Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2025 Aug 21;29(1):377.
doi: 10.1186/s13054-025-05618-x.

Hyperoxia and acute brain injury

Sylvain Diop  1   2   3 , Maxime Aparicio  4   5 , Hatem Kallel  4   6   7 , Roman Mounier  4   8   9
Affiliations
Comment

Hyperoxia and acute brain injury

Sylvain Diop et al. Crit Care. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

Declarations. Ethics approval and consent to participate: Not applicable. SysiPh group members: Roman Mounier, Sylvain Diop, Maxime Aparicio, Ariane Roujansky, Hatem Kallel. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
O2 journey: from the airways to the mitochondria. Figure 1 represents a schematic representation of the concentration of free O2 molecules during their journey from the atmosphere to the cells in a healthy subject. Airway’s cells are directly exposed to O2 molecules whose partial pressure varies linearly with the fraction of inspired O2. Then O2 molecules diffuse into the capillaries blood where they are loaded by hemoglobin. In standard condition of pressure and temperature, the solubility of O2 in blood is very low limiting the concentration of free O2 in whole blood. Then in tissue’s capillaries, O2 diffuse into the cells depending on their metabolic activities and O2 consumption’s rate. Thus, the concentration of O2 in blood decreases, allowing the release of O2 by hemoglobin according to the metabolic demand and local factors (such as pH through the Bohr’s effect). All the purpose of the blood carrier system is to ensure sufficient O2 supply, while limiting its toxicity. One can easily see that except from the airways, other parts of the body, especially the cells are not exposed to high O2 concentration and that hyperoxemia is not a surrogate for hyperoxia. In hyperbaric condition, the dissolved O2 in blood is dramatically increased so it will diffuse to the cells and increased cellular O2 concentration beyond their needs although arteriolar vasoconstriction tends to limit it until a threshold. ATM=atmosphere; PaO2= Arterial blood O2 partial pressure; PAO2= Alveolar O2 partial pressure formula image; O2= Dioxygen; CaO2=arterial content in O2 (formula image where SaO2 is the arterial blood O2 saturation).
See this image and copyright information in PMC

Comment on

References

    1. Romero-Garcia Nekane, Robba C, Monleón B, Ruiz-Zarco A, Pascual-González M, Ruiz-Pacheco A, et al. Neurological outcomes and mortality following hyperoxemia in adult patients with acute brain injury: an updated meta-analysis and meta-regression. Crit Care. 2025;29(1): 167. - PMC - PubMed
    1. Singer M, Young PJ, Laffey JG, et al. Dangers of hyperoxia. Crit Care. 2021;25:440. - PMC - PubMed
    1. Magder S. Reactive oxygen species: toxic molecules or spark of life? Crit Care. 2006;10:208. - PMC - PubMed
    1. Wolbarsht ML, Fridovich I. Hyperoxia during reperfusion is a factor in reperfusion injury. Free Radic Biol Med. 1989;6(1):61–2. - PubMed
    1. Turrens JF. Mitochondrial formation of reactive oxygen species. J Physiol. 2003;552:335–44. - PMC - PubMed

LinkOut - more resources