gms | German Medical Science

63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

13. - 16. Juni 2012, Leipzig

Role of Vasopressin-V1a-receptors for the Activation of the Cushing response

Meeting Abstract

  • K. Hockel - Institut für Chirurgische Forschung, Klinikum der Universität München, Campus Großhadern, München; Neurochirurgische Universitätsklinik, Universitätsklinikum Tübingen
  • K. Schöller - Institut für Chirurgische Forschung, Klinikum der Universität München, Campus Großhadern, München; Neurochirurgische Klinik, Klinikum der Universität München, Campus Großhadern, München
  • R. Trabold - Institut für Chirurgische Forschung, Klinikum der Universität München, Campus Großhadern, München; Neurochirurgische Klinik, Klinikum der Universität München, Campus Großhadern, München
  • N. Plesnila - Institut für Chirurgische Forschung, Klinikum der Universität München, Campus Großhadern, München; Institut für Schlaganfall- und Demenzforschung, Klinikum der Universität München, Campus Großhadern, München

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS). Leipzig, 13.-16.06.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. DocFR.02.03

DOI: 10.3205/12dgnc179, URN: urn:nbn:de:0183-12dgnc1793

Veröffentlicht: 4. Juni 2012

© 2012 Hockel 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 vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: In a previous experimental study on the role of Vasopressin (AVP) for the development of early brain injury following subarachnoid hemorrhage (SAH), rats under pharmacological Vasopressin-V1a-receptor inhibition failed to exhibit postictal compensatory arterial hypertension. The aim of the present study was to further elucidate the role of AVP and its V1a-receptors as mediators for the increase in arterial blood pressure (MABP) following acutely raised intracranial pressure (ICP), i.e. the Cushing response.

Methods: In ventilated Sprague-Dawley rats, SAH was induced by endovascular perforation and the spontaneous courses of ICP and MABP were monitored at high temporal resolution (n = 10). In a second series, ICP was raised to 35 or 75 mmHg for 1 minute by inflation of an epidurally placed balloon-microcatheter. MABP was monitored continuously and plasma AVP concentration was assessed at 3 and 30 minutes (n = 6). Subsequently, the rats received either a selective Vasopressin-V1a-receptor antagonist (V1880) or vehicle (0.9% NaCl) intravenously prior to balloon inflation or SAH, while ICP and MABP were monitored continuously (n = 10, 5).

Results: Both in SAH as well as in balloon-induced intracranial hypertension, MABP was increased by 30–40 mmHg for approximately 20 minutes (p < 0.05) and plasma AVP concentration simultaneously increased 35–40-fold (p < 0.05) within 3 minutes. By inhibition of systemic V1a-receptors, postictal arterial hypertension, i.e. the Cushing response, was almost completely suppressed (p < 0.05). In rats subjected to SAH, the preemptive treatment with a V1a-receptor antagonist reduced the rate of secondary rebleedings from 30 to 0%; the mortality rate was reduced from 50 to 20%.

Conclusions: The presented data show for the first time that the ICP-induced increase in MABP, the Cushing response, is greatly dependent on acutely released AVP and is mediated via V1a-receptors. The inhibition of these peripheral V1a-receptors prevents posthemorrhagic arterial hypertension, thus reducing the incidence of secondary bleeding events and improving the outcome following SAH. V1a-receptor antagonists could be a novel and safe therapeutic principle in the treatment of SAH.