gms | German Medical Science

58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. bis 29.04.2007, Leipzig

Influence of intraischemic versus postischemic induced normobaric hyperoxia on neurobehavioral deficits in a focal mass lesion in rodents

Einfluss einer intraischämisch versus postischämisch induzierten normobaren Hyperoxie auf das Outcome nach fokaler zerebraler Hirnläsion

Meeting Abstract

Suche in Medline nach

  • corresponding author R. Burger - Neurochirurgische Klinik, Georg-August Universität, Göttingen
  • A. Müller - Neurochirurgische Klinik, Georg-August Universität, Göttingen
  • N. Uzma - Neurochirurgische Klinik, Georg-August Universität, Göttingen
  • V. Rohde - Neurochirurgische Klinik, Georg-August Universität, Göttingen

Deutsche Gesellschaft für Neurochirurgie. 58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC). Leipzig, 26.-29.04.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. DocFR.03.07

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2007/07dgnc081.shtml

Veröffentlicht: 11. April 2007

© 2007 Burger et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: The effects of intra – versus postischemic arterial normobaric hyperoxia on a 2-week assessment of behavorial deficits were evaluated in a focal mass lesion model in rodents.

Methods: 58 Spraque Dawley rats were included in the study. Baseline measurement of ptiO2 and EEG was followed by induction of an epidural focal mass lesion. The endpoint of balloon inflation was defined by flattening of the EEG. Brain compression was prolonged over 60 min and followed by reperfusion (~60 min). Neurobehavior was assessed over 15 days by postural reflex (PR); open field (OF); beam balance (BB); beam walking (BW); Morris water maze (MWM). Study groups with arterial normoxia (paO2 ~100mmHg, n=25), intraischemic (n=13) and post-ischemic (n=8) arterial, normobaric hyperoxia (paO2 ~220mmHg) were compared to a sham group (n=12). The lesion was histologically evaluated by morphometric analysis.

Results: Sham-operated animals showed a normal EEG pattern, regular ptiO2 values and neurobehavior over time. All injured animals showed a significant worsening of EEG compared to the sham operated group (p<0.05), however no differences were found between treatment groups (p>0.05). PtiO2 increased to normal values under intraischemic and postischemic normobaric hyperoxia (p<0.05) while normoxic animals showed lower ptiO2 values. Neurobehavioral testing of injured animals showed a significant worsening (BB p<0.05, BW p<0.05, PR p<0.05, MWM p<0.05) compared to sham operated animals. Neurobehavioral deficits of animals treated with postischemic arterial hyperoxia were statistically not improved (BB, OF, BW, PR and WMT) compared to animals with intraischemic hyperoxia or normoxia, The histology showed no statistically significant difference in lesion size between injured study groups.

Conclusions: Induction of arterial hyperoxia increases oxygen delivery but did not improve outcome or structural damages.