Hyperbaric oxygen induces rapid protection against focal cerebral ischemia

Roland Veltkamp*, Dirk A. Siebing, Sabine Heiland, Philip Schoenffeldt-Varas, Claudia Veltkamp, Markus Schwaninger, Stefan Schwab

*Corresponding author for this work
56 Citations (Scopus)


Background and purpose. The timing and mechanisms of protection by hyperbaric oxygen (HBO) in cerebral ischemia have only been partially elucidated. We monitored the early in vivo effects of HBO after 2 h transient focal ischemia using repetitive MRI. Methods. Wistar rats underwent filament occlusion of the middle cerebral artery (MCAO). 40 min after MCAO, rats were placed in a HBO chamber and breathed either 100% O2 at 3.0 atmospheres absolute (ata; n = 24) or at 1.0 ata (control; n = 24) for 1 h. Diffusion, perfusion and T2-weighted MR-images were obtained after 15 min and 3, 6 and 24 h of reperfusion. In 6 axial MR slices, volume of abnormal diffusion and T2w signals were measured in the ischemic hemisphere. Furthermore, hemispheric mean apparent diffusion coefficient- (ADC) and T2 values were calculated for statistical analysis. Results. HBO significantly reduced volume of abnormal DWI signal beginning immediately after reperfusion (control: 92 ± 28 mm3; HBO: 64 ± 17) and lesion size on T2w (control: 375 ± 91 mm3; HBO: 225 ± 39) after 24 h. Correspondingly, mean ADC levels were lower and T2 values higher in the ischemic hemisphere in the control group. HBO reduced histological infarct size at 24 h. Conclusion. High-dose intraischemic HBO therapy has an immediate protective on the brain which is superior to normobaric oxygen.

Original languageEnglish
JournalBrain Research
Issue number1-2
Pages (from-to)134-138
Number of pages5
Publication statusPublished - 10.03.2005

Research Areas and Centers

  • Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)


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