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 language | English |
|---|---|
| Pages (from-to) | 952-958 |
| Number of pages | 7 |
| Journal | Journal of Neurosurgery |
| Volume | 98 |
| Issue number | 5 |
| Publication status | Published - May 1 2003 |
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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 journal › Article
}
TY - JOUR
T1 - Lack of improvement in cerebral metabolism after hyperoxia in severe head injury
T2 - A microdialysis study
AU - Magnoni, Sandra
AU - Ghisoni, Laura
AU - Locatelli, Marco
AU - Caimi, Mariangela
AU - Colombo, Angelo
AU - Valeriani, Valerio
AU - Stocchetti, Nino
PY - 2003/5/1
Y1 - 2003/5/1
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.
KW - Brain metabolism
KW - Head injury
KW - Hyperoxia
KW - Lactate
KW - Microdialysis
UR - http://www.scopus.com/inward/record.url?scp=0344837722&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0344837722&partnerID=8YFLogxK
M3 - Article
C2 - 12744353
AN - SCOPUS:0344837722
VL - 98
SP - 952
EP - 958
JO - Journal of Neurosurgery
JF - Journal of Neurosurgery
SN - 0022-3085
IS - 5
ER -