Cerebral oxygen vasoreactivity and cerebral tissue oxygen reactivity†

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Presentation transcript:

Cerebral oxygen vasoreactivity and cerebral tissue oxygen reactivity† A.J. Johnston, L.A. Steiner, A.K. Gupta, D.K. Menon British Journal of Anaesthesia Volume 90, Issue 6, Pages 774-786 (June 2003) DOI: 10.1093/bja/aeg104 Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

Fig 1 The influence of arterial oxygen content (CaO2) and arterial partial pressure of oxygen (PaO2) on cerebral blood flow (CBF). Below PaO2 ∼7 kPa (53 mm Hg), CBF increases. Within a normal physiological range of PaO2 there is little change in CBF (shaded box). Adapted with permission.43 British Journal of Anaesthesia 2003 90, 774-786DOI: (10.1093/bja/aeg104) Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

Fig 2 Non-linear curve-fitting regression model between cerebral blood flow (CBF) on 35% inspired oxygen (FIO2) and the percentage decrease in CBF on 60% oxygen in a sequential double CBF study in six patients with severe traumatic brain injury. (a) CBF changes in a region of interest in the right frontal lobe that appeared to be normal on CT scan. (b) Global CBF changes. Adapted with permission.58 British Journal of Anaesthesia 2003 90, 774-786DOI: (10.1093/bja/aeg104) Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

Fig 3 Two hypothetical models of the relationships between brain tissue oxygen (PbO2) and arterial oxygen content (CaO2) (solid line) and between PbO2 and arterial partial pressure of oxygen (PaO2) (dashed line). Hyperoxia (PaO2 >15 kPa) is indicated by the shaded area; within this region the relationship does not fit either model but falls between the two (see text). Note the non-linear CaO2 axis. *There are very little data to support either model under hypoxic conditions. British Journal of Anaesthesia 2003 90, 774-786DOI: (10.1093/bja/aeg104) Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

Fig 4 Neurotrend printout showing pH, carbon dioxide and brain tissue oxygen in response to changes in inspired oxygen (FIO2) in a head-injured patient. A, FIO2 0.25 (start of monitoring); B, FIO2 0.5; C, FIO2 0.73; D, FIO2 0.98. All other physiological variables were stable during the study. British Journal of Anaesthesia 2003 90, 774-786DOI: (10.1093/bja/aeg104) Copyright © 2003 British Journal of Anaesthesia Terms and Conditions

Fig 5 Many physiologically relevant genes are activated during conditions of hypoxia, including those encoding erythropoietin, vascular endothelial growth factor, inducible nitric oxide synthase and glycolytic enzymes. At the transcriptional level these diverse genes are all under the control of a crucial transcription factor: hypoxia-inducible factor 1 (HIF-1). HIF-1 is a heterodimeric protein complex composed of an α and β subunit. During normoxia, HIF-1α is rapidly degraded by the ubiquitin proteasome system, whereas exposure to hypoxic conditions prevents its degradation. This oxygen-dependent instability may provide a means by which gene expression is controlled during changes in oxygen tension. British Journal of Anaesthesia 2003 90, 774-786DOI: (10.1093/bja/aeg104) Copyright © 2003 British Journal of Anaesthesia Terms and Conditions