gms | German Medical Science

56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
3èmes journées françaises de Neurochirurgie (SFNC)

Deutsche Gesellschaft für Neurochirurgie e. V.
Société Française de Neurochirurgie

07. bis 11.05.2005, Strasbourg

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Microvascular basal lamina damage after subarachnoid hemorrhage (SAH) in rats

Schädigung der mikrovaskulären Basalmembran nach Subarachnoidalblutung am Rattenmodell

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

Deutsche Gesellschaft für Neurochirurgie. Société Française de Neurochirurgie. 56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3èmes journées françaises de Neurochirurgie (SFNC). Strasbourg, 07.-11.05.2005. Düsseldorf, Köln: German Medical Science; 2005. Doc10.05.-15.05

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2005/05dgnc0167.shtml

Published: May 4, 2005

© 2005 Schöller et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

Text

Objective

Mechanisms of early cerebral edema following SAH are poorly understood. Previously, we demonstrated a peak of edema evolution at 24 hours after experimental SAH in rats. Furthermore, brain water content correlated with neurological deficits of animals. In focal cerebral ischemia, alteration of the microvascular basal lamina and its relevance for development of hemorrhagic transformation and cerebral edema has previously been demonstrated. The present study was designed to demonstrate microvascular basal lamina damage as a potential target for therapeutical interventions to reduce vasogenic brain edema following SAH.

Methods

27 rats were subjected to SAH by an endovascular filament. Animals were randomly assigned to 1 sham (n=9) and 2 SAH groups (n=9 each; 6 and 24h survival). Microvascular basal lamina alteration was quantified by anticollagen type IV immunochemistry with subsequent counting of stained cerebral microvessels/region of interest (ROI) in cerebral cortex and basal ganglia of both hemispheres; Western Blot was used to define the collagen type IV protein content in the same brain regions.

Results

Significant (p<0.001) reduction of Collagen Type IV stained microvessels/ ROI occurred after 6 and 24 hours in both hemispheres with predominance of the ipsilateral cortex, respectively. Consistently, Collagen type IV protein content was significantly reduced after 6 and 24 hours with predominance of the ipsilateral cortex. We found no alteration of the microvascular basal lamina in the basal ganglia of both hemispheres, neither evaluated by immunohistochemistry nor by Western Blot.

Conclusions

Significant alteration of cerebral microvessels in the cortex of both hemispheres was demonstrated 6 and 24 hours after experimental SAH with predominance at the time point of maximum edema evolution. The importance of these findings for the development of vasogenic cerebral edema need to be determined by a correlation with blood-brain barrier integrity. Further investigations with survival of animals 48 and 72 hours after SAH are ongoing. Furthermore, the role of proteolytic systems as potential target for therapeutical interventions needs to be defined.