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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

The neuroprotective effect of Erythropoietin (Epo) in acute subdural hematoma (ASDH): A double-edged sword?

Meeting Abstract

  • H. Baechli - Neurochirurgische Universitätsklinik Basel
  • M. Rahimi - Institut für Neurochirurgische Pathophysiologie, Johannes-Gutenberg-Universität Mainz
  • A. Heimann - Institut für Neurochirurgische Pathophysiologie, Johannes-Gutenberg-Universität Mainz
  • O. Kempski - Institut für Neurochirurgische Pathophysiologie, Johannes-Gutenberg-Universität Mainz
  • B. Alessandri - Institut für Neurochirurgische Pathophysiologie, Johannes-Gutenberg-Universität Mainz

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. DocP09-05

DOI: 10.3205/09dgnc345, URN: urn:nbn:de:0183-09dgnc3453

Veröffentlicht: 20. Mai 2009

© 2009 Baechli 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: Epo is a well known doping drug. In previous studies with ASDH we could show that Epo is already neuroprotective in low concentrations of 200 IU i.v. injections. The aim of our study is to proof the efficacy of subdural applied Epo after clot evacuation and which concentration is needed to reduce brain damage.

Methods: Male Sprague-Dawley rats (n=9/group, weight 300–350g) were divided in 5 groups receiving subdurally 150μl of Epo 0.02, 2, 200IU, NaCl 0.9% (vehicle) or no treatment (sham). Anesthetic/medication: chloral hydrate (36mg/ml) i.p. initially afterwards 1ml/100g and 1ml/h; 1ml atropine 1mg s.c. Operation: Jugular vein catheter for collecting 400μl autologous blood and craniotomy (Ø3mm) were prepared. A blunt L-shaped cannula (G23) was inserted subdurally and fixed with histoacryl/dental cement. Laser Doppler probe, ptiO2 sensor (Licox) and parenchymal ICP (Raumedics, Ø 3F) were used for acute monitoring. ASDH: infusion of 400μl unheparinized blood with a flow rate of 50μl/min. (sham no infusion). At 60-min. post-ASDH, blood was evacuated, the opened craniotomy re-sealed. Then 150μl NaCl or Epo were directly applied on the cortex through a small burr hole above the injury site. Lesion volume was assessed on hematoxylin-eosin stained sections 48h after the trauma.

Results: There are no differences between injured groups in ICP, CBF and MAP values, but clot removal reduced ICP and increased local CBF. The evaluation of lesion volumes 48h after ASDH showed significant neuroprotection already in Epo concentrations of 0.02IU (lesion volume:11,2±2 mm3), p<0,05, but not with 2IU (67,9±10,4mm3) compared to the vehicle group (49,8±14,4 mm3). Epo concentrations of 200iU showed toxic effects with significantly increased lesion volumes (173.1±38 mm3, p<0.005 vs. vehicle).

Conclusions: Epo can be applied subdurally and its neuroprotective effect is dose-dependent. Compared to systemic injection with which 200IU was the lowest effective dose, already an extremely low Epo dose of 0.002IU was subdurally sufficient to induce neuroprotection. However, Epo exerts adverse effects on brain damage at concentrations higher than 2IU.