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

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.