Lack of improvement in cerebral metabolism after hyperoxia in severe head injury: A microdialysis study

Sandra Magnoni, Laura Ghisoni, Marco Locatelli, Mariangela Caimi, Angelo Colombo, Valerio Valeriani, Nino Stocchetti

Research output: Contribution to journalArticle

114 Citations (Scopus)

Abstract

Object. The authors investigated the effects of hyperoxia on brain tissue PO2 and on glucose metabolism in cerebral and adipose tissue after traumatic brain injury (TBI). Methods. After 3 hours of ventilation with pure O2, 18 tests were performed on different days in eight comatose patients with TBI. Lactate, pyruvate, glucose, glutamate, and brain tissue PO2 were measured in the cerebral extracellular fluid (ECF) by using microdialysis. Analytes were also measured in the ECF of abdominal adipose tissue. After 3 hours of increase in the fraction of inspired O2, brain tissue PO2 rose from the baseline value of 32.7 ± 18 to 122.6 ± 45.2 mm Hg (p <0.0001), whereas brain lactate dropped from its baseline (3.21 ± 2.77 mmol/L), reaching its lowest value (2.90 ± 2.58 mmol/L) after 3 hours of hyperoxia (p <0.01). Pyruvate dropped as well, from 153 ± 56 to 141 ± 56 μmol/L (p <0.05), so the lactate/pyruvate ratio did not change. No significant changes were observed in glucose and glutamate. The arteriovenous difference in O2 content dropped, although not significantly, from a baseline of 4.52 ± 1.22 to 4.15 ± 0.76 ml/100 ml. The mean concentration of lactate in adipose tissue fell significantly as well (p <0.01), but the lactate/pyruvate ratio did not change. Conclusions. Hyperoxia slightly reduced lactate levels in brain tissue after TBI. The estimated redox status of the cells, however, did not change and cerebral O2 extraction seemed to be reduced. These data indicate that oxidation of glucose was not improved by hyperoxia in cerebral and adipose tissue, and might even be impaired.

Original languageEnglish
Pages (from-to)952-958
Number of pages7
JournalJournal of Neurosurgery
Volume98
Issue number5
Publication statusPublished - May 1 2003

Fingerprint

Hyperoxia
Microdialysis
Craniocerebral Trauma
Lactic Acid
Pyruvic Acid
Brain
Adipose Tissue
Glucose
Extracellular Fluid
Glutamic Acid
Abdominal Fat
Coma
Oxidation-Reduction
Ventilation
Traumatic Brain Injury

Keywords

  • Brain metabolism
  • Head injury
  • Hyperoxia
  • Lactate
  • Microdialysis

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Lack of improvement in cerebral metabolism after hyperoxia in severe head injury : A microdialysis study. / Magnoni, Sandra; Ghisoni, Laura; Locatelli, Marco; Caimi, Mariangela; Colombo, Angelo; Valeriani, Valerio; Stocchetti, Nino.

In: Journal of Neurosurgery, Vol. 98, No. 5, 01.05.2003, p. 952-958.

Research output: Contribution to journalArticle

Magnoni, Sandra ; Ghisoni, Laura ; Locatelli, Marco ; Caimi, Mariangela ; Colombo, Angelo ; Valeriani, Valerio ; Stocchetti, Nino. / Lack of improvement in cerebral metabolism after hyperoxia in severe head injury : A microdialysis study. In: Journal of Neurosurgery. 2003 ; Vol. 98, No. 5. pp. 952-958.
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AU - Colombo, Angelo

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N2 - Object. The authors investigated the effects of hyperoxia on brain tissue PO2 and on glucose metabolism in cerebral and adipose tissue after traumatic brain injury (TBI). Methods. After 3 hours of ventilation with pure O2, 18 tests were performed on different days in eight comatose patients with TBI. Lactate, pyruvate, glucose, glutamate, and brain tissue PO2 were measured in the cerebral extracellular fluid (ECF) by using microdialysis. Analytes were also measured in the ECF of abdominal adipose tissue. After 3 hours of increase in the fraction of inspired O2, brain tissue PO2 rose from the baseline value of 32.7 ± 18 to 122.6 ± 45.2 mm Hg (p <0.0001), whereas brain lactate dropped from its baseline (3.21 ± 2.77 mmol/L), reaching its lowest value (2.90 ± 2.58 mmol/L) after 3 hours of hyperoxia (p <0.01). Pyruvate dropped as well, from 153 ± 56 to 141 ± 56 μmol/L (p <0.05), so the lactate/pyruvate ratio did not change. No significant changes were observed in glucose and glutamate. The arteriovenous difference in O2 content dropped, although not significantly, from a baseline of 4.52 ± 1.22 to 4.15 ± 0.76 ml/100 ml. The mean concentration of lactate in adipose tissue fell significantly as well (p <0.01), but the lactate/pyruvate ratio did not change. Conclusions. Hyperoxia slightly reduced lactate levels in brain tissue after TBI. The estimated redox status of the cells, however, did not change and cerebral O2 extraction seemed to be reduced. These data indicate that oxidation of glucose was not improved by hyperoxia in cerebral and adipose tissue, and might even be impaired.

AB - Object. The authors investigated the effects of hyperoxia on brain tissue PO2 and on glucose metabolism in cerebral and adipose tissue after traumatic brain injury (TBI). Methods. After 3 hours of ventilation with pure O2, 18 tests were performed on different days in eight comatose patients with TBI. Lactate, pyruvate, glucose, glutamate, and brain tissue PO2 were measured in the cerebral extracellular fluid (ECF) by using microdialysis. Analytes were also measured in the ECF of abdominal adipose tissue. After 3 hours of increase in the fraction of inspired O2, brain tissue PO2 rose from the baseline value of 32.7 ± 18 to 122.6 ± 45.2 mm Hg (p <0.0001), whereas brain lactate dropped from its baseline (3.21 ± 2.77 mmol/L), reaching its lowest value (2.90 ± 2.58 mmol/L) after 3 hours of hyperoxia (p <0.01). Pyruvate dropped as well, from 153 ± 56 to 141 ± 56 μmol/L (p <0.05), so the lactate/pyruvate ratio did not change. No significant changes were observed in glucose and glutamate. The arteriovenous difference in O2 content dropped, although not significantly, from a baseline of 4.52 ± 1.22 to 4.15 ± 0.76 ml/100 ml. The mean concentration of lactate in adipose tissue fell significantly as well (p <0.01), but the lactate/pyruvate ratio did not change. Conclusions. Hyperoxia slightly reduced lactate levels in brain tissue after TBI. The estimated redox status of the cells, however, did not change and cerebral O2 extraction seemed to be reduced. These data indicate that oxidation of glucose was not improved by hyperoxia in cerebral and adipose tissue, and might even be impaired.

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