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61. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC) im Rahmen der Neurowoche 2010
Joint Meeting mit der Brasilianischen Gesellschaft für Neurochirurgie am 20. September 2010

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

21. - 25.09.2010, Mannheim

Release of thrombin following acute subdural hematoma does not influence lesion development

Meeting Abstract

  • Tobias Krämer - Universitätsmedizin Mainz, Institute for Neurosurgical Pathophysiology, Mainz, Germany
  • Axel Heimann - Universitätsmedizin Mainz, Institute for Neurosurgical Pathophysiology, Mainz, Germany
  • Oliver Kempski - Universitätsmedizin Mainz, Institute for Neurosurgical Pathophysiology, Mainz, Germany
  • Beat Alessandri - Universitätsmedizin Mainz, Institute for Neurosurgical Pathophysiology, Mainz, 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. DocP1858

DOI: 10.3205/10dgnc329, URN: urn:nbn:de:0183-10dgnc3291

Veröffentlicht: 16. September 2010

© 2010 Krämer 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: Acute subdural hemorrhage is a major complication following traumatic brain injury and is associated with high mortality. Beside the subdural mass, components from blood coagulation have been proposed to play an important role in lesion development. In this respect thrombin is known to be neurotoxic and produced immediately following extravasation of blood. The goal of the present study was to investigate whether thrombin from subdural blood augments brain damage after acute subdural hematoma in rats..

Methods: Male sprague-Dawley rats were anesthtized and surgically prepared for ASDH. Tail artery and jugular vein were cannulated and a craniotomy (3 mm) was drilled over the left cortex to subdurally insert a L-shaped, blunted needle (fixed with Histoacryl® and dental cement). Cerebral blood flow (lCBF) was measured frontal to the craniotomy using a Laser-Doppler probe. ASDH was induced with 300 µl venous, autologous blood. Animals were divided randomly into three groups, a sham-operated group (n=10), an ASDH group (n=11) and an ASDH group that received subdural blood that was mixed with a thrombin inhibitor just before subdural infusion(1 µg Argatra®/300 µl blood; n=9). Animals survived for 14 days and lesion size was assessed on hematoxylin-eosin stained sections.

Results: All values are given as means ± SD. Mean arterial blood pressure (MABP) was 66.0±4 (sham), 71±8 (ASDH), 68.1±13 mmHg (ASDH+Argatra) shortly before blood infusion. Due to injury MABP showed a Cushing reflex and rose to a maximum of 68.5±6, 83.5±9 and 87.9±19. 60 minutes post-injury MABP had normalized with 72.9±11 and 73.4±14 mmHg (sham: 68.3±4). lCBF dropped during infusion from 33.3±1.8 to 21.8±7.1 LDU (ASDH) and from 32.0±1.0 to 21.0±7.1 LDU (ASDH+Argatra). lCBF remained decreased to the end of monitoring (ASDH: 24.7±5.7, ASDH+Argatra: 23.3±5.6 LDU). Cortical lesion at 14 days post-injury was 1.7±1.6 (sham), 8.9±7.3 (ASDH) and 7.6±4.2 (ASDH+Argatra). Injury groups did not differ significantly from each other.

Conclusions: We blocked production of thrombin in the subdurally infused blood by Argatra® and thus prevented direct effects of thrombin on lesion development. Since we could not detect a significant difference in lesion size between injury groups at 14 days post-injury we suggest that thrombin is not released from coagulation in sufficient concentrations to harm neuronal tissue after acute subdural hematoma.