gms | German Medical Science

60th Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Benelux countries and Bulgaria

German Society of Neurosurgery (DGNC)

24 - 27 May 2009, Münster

Reduced vasospasm in S100A9 knock-out mice after experimental SAH

Meeting Abstract

  • B. Fischer - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster
  • O. Penz - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster
  • H. Hüsken - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster
  • W. Nacken - Institut für Immunologie, Universitätsklinikum Münster
  • H. Wassmann - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocDI.03-03

doi: 10.3205/09dgnc120, urn:nbn:de:0183-09dgnc1200

Published: May 20, 2009

© 2009 Fischer et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Objective: Vasospasms after intracranial aneurysmatic haemorrhage occur in up to 70% of patients surviving the initial bleeding. In up to 50% of them, vasospasms end in severe neurological deficits or death. Inflammatory reactions due to the subarachnoid blood seem to be the cause of vasospasm. S100A9, a calcium binding protein expressed from neutrophils and macrophages is a key protein in the acute phase of inflammatory reactions for adhesion of inflammatory cells to endothelial cells and transmigration. Aim of this study was to determine if S100A9 is one of the main mediators in pathogenesis of cerebral vasospasm after experimental subarachnoid haemorrhage (SAH). This study was performed in wild-type (n = 10) as well as in S100A9 knock-out mice (n = 10).

Methods: Experimental SAH was performed by injection of autologous blood, taken form the femoral artery (0.08 ml) or saline (0.08 ml) in sham surgery, into the cisterna magna. The injection was repeated within 24 hours. Body temperature, pulse rate and blood gases were recorded before, during and after injection. The neurological deficits were scored every day. 4 days after last blood injection, animals were killed by perfusion fixation with a mixture of gelatine and ink. After fixation of the brain with 10% formalin (pH 7.4 at 37°C) the diameters of the cerebral arteries were measured at defined locations (basilar, medial and anterior cerebral artery).

Results: In all mice breathing rate decreases dramatically immediately after blood or saline injection with spontaneous recovery. Mice showed a loss of body weight in the first two days after injection (10 %). Mortality of the animals was nearly 30 %. The neurological score of the S100A9 knock-out mice was 2 points better then the controls (10%). The diameter of the cerebral arteries in mean was 10 % larger in S100A9 knock-out mice compared with wild-type mice.

Conclusions: S100A9 knock-out mice had a better neurological outcome maybe due to reduced inflammatory reaction after experimental SAH. These results suggest that S100A9 is one of the key protein mediating inflammation and vasospasm after SAH. Further experimental data are necessary to verify theses data.