gms | German Medical Science

67th Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Korean Neurosurgical Society (KNS)

German Society of Neurosurgery (DGNC)

12 - 15 June 2016, Frankfurt am Main

Xenon reduces neuronal hippocampal damage and alters the pattern of microglial activation after experimental subarachnoid hemorrhage

Meeting Abstract

  • Michael Veldeman - Neurochirurgische Klinik, Universitätsklinikum der RWTH Aachen, Germany; Klinik für Anästhesiologie, Universitätsklinikum der RWTH Aachen, Germany
  • Mark Coburn - Klinik für Anästhesiologie, Universitätsklinikum der RWTH Aachen, Germany
  • Rolf Rossaint - Klinik für Anästhesiologie, Universitätsklinikum der RWTH Aachen, Germany
  • Hans Clusmann - Neurochirurgische Klinik, Universitätsklinikum der RWTH Aachen, Germany
  • Anke Höllig - Neurochirurgische Klinik, Universitätsklinikum der RWTH Aachen, Germany

Deutsche Gesellschaft für Neurochirurgie. 67. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 1. Joint Meeting mit der Koreanischen Gesellschaft für Neurochirurgie (KNS). Frankfurt am Main, 12.-15.06.2016. Düsseldorf: German Medical Science GMS Publishing House; 2016. DocDI.02.08

doi: 10.3205/16dgnc098, urn:nbn:de:0183-16dgnc0983

Published: June 8, 2016

© 2016 Veldeman et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at



Objective: The neuroprotective properties of the noble gas xenon have already been demonstrated using different injury models. Here, we examine xenon' possible neuroprotective effect as well as its influence on posthemorrhagic microglial neuroinflammation in an in vivo rat model of subarachnoid hemorrhage (SAH).

Method: Sprague Dawley rats (n=22) were randomly assigned to receive either Sham surgery (n=9) or SAH induction via endovascular perforation (n=13). Of those randomized for SAH, 7 animals were post-operatively ventilated with 50 vol% oxygen/50 vol% xenon for one hour and 6 received 50 vol% oxygen/50 vol% nitrogen (control). Of each animal 2 coronal sections (-3.60 and +1.0 mm from bregma) were selected for assessment of histological damage 24 h after SAH. A 5-point neurohistopathological severity score was applied to assess neuronal cell damage in H&E and NeuN stained sections in a total of 4 predefined anatomical regions of interest. Microglial neuroinflammation was evaluated by a software assisted cell count of Iba-1 stained slices in 3 cortical regions of interest.

Results: A diffuse cellular damage was apparent in all regions of the ipsilateral hippocampus 24 h after SAH. Xenon treated animals presented with a milder damage after SAH. This effect was found to be particularly pronounced in the medial regions of the hippocampus, CA3 (p=0.040) and DG (p=0.040). However, for the CA1 and CA2 regions no statistical difference in neuronal damage according to our histological scoring (p=0.428; p=0.071). A microglial cell count was significantly lower in the right hemisphere (p=0.032) of the xenon group when comparing the summed scores of all 3 cortical regions to the control group. This difference was especially apparent in the right piriform cortex (p=0.009). Left side microglial activation did not differ significantly between treatment groups (p=0.428).

Conclusions: Postconditioning with 50 vol% xenon for one hour after SAH resulted in a decrease of ipsilateral neuronal hippocampal damage (CA3, DG), when compared to the control group. We presume an immunomodulatory effect of xenon mediating this protective effect and a bilateral and more global protection could become apparent in a larger trial. As for now, these results cannot be generalized as only some hippocampal regions are affected. Future studies should assess the time and localization dependency of xenon´s beneficial properties after SAH.