Exposure to 16 h of normobaric hypoxia induces ionic edema in the healthy brain

• Verfasst von: Biller, Armin [VerfasserIn]
• Verfasst von: Badde, Stephanie [VerfasserIn]
• Verfasst von: Heckel, Andreas [VerfasserIn]
• Verfasst von: Guericke, Philipp [VerfasserIn]
• Verfasst von: Bendszus, Martin [VerfasserIn]
• Verfasst von: Nagel, Armin Michael [VerfasserIn]
• Verfasst von: Heiland, Sabine [VerfasserIn]
• Verfasst von: Mairbäurl, Heimo [VerfasserIn]
• Verfasst von: Bärtsch, Peter [VerfasserIn]
• Verfasst von: Schommer, Kai [VerfasserIn]
• Titel: Exposure to 16 h of normobaric hypoxia induces ionic edema in the healthy brain
• Verf.angabe: Armin Biller, Stephanie Badde, Andreas Heckel, Philipp Guericke, Martin Bendszus, Armin M. Nagel, Sabine Heiland, Heimo Mairbäurl, Peter Bärtsch & Kai Schommer
• E-Jahr: 2021
• Jahr: 13 October 2021
• Umfang: 12 S.
• Fussnoten: Gesehen am 09.02.2022
• Titel Quelle: Enthalten in: Nature Communications
• Ort Quelle: [London] : Nature Publishing Group UK, 2010
• Jahr Quelle: 2021
• Band/Heft Quelle: 12(2021), Artikel-ID 5987, Seite 1-12
• ISSN Quelle: 2041-1723
• DOI: doi:10.1038/s41467-021-26116-y
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Blood-brain barrier
• Sach-SW: Translational research
• Sach-SW: White matter injury
• K10plus-PPN: 1789102340
• K10plus-PPN:
  Universitätsbibliothek
• Lokale URL UB: Zum Volltext

Abstract

Following prolonged exposure to hypoxic conditions, for example, due to ascent to high altitude, stroke, or traumatic brain injury, cerebral edema can develop. The exact nature and genesis of hypoxia-induced edema in healthy individuals remain unresolved. We examined the effects of prolonged, normobaric hypoxia, induced by 16 h of exposure to simulated high altitude, on healthy brains using proton, dynamic contrast enhanced, and sodium MRI. This dual approach allowed us to directly measure key factors in the development of hypoxia-induced brain edema: (1) Sodium signals as a surrogate of the distribution of electrolytes within the cerebral tissue and (2) Ktrans as a marker of blood-brain-barrier integrity. The measurements point toward an accumulation of sodium ions in extra- but not in intracellular space in combination with an intact endothelium. Both findings in combination are indicative of ionic extracellular edema, a subtype of cerebral edema that was only recently specified as an intermittent, yet distinct stage between cytotoxic and vasogenic edemas. In sum, here a combination of imaging techniques demonstrates the development of ionic edemas following prolonged normobaric hypoxia in agreement with cascadic models of edema formation.