gms | German Medical Science

57th Annual Meeting of the German Society of Neurosurgery
Joint Meeting with the Japanese Neurosurgical Society

German Society of Neurosurgery (DGNC)

11 - 14 May, Essen

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Formation of reactive oxygen species induced by a focal mass lesion in rodents: Dependency on arterial and brain tissue oxygenation

Bildung reaktiver Sauerstoffradikale bei fokaler Hirnläsion im Rattenmodell: Einfluss der arteriellen und der Hirngewebsoxygenierung

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  • corresponding author J. Warnat - Klinik für Neurochirurgie, Universität Regensburg
  • E.-A. Stoerr - Klinik für Neurochirurgie, Universität Regensburg
  • M. Gruber - Klinik für Anästhesiologie, Universität Regensburg
  • T. Finkenzeller - Klinik für Radiologie, Universität Regensburg
  • A. Brawanski - Klinik für Neurochirurgie, Universität Regensburg
  • R. Burger - Klinik für Neurochirurgie, Universität Göttingen

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 57. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie. Essen, 11.-14.05.2006. Düsseldorf, Köln: German Medical Science; 2006. DocP 03.38

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2006/06dgnc255.shtml

Published: May 8, 2006

© 2006 Warnat et al.
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Objective: The effect of normobaric arterial hyperoxia on the formation of reactive oxygen species and protein oxidation was studied during and after induction of an extraaxial mass lesion in rodents.

Methods: Intracranial pressure (ICP), brain tissue partial oxygen pressure [p(ti)O2], electroencephalography (EEG) and microdialysis-based estimation of reactive oxygen species (ROS) by the salicylate trapping method [reaction of hydroxyl radicals with salicylate forming 2,3 - and 2,5 - dihydroxy benzoic acid (DHBA)] was monitored in sham-operated animals (n=9, 298±32g) and in animals with an epidural mass lesion. After baseline measurement (60 min), epidural brain compression was initiated with a balloon device as long as EEG was isoelectric, followed by prolonged balloon inflation (60 min), rapid deflation and reperfusion (120 min). Formation of ROS was compared between animals with arterial normoxia (n=11, 284±29g, paO2 ~ 100 mmHg) and intraischemically induced normobaric arterial hyperoxia (n=9, 282±20g, paO2 ~ 250mmHg). Results were correlated with brain tissue pO2. The tissue in the area of the microdialysis probe was prepared and the extent of protein oxidation was detected by western blot analysis (OxyBlot).

Results: After epidural mass lesion the level of 2,3 - dihydroxy benzoic acid was increased by factor 1,55±0,37 (p<0.001) under normoxic conditions and by factor 1,55±0,61 (p<0.001) with arterial hyperoxia. Throughout reperfusion the level of 2,3 - DHBA was still increased by the 1,54±1,9 fold (p<0,05) in the normoxic and by the 1,49±0,66 fold (p<0,05) in the hyperoxic group. Under normoxic conditions the p(ti)O2 decreased from 19,5±3,2 mmHg to 8,2±3,1 mm Hg while with hyperoxia the p(ti)O2 remained almost stable at 16,0±2,7 mmHg. During reperfusion p(ti)O2 normalized to 20,8±3,8 mmHg (normoxic group) and to 19,8±2,8 mmHg (hyperoxic group). Protein oxidation in the putative penumbra region was increased by factor 1,28±5,07 (normoxia, p<0,001) and by 1,89±16,92 (hyperoxia, p<0,001). Core temperature, CPP and paCO2 remained stable in sham-operated and lesioned animals over time course.

Conclusions: In this model the epidural mass lesion promotes the formation of ROS in the penumbra region during brain compression and reperfusion significantly. Intraischemic arterial hyperoxia does not lead to further ROS formation but significantly increases the extent of protein oxidation.