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

Neuroprotective effects of Argon ventilation in a rat model of subarachnoid hemorrhage

Meeting Abstract

  • Naureen Keric - Neurochirurgische Klinik und Poliklinik, Universitätsmedizin Mainz, Mainz, Germany
  • Dominik Wesp - Neurochirurgische Klinik und Poliklinik, Universitätsmedizin Mainz, Mainz, Germany
  • Julia Masomi - Neurochirurgische Klinik und Poliklinik, Universitätsmedizin Mainz, Mainz, Germany
  • Anika Korinek - Neurochirurgische Klinik und Poliklinik, Universitätsmedizin Mainz, Mainz, Germany
  • Axel Heimann - Institut für Neurochirurgische Pathophysiologie, Universitätsmedizin Mainz, Mainz, Germany
  • Clemens Sommer - Institut für Neuropathologie, Universitätsmedizin Mainz, Mainz, 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.02.10

doi: 10.3205/16dgnc100, urn:nbn:de:0183-16dgnc1008

Published: June 8, 2016

© 2016 Keric 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: Subarachnoid hemorrhage (SAH) is still a life threatening disease. Vasospasm resulting in hypoperfusion and ischemia leads to secondary brain injury. Modern diagnostic procedures and therapeutic strategies led to better outcome, nevertheless new neuroprotective approaches are highly sought after. Recently neuroprotective effects of noble gases like Xenon and Argon have been shown in animal models of ischemia. We investigated the effects of Argon in a SAH rat model.

Method: 24 male Wistar rats were operated and randomized in 3 groups. 2 groups had a SAH induction, using an endovascular perforation model. Group A received 2 hours of ventilation by 50% Argon/50% O2 via a face mask immediately following SAH. Group B underwent a sham operation (n=8), and was also ventilated by Argon/O2. Group C received a SAH but no further treatment (n=8). Bilateral Laser Doppler Flow monitoring, arterial blood pressure and body temperature were measured continuously throughout the experiments. Rats were sacrificed and perfused with PFA 24-72 h following SAH. Pre- and postoperatively neurological and behavioral testing was performed. Histology and immunohistochemistry were used to evaluate the extent of brain injury and vasospasm.

Results: Laser Doppler Flow decreased immediately at the time of SAH induction and recovered in groups A and C equally during 30 minutes following SAH, while it remained unchanged in the sham group. However in the groups A and C arterial blood pressure decreased when opening of carotid artery, rose significantly at onset of SAH and decreased again after 1-2 minutes. Post-interventional neurological score showed no significant difference among group A and B. Group C showed a tendency of a deteriorated neurological score. Rats with large hematomas showed a more impaired gait and a higher mortality rate compared to the mild SAH's (16% vs. 53%). Histology and immunohistochemistry revealed lower amount of secondary brain injury in the Argon ventilated SAH group. Vasospasm was found in the basal arteries of both SAH groups.

Conclusions: In the present study immunohistochemistry demonstrated a decrease of secondary brain injury in the Argon ventilated group compared to the control group. No clear impact of Argon was found on the extent of vasospasm. Argon seems to have a neuroprotective potential in the experimental SAH. The concentration of the noble gas and the duration of treatment need to be further investigated to optimize the treatment.