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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

Roles of ADMA and endothelin-1 in cerebral vasospasm after subarachnoid hemorrhage

Meeting Abstract

  • Carla S. Jung - Abteilung für Neurochirurgie, Universitätsklinikum Heidelberg, Deutschland
  • Bettina Lange - Neurochirurgische Klinik, Universitätsklinikum Frankfurt/Main, Deutschland
  • Klaus Zweckberger - Abteilung für Neurochirurgie, Universitätsklinikum Heidelberg, Deutschland
  • Daniel Haux - Abteilung für Neurochirurgie, Universitätsklinikum Heidelberg, Deutschland
  • Volker Seifert - Neurochirurgische Klinik, Universitätsklinikum Frankfurt/Main, Deutschland
  • Andreas W. Unterberg - Abteilung für Neurochirurgie, Universitätsklinikum Heidelberg, 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. DocP1838

DOI: 10.3205/10dgnc309, URN: urn:nbn:de:0183-10dgnc3091

Published: September 16, 2010

© 2010 Jung et al.
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Outline

Text

Objective: Delayed cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) leading to delayed ischemic neurological deficits, may be evoked by a disturbance in vasomotor equilibrium, to which two major physiologically antagonistic compounds nitric oxide (NO) and ET-1 may contribute. Increased CSF levels of ADMA have been associated with the course and degree of cerebral vasospasm in a primate model and in patients after SAH. We sought to determine, if alterations of ADMA and ET-1 levels are associated with cerebral vasospasm and/or ischemic lesions after SAH.

Methods: Levels of ADMA and ET-1 were determined in CSF from 35 patients after SAH. Cerebral arteriograms were performed to detect vasospasm and CT-scans to verify ischemic brain lesions. Results: CSF ADMA levels were correlated with the development of vasospasm (p<0.01) and increased only in patients with vasospasm (p<0.01). ET-1 CSF levels remained unchanged in patients with and without vasospasm.

Results: CSF ADMA levels were correlated with the development of vasospasm (p<0.01) and increased only in patients with vasospasm (p<0.01). ET-1 CSF levels remained unchanged in patients with and without vasospasm.

Conclusions: Levels of CSF ADMA, but not ET-1, significantly correlate with development of vasospasm after SAH. ADMA and ET-1 were not correlated with ischemia verified on follow-up CCT scans. ADMA via NO, seems to be involved in the development of cerebral vasospasm after SAH, causing an imbalance of vasodilative and vasoconstrictive components, whereas ET-1 may sustain and/or enforce this imbalance.