür C, Stocker R, Stover JF - Crit Care (2010)

Bottom Line: Occult metabolic alterations were determined by calculating the lactate- pyruvate (L/P), lactate- glucose (L/Glc), and lactate- glutamate (L/Glu) ratios.Arterial blood glucose levels appear to be optimal at 6-9 mM.Pathogenity of elevated glutamate appears to be relativized by L/Glu and suggests to exclude insulin- induced brain injury.

View Article: PubMed Central - HTML - PubMed

Affiliation: Surgical Intensive Care, University Hospital Zürich, Rämistrasse 100, 8091 Zürich, Switzerland. roman.meierhans@usz.ch.

ABSTRACT

Introduction: The optimal blood glucose target following severe traumatic brain injury (TBI) must be defined. Cerebral microdialysis was used to investigate the influence of arterial blood and brain glucose on cerebral glucose, lactate, pyruvate, glutamate, and calculated indices of downstream metabolism.

Methods: In twenty TBI patients, microdialysis catheters inserted in the edematous frontal lobe were dialyzed at 1 microl/min, collecting samples at 60 minute intervals. Occult metabolic alterations were determined by calculating the lactate- pyruvate (L/P), lactate- glucose (L/Glc), and lactate- glutamate (L/Glu) ratios.

Results: Brain glucose was influenced by arterial blood glucose. Elevated L/P and L/Glc were significantly reduced at brain glucose above 1 mM, reaching lowest values at blood and brain glucose levels between 6-9 mM (P < 0.001). Lowest cerebral glutamate was measured at brain glucose 3-5 mM with a significant increase at brain glucose below 3 mM and above 6 mM. While L/Glu was significantly increased at low brain glucose levels, it was significantly decreased at brain glucose above 5 mM (P < 0.001). Insulin administration increased brain glutamate at low brain glucose, but prevented increase in L/Glu.

Conclusions: Arterial blood glucose levels appear to be optimal at 6-9 mM. While low brain glucose levels below 1 mM are detrimental, elevated brain glucose are to be targeted despite increased brain glutamate at brain glucose >5 mM. Pathogenity of elevated glutamate appears to be relativized by L/Glu and suggests to exclude insulin- induced brain injury.

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Changes in brain glutamate (grey box plots) and calculated brain lactate-to-glutamate (white box plots) ratio determined by microdialysis reflecting influence of brain glucose on downstream cerebral metabolism in pre-defined brain glucose clusters, ranging from less than 1 mM to more than 9 mM in 1 mM buckets. At brain glucose levels exceeding 5 mM brain glutamate was significantly increased. In parallel lactate-to-glutamate was significantly decreased. Changes across the pre-defined brain glucose clusters compared with low brain glucose levels were significant (*P < 0.001; analysis of variance on ranks, post hoc Dunn's test).
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Figure 5: Changes in brain glutamate (grey box plots) and calculated brain lactate-to-glutamate (white box plots) ratio determined by microdialysis reflecting influence of brain glucose on downstream cerebral metabolism in pre-defined brain glucose clusters, ranging from less than 1 mM to more than 9 mM in 1 mM buckets. At brain glucose levels exceeding 5 mM brain glutamate was significantly increased. In parallel lactate-to-glutamate was significantly decreased. Changes across the pre-defined brain glucose clusters compared with low brain glucose levels were significant (*P < 0.001; analysis of variance on ranks, post hoc Dunn's test).

Mentions: Brain glucose levels exceeding 5 mM was associated with a significant increase in cerebral glutamate concentrations and in parallel with a significant decrease in calculated L/Glu ratio (P < 0.001, ANOVA on ranks, post hoc Dunn's test; Figure 5).


Brain metabolism is significantly impaired at blood glucose below 6 mM and brain glucose below 1 mM in patients with severe traumatic brain injury.

Meierhans R, Béchir M, Ludwig S, Sommerfeld J, Brandi G, Haberthür C, Stocker R, Stover JF - Crit Care (2010)

Changes in brain glutamate (grey box plots) and calculated brain lactate-to-glutamate (white box plots) ratio determined by microdialysis reflecting influence of brain glucose on downstream cerebral metabolism in pre-defined brain glucose clusters, ranging from less than 1 mM to more than 9 mM in 1 mM buckets. At brain glucose levels exceeding 5 mM brain glutamate was significantly increased. In parallel lactate-to-glutamate was significantly decreased. Changes across the pre-defined brain glucose clusters compared with low brain glucose levels were significant (*P < 0.001; analysis of variance on ranks, post hoc Dunn's test).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2875528&req=5

Figure 5: Changes in brain glutamate (grey box plots) and calculated brain lactate-to-glutamate (white box plots) ratio determined by microdialysis reflecting influence of brain glucose on downstream cerebral metabolism in pre-defined brain glucose clusters, ranging from less than 1 mM to more than 9 mM in 1 mM buckets. At brain glucose levels exceeding 5 mM brain glutamate was significantly increased. In parallel lactate-to-glutamate was significantly decreased. Changes across the pre-defined brain glucose clusters compared with low brain glucose levels were significant (*P < 0.001; analysis of variance on ranks, post hoc Dunn's test).
Mentions: Brain glucose levels exceeding 5 mM was associated with a significant increase in cerebral glutamate concentrations and in parallel with a significant decrease in calculated L/Glu ratio (P < 0.001, ANOVA on ranks, post hoc Dunn's test; Figure 5).

Bottom Line: Occult metabolic alterations were determined by calculating the lactate- pyruvate (L/P), lactate- glucose (L/Glc), and lactate- glutamate (L/Glu) ratios.Arterial blood glucose levels appear to be optimal at 6-9 mM.Pathogenity of elevated glutamate appears to be relativized by L/Glu and suggests to exclude insulin- induced brain injury.

View Article: PubMed Central - HTML - PubMed

Affiliation: Surgical Intensive Care, University Hospital Zürich, Rämistrasse 100, 8091 Zürich, Switzerland. roman.meierhans@usz.ch.

ABSTRACT

Introduction: The optimal blood glucose target following severe traumatic brain injury (TBI) must be defined. Cerebral microdialysis was used to investigate the influence of arterial blood and brain glucose on cerebral glucose, lactate, pyruvate, glutamate, and calculated indices of downstream metabolism.

Methods: In twenty TBI patients, microdialysis catheters inserted in the edematous frontal lobe were dialyzed at 1 microl/min, collecting samples at 60 minute intervals. Occult metabolic alterations were determined by calculating the lactate- pyruvate (L/P), lactate- glucose (L/Glc), and lactate- glutamate (L/Glu) ratios.

Results: Brain glucose was influenced by arterial blood glucose. Elevated L/P and L/Glc were significantly reduced at brain glucose above 1 mM, reaching lowest values at blood and brain glucose levels between 6-9 mM (P < 0.001). Lowest cerebral glutamate was measured at brain glucose 3-5 mM with a significant increase at brain glucose below 3 mM and above 6 mM. While L/Glu was significantly increased at low brain glucose levels, it was significantly decreased at brain glucose above 5 mM (P < 0.001). Insulin administration increased brain glutamate at low brain glucose, but prevented increase in L/Glu.

Conclusions: Arterial blood glucose levels appear to be optimal at 6-9 mM. While low brain glucose levels below 1 mM are detrimental, elevated brain glucose are to be targeted despite increased brain glutamate at brain glucose >5 mM. Pathogenity of elevated glutamate appears to be relativized by L/Glu and suggests to exclude insulin- induced brain injury.

Show MeSH
Related in: MedlinePlus