Artikel
Roles of ADMA and endothelin-1 in cerebral vasospasm after subarachnoid hemorrhage
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Autoren
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Carla S. Jung
- Abteilung für Neurochirurgie, Universitätsklinikum Heidelberg, Deutschland
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Bettina Lange
- Neurochirurgische Klinik, Universitätsklinikum Frankfurt/Main, Deutschland
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Klaus Zweckberger
- Abteilung für Neurochirurgie, Universitätsklinikum Heidelberg, Deutschland
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Daniel Haux
- Abteilung für Neurochirurgie, Universitätsklinikum Heidelberg, Deutschland
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Volker Seifert
- Neurochirurgische Klinik, Universitätsklinikum Frankfurt/Main, Deutschland
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Andreas W. Unterberg
- Abteilung für Neurochirurgie, Universitätsklinikum Heidelberg, Deutschland
| Veröffentlicht: | 16. September 2010 |
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Gliederung
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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.
