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61. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC) im Rahmen der Neurowoche 2010
Joint Meeting mit der Brasilianischen Gesellschaft für Neurochirurgie am 20. September 2010

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

21. - 25.09.2010, Mannheim

Role of Arginine-Vasopressin V1a receptors for secondary brain damage following controlled cortical impact in mice

Meeting Abstract

Suche in Medline nach

  • Raimund Trabold - Department of Neurosurgery, University of Munich Medical Center – Grosshadern, Ludwig Maximilians University, Munich, Germany
  • Katrin Rauen - Department of Neurosurgery, University of Munich Medical Center – Grosshadern, Ludwig Maximilians University, Munich, Germany
  • Nikolaus Plesnila - Royal College of Surgeons in Ireland (RCSI), Dublin, Ireland

Deutsche Gesellschaft für Neurochirurgie. 61. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC) im Rahmen der Neurowoche 2010. Mannheim, 21.-25.09.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. DocV1586

DOI: 10.3205/10dgnc061, URN: urn:nbn:de:0183-10dgnc0615

Veröffentlicht: 16. September 2010

© 2010 Trabold 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: Brain edema formation and subsequent intracranial hypertension are well known to result in secondary brain damage and, hence, unfavorable outcome following traumatic brain injury (TBI). So far the knowledge on the molecular mechanisms of brain edema formation is still insufficient. Previously we showed that Arginin-Vasopressin (AVP) receptor antagonists reduce post-traumatic and post-ischemic brain edema formation. In the current study we investigated the relevance of Vasopressin V1a receptors for secondary brain damage after TBI by using V1a-receptor knock-out mice.

Methods: C57/BL6 mice and V1a-receptor knock-out mice (V1a-/-) were subjected to controlled cortical impact (CCI; 8 m/s, 1 mm). As parameters we quantified brain water content (baseline and 24 h after CCI), secondary contusion volume (15 min, 24 h and 7 d after CCI), neurological outcome (1 d before and at 7 d after CCI), body weight (in % at 7 d after CCI), and mortality.

Results: V1a-receptor deficiency significantly decreased brain water content by 29% (Mean ± SEM: 79.8%±0.3 vs. 80.6%±0.2 in controls) and secondary contusion volume by 29% (38.2±1.7 mm3 vs. 45.1±1.5 mm3 in controls) 24 h after CCI. Furthermore lack of V1a-receptor ameliorated neurological dysfunction (3.2±0.8 vs. 7.0±1.4 in controls) and reduced weight-loss (96±1.6% vs 91.0± 2.0) 7 days after CCI. All animals survived the observation period of 7 days.

Conclusions: Our data show that deficiency of V1a-receptor decreases secondary brain damage after experimental traumatic brain injury (TBI). We conclude from these findings that the V1a-receptor is a new potential drug target for the therapy of post-traumatic brain edema.