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61st Annual Meeting of the German Society of Neurosurgery (DGNC) as part of the Neurowoche 2010
Joint Meeting with the Brazilian Society of Neurosurgery on the 20 September 2010

German Society of Neurosurgery (DGNC)

21 - 25 September 2010, Mannheim

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Changes in cortex oxygen distribution during an epidural mass lesion in rodents

Meeting Abstract

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  • Jan Warnat - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Regensburg, Germany
  • Eva-Maria Stoerr - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Regensburg, Germany
  • Gregor Liebsch - Biocam, Regensburg, Germany
  • Martin Proescholdt - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Regensburg, Germany
  • Alexander Brawanski - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Regensburg, Germany

Deutsche Gesellschaft für Neurochirurgie. 61. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC) im Rahmen der Neurowoche 2010. Mannheim, 21.-25.09.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. DocP1862

doi: 10.3205/10dgnc333, urn:nbn:de:0183-10dgnc3337

Published: September 16, 2010

© 2010 Warnat 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

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Objective: The measurement of brain parenchyma pO2 is a valuable standard procedure for neurocritically ill patients. Here we utilize a opto-chemical method of planar oxygen detection for measuring changes of cortex pO2 during a reversibly introduced epidural mass lesion.

Methods: 17 male wistar rats (m = 303±21 g) were sedated (midazolam, fentanyl, medetomidin), intubated and ventilated. A 2*2 mm cortical window was prepared with a translucent porphyrine containing sensor foil. The sensor was excited by short light pulses (λ = 405 nm) and it’s pO2 dependant light emissions were recorded with a CCD camera of the measurement device (Biocam, Regensburg). A balloon device, which allowed to trigger an epidural mass lesion was placed over the contra lateral hemisphere. Throughout the experiment, the balloon was inflated up to an ICP of approx. 40 mmHg for 60 minutes and then deflated. ICP, RR, body temperature, EEG and cortex pO2 were recorded and blood gas samples were drawn.

Results: ICP increased from a baseline of 5,3±3,5 mmHg to 39,9±14,7 mmHg (p<0,001) due to the balloon inflation. Cortical surface pO2 over arterioles changed from 51,8±10,7 mmHg to 42,1±10,8 mmHg (p<0,001), over venoles from 41,2±7,4 mmHg to 35,4±8,8 mmHg (p<0,001) and over parenchyma (defined as area without visible vessels) from 32,9±6,0 mmHg to 29,9±5,1 mmHg respectively (p<0,001). Arterial pO2 (mean 176 mmHg) and pCO2 (mean 41,8 mmHg) remained constant (p>0,05).

Conclusions: In this animal model, a moderate epidural mass lesion causes significant decrease in cortical pO2. The parenchyma shows the smallest, although still significant pO2 changes. This may reflect autoregulative processes. The measurement system utilized here proves to be suitable for the simultaneous pO2 measurement of distinct anatomical structures of the cortex under pathophysiological conditions and may be useful as a monitoring device.