Improvement of oxygen supply by an artificial carrier in combination with normobaric oxygenation decreases the volume of tissue hypoxia and tissue damage from transient focal cerebral ischemia

David J. Seiffge, Natalia E. Lapina, Charalambos Tsagogiorgas, Bastian Theisinger, Robert H. Henning, Lothar Schilling*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

15 Citations (Scopus)

Abstract

Tissue hypoxia may play an important role in the development of ischemic brain damage. In the present study we investigated in a rat model of transient focal brain ischemia the neuroprotective effects of increasing the blood oxygen transport capacity by applying a semifluorinated alkane (SFA)-containing emulsion together with normobaric hyperoxygenation (NBO). The spread of tissue hypoxia was studied using pimonidazole given prior to filament-induced middle cerebral artery occlusion (MCAO, 2 h). Treatment consisted of intravenous injection of saline or the SFA-containing emulsion (0.5 or 1.0 ml/100 g body weight; [SFA(0.5) or SFA(1.0)]) either upon establishing MCAO (early treatment) or after filament removal (delayed treatment). After injection NBO was administered for 8 h (early treatment) or 6 h (delayed treatment). Experiments were terminated 8 or 24 h after MCAO. In serial brain sections tissue hypoxia and irreversible cell damage were quantitatively determined. Furthermore, we studied hypoxia-related gene expression (VEGF, flt-1). Early treatment significantly (p

Original languageEnglish
Pages (from-to)18-25
Number of pages8
JournalExperimental Neurology
Volume237
Issue number1
DOIs
Publication statusPublished - Sept-2012

Keywords

  • Artificial oxygen carrier
  • Focal brain ischemia
  • Normobaric hyperoxygenation
  • Rat
  • Tissue hypoxia
  • ARTERY OCCLUSION
  • RAT-BRAIN
  • PERFLUOROCARBON EMULSIONS
  • HYPERBARIC OXYGENATION
  • REPERFUSION
  • EXPRESSION
  • MODEL
  • PERFUSION
  • THERAPY
  • FLUOSOL

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