gms | German Medical Science

56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
3èmes journées françaises de Neurochirurgie (SFNC)

Deutsche Gesellschaft für Neurochirurgie e. V.
Société Française de Neurochirurgie

07. bis 11.05.2005, Strasbourg

The family of methylated L-arginines (L-NMMA, ADMA and SDMA) : endogenous nitric oxide synthase inhibitors and their role in the pathogenesis of cerebral vasospasm in vitro and in vivo

Die Familie der methylierten L-Arginine (L-NMMA, ADMA and SDMA): endogene NO-Synthetase Inhibitoren und ihre Rolle in der Pathogenese des zerebralen Vasospasmus

Meeting Abstract

Suche in Medline nach

  • corresponding author C. S. Jung - Neurochirurgische Klinik, Johann-Wolfgang-Goethe-Universität, Frankfurt am Main
  • R. M. Pluta - Surgical Neurology Branch, NINDS, NIH, Bethesda, USA
  • E. H. Oldfield - Surgical Neurology Branch, NINDS, NIH, Bethesda, USA

Deutsche Gesellschaft für Neurochirurgie. Société Française de Neurochirurgie. 56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3èmes journées françaises de Neurochirurgie (SFNC). Strasbourg, 07.-11.05.2005. Düsseldorf, Köln: German Medical Science; 2005. Doc11.05.-13.08

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2005/05dgnc0246.shtml

Veröffentlicht: 4. Mai 2005

© 2005 Jung et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective

Endothelial dysfunction was observed in cerebral vasospasm after subarachnoid hemorrhage (SAH). Monomethyl-L-arginine (L-NMMA), asymmetric- and symmetric dimethyl-L-arginine (ADMA, SDMA) are produced by endothelial cells. They can inhibit endothelial nitric oxide synthase and produce endothelial dysfunction. Subarachnoid hemorrhage may evoke production and release of methylated arginines. We sought to determine L-NMMA, ADMA and SDMA level in vitro and in vivo and elucidate their role in cerebral vasospasm after SAH.

Methods

L-NMMA, ADMA, SDMA and NO metabolite levels were determined in CSF and serum samples from 30 patients and 22 animals after SAH as well as in human endothelial cell cultures treated with blood derived spasmogens.

Results

ADMA levels remained unchanged in patients and animals without vasospasm, but significantly increased during vasospasm: (6.2mM±1.7mM and 2.8mM±1.9mM vs. 15.7±6.3mM and 7.2mM±1.9mM;p<0.001) and decreased with resolution of vasospasm. Levels of L-NMMA and SDMA showed no significant alterations during vasospasm. ADMA levels were correlated with the degree of vasospasm (cc=0.82;p<0.0001) and negatively correlated with NO metabolite levels (cc=-0.32;p=0.008;cc=-0.25; p=0.04). ADMA increased after treatment with blood derived spasmogens from 7pM±3.7 to 12,3±3.7pM/mg Protein.

Conclusions

Blood derived spasmogens lead to increased levels of methylated arginines in vitro. ADMA levels significantly increased during vasospasm and were correlated with cerebral vasospasm and NO metabolite levels. Thus, the family of methylated arginines, especially ADMA, seem to be involved in the development of cerebral vasospasm.