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 language | English |
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Pages (from-to) | 18-25 |
Number of pages | 8 |
Journal | Experimental Neurology |
Volume | 237 |
Issue number | 1 |
DOIs | |
Publication status | Published - 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