Artikel
Persistence of the endothelium and nitric oxide dependent relaxant pathway of cerebral vessels during experimental cerebral vasospasm
Erhalt des endothel- und stickstoffmonoxidabhängigen relaxierenden Stoffwechsels zerebraler Gefäße während eines experimentellen zerebralen Vasospasmus
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Autoren
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H. Vatter
- Klinik für Neurochirurgie, Johann Wolfgang Goethe-Universität, Frankfurt am Main
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S. Dias
- Klinik für Neurochirurgie, Johann Wolfgang Goethe-Universität, Frankfurt am Main
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S. Weidauer
- Institut für Neuroradiologie, Johann Wolfgang Goethe-Universität, Frankfurt am Main
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A. Raabe
- Klinik für Neurochirurgie, Johann Wolfgang Goethe-Universität, Frankfurt am Main
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M. Zimmermann
- Klinik für Neurochirurgie, Johann Wolfgang Goethe-Universität, Frankfurt am Main
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V. Seifert
- Klinik für Neurochirurgie, Johann Wolfgang Goethe-Universität, Frankfurt am Main
| Veröffentlicht: | 8. Mai 2006 |
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Gliederung
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Objective: An impaired endothelium dependent and nitric oxide (NO) mediated cerebrovascular response was frequently charged to represent a part of the pathophysiological pathway leading to cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH). Application of particular compounds of this pathway, however, was partial successful in the treatment of CVS. The aim of the present study was, therefore, to characterize this pathway vasospastic altered cerebral vessels.
Methods: CVS was induced by twofold application of 0.2 ml arterial blood in the cisterna magna of rats (double hemorrhage model) and proven by perfusion weighted magnet resonance imaging (MR PWI). Ring segments from the basilar artery BA were prepared for immunohistochemical staining and for the measurement of isometric force in an organ bath. Concentration-effect curves (CECs) were constructed by cumulative application of Acetylcholine (Ach) (10-8-10-4M), sodium nitroprusside (SNP) and 8-Bromo-cGMP (10-7-10-3M) after pre-contraction. Relaxation was measured in per cent of pre-contraction. Staining was performed with antibodies against eNOS, and the α- and β-subunit of the soluble guanylate cyclase (sGC).
Results: Relative regional cerebral blood flow (CBF) was reduced to 47% on day (d) 3 and to 22% on d5 after SAH compared to the control. Relaxation of BA ring segments by ACH and 8-Bromo-cGMP was not significantly different in vessels from controls and from the SAH (d5). SNP, however, induced an enhanced relaxation in case of CVS (control: 88±12%, SAH d5: 117±26%). Immunohistochemical staining of eNOS trends to increase on d5 versus control. Expression of the α- and β-subunit of the sGC was reduced on d3 but recoverd to the base level on day 5 after SAH.
Conclusions: The present data indicate the persistence or even an increase of the function and the expression of the cerebrovascular NO dependent vasodilatory pathway during CVS. Activation of the NO pathway on different levels could, therefore, represent a reasonable approach for the treatment of CVS.
