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

• Verfasst von: Seiffge, David [VerfasserIn]
• Verfasst von: Lapina, Natalia [VerfasserIn]
• Verfasst von: Tsagogiorgas, Charalambos [VerfasserIn]
• Verfasst von: Schilling, Lothar [VerfasserIn]
• Titel: 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
• Verf.angabe: David J. Seiffge, Natalia E. Lapina, Charalambos Tsagogiorgas, Bastian Theisinger, Robert H. Henning, Lothar Schilling
• Jahr: 2012
• Umfang: 8 S.
• Fussnoten: Available online 21 June 2012 ; Gesehen am 29.06.2018
• Titel Quelle: Enthalten in: Experimental neurology
• Ort Quelle: Amsterdam [u.a.] : Elsevier, 1959
• Jahr Quelle: 2012
• Band/Heft Quelle: 237(2012), 1, Seite 18-25
• ISSN Quelle: 1090-2430
• DOI: doi:10.1016/j.expneurol.2012.06.007
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Artificial oxygen carrier
• Sach-SW: Focal brain ischemia
• Sach-SW: Normobaric hyperoxygenation
• Sach-SW: Rat
• Sach-SW: Tissue hypoxia
• K10plus-PPN: 1577048784

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, 2h). Treatment consisted of intravenous injection of saline or the SFA-containing emulsion (0.5 or 1.0ml/100g body weight; [SFA0.5 or SFA1.0]) either upon establishing MCAO (early treatment) or after filament removal (delayed treatment). After injection NBO was administered for 8h (early treatment) or 6h (delayed treatment). Experiments were terminated 8 or 24h 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<0.05) reduced the volumes of tissue damage (8h after MCAO: SFA1.0, 57±34mm³; controls, 217±70mm³; 24h after MCAO: SFA1.0, 189±82mm³; controls, 317±60mm³) and of P-Add immunoreactivity (8h after MCAO: SFA1.0, 261±37mm³; controls, 339±26mm³; 24h after MCAO: SFA1.0, 274±47mm³; controls, 364±46mm³). Delayed treatment was comparably successful. The volume of the hypoxic penumbra was not decreased by the treatment. Similarly, VEGF and flt-1 mRNA levels did not differ between the experimental groups. From these data we conclude that increasing the blood oxygen transport capacity in the plasma compartment provides a neuroprotective effect by alleviating the severity of hypoxia to a level sufficient to prevent cells from transition into irreversible damage.