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@ARTICLE{Biller:177041,
      author       = {A. Biller and S. Badde and A. Heckel and P. Guericke and M.
                      Bendszus and A. Nagel$^*$ and S. Heiland and H. Mairbäurl
                      and P. Bärtsch and K. Schommer},
      title        = {{E}xposure to 16 h of normobaric hypoxia induces ionic
                      edema in the healthy brain.},
      journal      = {Nature Communications},
      volume       = {12},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2021-02269},
      pages        = {5987},
      year         = {2021},
      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.},
      cin          = {E020},
      ddc          = {500},
      cid          = {I:(DE-He78)E020-20160331},
      pnm          = {315 - Bildgebung und Radioonkologie (POF4-315)},
      pid          = {G:(DE-HGF)POF4-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34645793},
      doi          = {10.1038/s41467-021-26116-y},
      url          = {https://inrepo02.dkfz.de/record/177041},
}