gms | German Medical Science

61st Annual Meeting of the German Society of Neurosurgery (DGNC) as part of the Neurowoche 2010
Joint Meeting with the Brazilian Society of Neurosurgery on the 20 September 2010

German Society of Neurosurgery (DGNC)

21 - 25 September 2010, Mannheim

Neuroprotective effects of argon in an in vivo model of ischemic stroke in the rat

Meeting Abstract

  • Yu-Mi Ryang - Neurochirurgische Klinik, Klinikum rechts der Isar, Technische Universität München, Deutschland; Neurochirurgische Klinik, Universitätsklinikum, Rheinisch-Westfälische Technische Hochschule Aachen, Deutschland
  • Jens Gempt - Neurochirurgische Klinik, Klinikum rechts der Isar, Technische Universität München, Deutschland
  • Astrid Fahlenkamp - Klinik für Anästhesiologie, Universitätsklinikum, Rheinisch-Westfälische Technische Hochschule Aachen, Deutschland
  • Rolf Rossaint - Klinik für Anästhesiologie, Universitätsklinikum, Rheinisch-Westfälische Technische Hochschule Aachen, Deutschland
  • Mark Coburn - Klinik für Anästhesiologie, Universitätsklinikum, Rheinisch-Westfälische Technische Hochschule Aachen, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 61. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC) im Rahmen der Neurowoche 2010. Mannheim, 21.-25.09.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. DocP1842

doi: 10.3205/10dgnc313, urn:nbn:de:0183-10dgnc3137

Published: September 16, 2010

© 2010 Ryang et al.
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Outline

Text

Objective: Argon (Ar) like xenon is a noble gas which excerpts no hypnotic effects under normobaric conditions. Numerous studies showed neuroprotection by xenon in ischemic stroke and brain trauma, but only scarce reports on neuroprotective effects of argon exist. Whereas ubiquitary use of xenon is impossible due to its scarceness and cost-intensity argon is substantially less expensive and could be a feasible alternative to xenon.

Methods: 22 adult male SD rats (250–295 g) underwent 2 h-transient middle cerebral artery occlusion (tMCAO) by use of the endoluminal thread model. Animals were randomized to a control group (n=11) which received 50% N2/50% O2 and an argon group (n=11) which received 50% Ar/50% O2 by mask ventilation 1 hour after tMCAO induction for 1 hour. 24 hours post-reperfusion mortality and neuroscores (modified Bederson score (MBS)) were assessed and animals sacrificed. Rat brains were TTC stained (2, 3, 5-triphenyltetrazolium chloride) and infarct volumes were evaluated.

Results: Edema corrected total infarct volumes showed a significant 15% reduction in mean total stroke volume in argon treated (mean±SD, controls 323 mm3 ±25; Ar 276 ±41; p=0.004) compared to control animals. Neurological deficits (MBS 0 worst, 5 best) were significantly more pronounced in the control group (n=1 MBS 2, n=10 MBS 0) compared to the argon group (n=4 MBS 2, n=2 MBS 1, n=5 MBS 0) (p=0.034). Mortality was also higher in the control group (5/11) compared to the argon group (2/11). These results however were not significant (p=0.3).

Conclusions: Argon seems to have neuroprotective effects in an experimental stroke model of the rat. A significant reduction in infarct volumes and a significantly improved outcome could be achieved in the argon group compared to controls. Even though not significant, the mortality rate was also in favour of the argon treated animals.