gms | German Medical Science

57th Annual Meeting of the German Society of Neurosurgery
Joint Meeting with the Japanese Neurosurgical Society

German Society of Neurosurgery (DGNC)

11 - 14 May, Essen

Deprivation of the vasoactive Endothelin (B)- receptor function after experimental subarachnoid hemorrhage in the rat

Verlust der vasoaktiven Endothelin (B)-Rezeptor-Funktion nach experimenteller Subarachnoidalblutung an der Ratte

Meeting Abstract

  • corresponding author H. Vatter - Klinik für Neurochirurgie, Johann Wolfgang Goethe-Universität, Frankfurt am Main
  • J. Konczalla - Klinik für Neurochirurgie, Johann Wolfgang Goethe-Universität, Frankfurt am Main
  • S. Weidauer - Institut für Neuroradiologie, Johann Wolfgang Goethe-Universität, Frankfurt am Main
  • A. Raabe - Klinik für Neurochirurgie, Johann Wolfgang Goethe-Universität, Frankfurt am Main
  • M. Zimmermann - Evangelisches und Johanniter Klinikum, Duisburg-Nord
  • V. Seifert - Klinik für Neurochirurgie, Johann Wolfgang Goethe-Universität, Frankfurt am Main

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 57. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie. Essen, 11.-14.05.2006. Düsseldorf, Köln: German Medical Science; 2006. DocFR.10.08

The electronic version of this article is the complete one and can be found online at:

Published: May 8, 2006

© 2006 Vatter 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: Numerous experimental and recently also clinical investigations evidence the central role of Endothelin (ET)-1 in the development of cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH). However, the role and the function of the cerebrovascular ET(B)-receptor (ETBR) remains unclear so far. Therefore the aim of the present investigation was the characterization of the expression and the function of this receptor subtype after SAH.

Methods: CVS was induced employing the rat double hemorrhage model and proven by the reduction of the cerebral blood flow (CBF) by MR perfusion weighted imaging (PWI). The basilar arteries (BA) were dissected from animals on the days 3 (d3) and 5 (d5) after SAH. They were cut into ring segments for measurement of isometric force in an organ bath or embedded for immunohistochemical staining. Concentration-effect curves (CECs) were constructed by cumulative application of ET-1 or Sarafotoxin S6c (S6c) in segments with (E+) and without (E-) endothelium. CECs were compared by the maximum effect (E(max)) and the pD2. Staining was performed with an antibody against the ETBR.

Results: Relative regional CBF was reduced to 63% (d3) and to 32% (d5) after SAH compared to the controls. The ET-1 induced contraction was not significantly changed in respect to the E(max). However, the pD2 was significantly enhanced after SAH (control: 7.7±0.1 (mean±SEM), d3: 8.1±0.1, d5: 8.3±0.1). S6c did not induce a significant contraction in segments from any group. Relaxation by S6c, however, disappeared during CVS (E(max): 73±11% (control), 21±13% (d3), 13±8% (d5)), whereas relaxation by Ach was not significantly altered. No significant changes of the endothelial ETBR expression was observed by immunohistochemical staining.

Conclusions: Present data indicate a decoupling of the vasoactive ETBR function and expression in cerebral arteries after SAH. The loss of the ETBR relaxation may be an additional pathophysiological mechanism leading to CVS.