gms | German Medical Science

55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

25. bis 28.04.2004, Köln

Role of Bradykinin B2 receptors for secondary brain damage after traumatic brain injury in mice

Rolle von Bradykinin-B2-Rezeptoren für den sekundären Hirnschaden nach Schädel-Hirn-Trauma bei der Maus

Meeting Abstract

  • corresponding author Christian A. Erös - Institute for Surgical Research, University of Munich, Munich
  • S. W. Kim - Institute for Surgical Research, University of Munich, Munich
  • K. Zweckberger - Institute for Surgical Research, University of Munich, Munich
  • R. Zimmermann - Institute for Surgical Research, University of Munich, Munich
  • A. Baethmann - Institute for Surgical Research, University of Munich, Munich
  • N. Plesnila - Institute for Surgical Research, University of Munich, Munich

Deutsche Gesellschaft für Neurochirurgie. Ungarische Gesellschaft für Neurochirurgie. 55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie. Köln, 25.-28.04.2004. Düsseldorf, Köln: German Medical Science; 2004. DocDI.04.07

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2004/04dgnc0185.shtml

Published: April 23, 2004

© 2004 Erös et al.
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Outline

Text

Objective

Bradykinin B2 receptors may be involved in the pathophysiology of traumatic brain injury (TBI). However, direct evidence is still missing. In the present study we have investigated contusion volume, brain edema and functional outcome of bradykinin B2 receptor knock out (B2 Ko) and wild type (WT) mice after experimental TBI.

Methods

B2 Ko and WT mice (n=7 each) were subjected to controlled cortical impact injury (CCI, 8 m/s, 1 mm indentation). Brain water content and contusion volume were assessed after 24 h and after 7 days, respectively. Hind paw misplacements during beam walking were counted daily 4 days before and 7 days after CCI. WT mice had a contusion volume of 7 days after CCI.

Results

Deletion of the B2 gene resulted in a reduction of contusion volume by 33% as compared to WT mice (9.1±1.4 mm3 vs. 13.5±4.5 mm3; p<0.02). In B2 Ko mice cerebral water content 24 h after trauma was reduced from 81.1±0.7% in WT mice to 79.6±0.4% (- 51%; p<0.05). Functional outcome was significantly better on day 5 post trauma in B2 Ko mice as compared to WT mice (6.7±3.2 and 12.2±5.8 foot misplacements, respectively. p<0.05).

Conclusions

Bradykinin B2 receptors mediate brain edema formation, loss of brain parenchyma, and loss of function after TBI. Therefore the bradykinin B2 receptor might represent a good target molecule for the development of drugs against secondary brain damage after TBI in man.