gms | German Medical Science

60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit den Benelux-Ländern und Bulgarien

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

24. - 27.05.2009, Münster

Inflammatory signaling via bradykinin receptors plays a role for the development of secondary brain damage after subarachnoid hemorrhage in mice

Meeting Abstract

  • K. Schöller - Neurochirurgische Klinik und Poliklinik, Klinikum Großhadern, Ludwig-Maximilians-Universität, München
  • S. Feiler - Institut für Chirurgische Forschung, Klinikum Großhadern, Ludwig-Maximilians-Universität, München
  • S. Anetsberger - Institut für Chirurgische Forschung, Klinikum Großhadern, Ludwig-Maximilians-Universität, München
  • N. Plesnila - Neurochirurgische Klinik und Poliklinik, Klinikum Großhadern, Ludwig-Maximilians-Universität, München

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocP05-06

DOI: 10.3205/09dgnc298, URN: urn:nbn:de:0183-09dgnc2986

Veröffentlicht: 20. Mai 2009

© 2009 Schöller 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: The kallikrein-kinin system is involved in inflammatory signaling after traumatic brain injury and cerebral ischemia via bradykinin B2 receptors. The current study was conducted to clarify the role of both bradykinin receptor subtypes (B1 and B2) for the development of secondary brain damage after experimental subarachnoid hemorrhage (SAH).

Methods: 6–8 week old C57/Bl6 mice (controls) and bradykinin B1- and B2-receptor knock-out (-/-) mice were anesthetized, intubated and mechanically ventilated. The SAH was induced by endovascular puncture. Intracranial pressure (ICP, parenchymal probe) and cerebral blood flow (CBF, Laser-Doppler flowmetry) were continuously measured from 15 minutes before until 15 minutes after SAH. 24 hours after SAH ICP measurement was repeated and animals were subsequently sacrificed to quantify the brain water content. Mortality, neurological function and postoperative weight gain was quantified over a period of 7 days after SAH.

Results: ICP and CBF did not differ between groups in the first 15 minutes after SAH. 24 hours after SAH, however, ICP (p<0.05) and brain water content (p<0.05 B2 -/-) was reduced in bradykinin receptor knock-out animals. 7-day mortality was 43%, 71% (p<0.05 vs. controls), and 14% (p<0.05 vs. controls) in control, B1 -/-, and B2 -/- mice, respectively. The neurological function was significantly better in B2 -/- mice (p<0.05) compared to control and B1 -/- mice on the first postoperative day. B2 -/- animals also exhibited a better weight gain on postoperative day 4 whereas the B1 -/- group showed a lesser weight gain from postoperative 3 through 7 compared to control animals (p<0.05).

Conclusions: An inflammatory response mediated by bradykinin B2 receptors plays a role for the development of secondary brain damage after SAH. Thus, pharmacological inhibition of B2 receptors might be a future candidate for the treatment of post-hemorrhagic cerebral edema.