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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

Article

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Extrinsic and intrinsic inhibition of the sympathetic noradrenergic system (SNS) – impact on CBF and O2 -Saturation in an animal model of AVM

Periphere und zentrale Noradrenalindepletion – Einfluss auf Hirndurchblutung und Sauerstoffsättigung in einem AV-Fistelmodell

Meeting Abstract

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  • corresponding author C. Stüer - Department of Neurosurgery, Rheinische Friedrich-Wilhelms University Bonn
  • T. Ikeda - Department of Neurosurgery, Rheinische Friedrich-Wilhelms University Bonn
  • M. Stoffel - Department of Neurosurgery, Rheinische Friedrich-Wilhelms University Bonn
  • G. Luippold - Department of Neurosurgery, Rheinische Friedrich-Wilhelms University Bonn
  • C. Schaller - Department of Neurosurgery, Rheinische Friedrich-Wilhelms University Bonn
  • B. Meyer - Department of Neurosurgery, Rheinische Friedrich-Wilhelms University Bonn

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. Doc11.05.-09.01

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2005/05dgnc0211.shtml

Published: May 4, 2005

© 2005 Stüer 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

To elucidate for the first time the influence of the intrinsic versus the extrinsic component of the cerebral noradrenergic system (SNS) on CBF and SO2 in an established animal model of AVM.

Methods

12 weeks after creation of an extracranial AV-Fistula [Morgan-Type in male Sprague-Dawley rats] (n=40) or sham-operation (n=40) rSO2 (spectrophotometry), rCBF (LDF) and cortical interstitial Noradrenaline concentrations (microdialysis) were measured before and after fistula occlusion. N=10 fistula or sham animals each underwent 1. no SNS manipulation (=controls), 2. peripheral SNS inhibition via bilateral sympathectomy (=scgx), 3. central SNS inhibition via the neurotoxin DSP-4 (=dsp) or 4. complete SNS inhibition (scgx/dsp).

Results

Resting blood flow (shams versus fistula pre) remained unaffected. After fistula occlusion rCBF/rSO2 increases were highest after complete and lowest after peripheral inhibition (control pre:224±49LDU, 44±12%SO2; post:235±64LDU, 48±9%SO2; scgx pre:221±53 LDU, 41±13% SO2; post:226±58LDU, 47±12%SO2; dsp pre:223±58LDU, 47±9%SO2; post:249±54LDU, 56±12%SO2, scgx/dsp pre:204±48LDU, 34±8%SO2; post: 226±60LDU, 39±11%SO2). Noradrenaline-concentrations were lowest in the scgx/dsp group and highest in the scgx group (NA (nMol): control pre:2,2±1,2; post:2,4±1,0; scgx pre:3,6±2,0; post:6,6±4,5; dsp pre:2,4±2,0; post 2,5±2,1; scgx/dsp pre:1,1±0,8; post 1,7±1,6).

Conclusions

Evidence for the hypothesized protective capacity of the central SNS against hyperperfusion syndromes could thus be established for the first time in vivo. The hitherto unknown predominant role of the intrinsic component could be demonstrated. Extrinsic depletion alone seems to be compensated by increased intrinsic activity in this situation, explaining some contradictory results in the literature to date.