gms | German Medical Science

62nd Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Polish Society of Neurosurgeons (PNCH)

German Society of Neurosurgery (DGNC)

7 - 11 May 2011, Hamburg

The role of SAH intensity and endothelin-1 increases in aneurysmal symptomatic cerebral vasospasm

Meeting Abstract

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  • S. Hendryk - Department of Neurosurgery, Medical University of Silesia in Katowice, Poland
  • P. Bażowski - Department of Neurosurgery, Medical University of Silesia in Katowice, Poland

Deutsche Gesellschaft für Neurochirurgie. Polnische Gesellschaft für Neurochirurgen. 62. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Polnischen Gesellschaft für Neurochirurgen (PNCH). Hamburg, 07.-11.05.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. DocP 050

doi: 10.3205/11dgnc271, urn:nbn:de:0183-11dgnc2719

Published: April 28, 2011

© 2011 Hendryk 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: The development of symptomatic cerebral vasospasm and brain ischemia (DIND) after SAH may be explained by a mechanism involving the vasospasmatic and proinflammatory effects of endothelin-1 (ET-1). This concept is supported by the rule that symptomatic cerebral vasospasm occurs more frequently in patients with more intensive SAH. The aim of this study was to estimate the potential role of SAH intensity and changes in ET-1 plasma concentrations in symptomatic vasospasm as well as their mutual time correlations occurring in SAH.

Methods: The connection between hemorrhage intensity, symptomatic cerebral vasospasm and brain ischemia was prospectively evaluated in a group of 331 patients treated surgically due to aneurysmal SAH. Out of 88 patients who underwent aneurysm clipping this year within 72 hours of SAH, 34 were selected for the assessment of changes in ET-1 concentration. ET-1 plasma levels were measured with the use of the RIA method and commercially available kits in patients with symptomatic cerebral vasospasm and without vasospasm and DIND.

Results: The results of the study confirmed a close correlation between symptomatic cerebral vasospasm and SAH intensity. The significant increase in ET-1 plasma concentration was associated with acute, subacute and delayed cerebral symptomatic aneurysmal vasospasm and DIND (2.5; 2.2; 2.5 pg/ml respectively). A significant ET-1 concentration increase in cerebral vasospasm was more likely to occur when SAH was more intensive.

Conclusions: Our results confirm the significant role of ET-1 in the development of cerebral symptomatic vasospasm and brain ischemia after aneurysmal SAH. ET-1 increases are related to SAH intensity.