gms | German Medical Science

58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. bis 29.04.2007, Leipzig

Mild Hypothermia (33°C) ameliorates BBB dysfunction and improves neurological outcome following experimental subarachnoid hemorrhage (SAH) in rats

Milde Hypothermie (33°C) reduziert die Dysfunktion der Blut-Hirnschranke und verbessert die neurologische Erholung nach experimenteller Subarachnoidalblutung (SAB) am Rattenmodell

Meeting Abstract

  • corresponding author K. Schöller - Neurochirurgische Klinik, Klinikum der Universität München-Großhadern
  • E. Török - Institut für Chirurgische Forschung, Klinikum der Universität München-Großhadern
  • A. Trinkl - Neurologische Klinik, Klinikum der Universität München-Großhadern
  • N. Plesnila - Neurochirurgische Klinik, Klinikum der Universität München-Großhadern
  • R. Schmid-Elsaesser - Neurochirurgische Klinik, Klinikum der Universität München-Großhadern
  • S. Zausinger - Neurochirurgische Klinik, Klinikum der Universität München-Großhadern

Deutsche Gesellschaft für Neurochirurgie. 58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC). Leipzig, 26.-29.04.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. DocP 061

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2007/07dgnc316.shtml

Veröffentlicht: 11. April 2007

© 2007 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 vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: There is no effective treatment available for early brain injury (EBI) following SAH. Mild hypothermia is known to reduce secondary brain damage as well as CBF and ICP under various pathological conditions. This study for the first time investigates acute and chronic effects of mild hypothermia applied in an experimental post-treatment regimen.

Methods: Rats were subjected to SAH using the endovascular puncture method and assigned to a control group and two groups with induction of two hours hypothermia 60 and 180 minutes after SAH (n=10 per group). ICP and bilateral rCBF were continuously monitored during the acute phase. The wet-and-dry method was utilized to measure brain water content after 24 hours. Neurological outcome and mortality were monitored for 7 days. Thereafter, BBB permeability was quantified by Bovine serum albumin Western Blot and microvascular basal lamina alteration by collagen type IV Western Blot in bilateral cortical and subcortical regions.

Results: Mild hypothermia had no effect on post-ictal ICP, mortality, and brain water content. When hypothermia was initiated 60 minutes following SAH ipsilateral rCBF showed a better recovery over time (p<0.05). Furthermore, the same animals had less neurological deficits (p=0.03) and BBB function as well as basal lamina integrity were better preserved in the ipsilateral cortex as compared to controls or animals with later hypothermia application (p<0,05).

Conclusions: Although mild hypothermia did not affect brain edema formation, intracranial hypertension, or survival after SAH, it significantly improved BBB integrity and functional outcome in surviving animals. Provided the effect observed in the present study is permanent, our data suggest that mild hypothermia may be considered as a treatment option for SAH-induced brain damage.