Abstract
New Viewpoint in Exaggerated Increase of PtiO2 With Normobaric Hyperoxygenation and Reasons to Limit Oxygen Use in Neurotrauma Patients.
Highlights
Specialty section: This article was submitted to Intensive Care Medicine and Anesthesiology, a section of the journal
Multiple studies have shown that some of cerebral metabolic abnormalities occurring after traumatic brain injuries (TBI) are not of ischemic origin [1,2,3,4]
normobaric hyperoxia (NH) induces a negligible increase in the amount of arterial O2 content and DO2, whereas it is associated with an important augmentation of PtiO2, without significant change in cerebral metabolic rate of O2 consumption (CMRO2) [11,12,13,14]
Summary
The circulated hypotheses of mitochondrial dysfunction as a contributor [21] to high PtiO2 and the loss of O2 homeostatic mechanisms in the injured tissue during NH [22] requires an alternative explanation based on the conformational change of hemoglobin (Hb) quaternary structure (Max Perutz—the Nobel prize in chemistry 1962) This change produces a significant decrease in Hb–O2 affinity, considerable Hb buffering capacity augmentation, and convert the sigmoidal form of ODC to hyperbola. In this commentary, we explain the mechanisms underlying the exaggerated rise in PtiO2 with NH and consider the factors that limiting oxygen use in the damaged cerebral tissue
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