gms | German Medical Science

60th Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Benelux countries and Bulgaria

German Society of Neurosurgery (DGNC)

24 - 27 May 2009, Münster

Time-dependent effects of arginine vasopressin V1 receptor inhibition on secondary brain damage after experimental brain injury

Meeting Abstract

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  • R. Trabold - Neurochirurgische Universitätsklinik, Klinikum Großhadern, Ludwig-Maximilians-Universität München
  • S. Krieg - Neurochirurgische Universitätsklinik, Klinikum Großhadern, Ludwig-Maximilians-Universität München
  • N. Plesnila - Neurochirurgische Universitätsklinik, Klinikum Großhadern, Ludwig-Maximilians-Universität München

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. DocP09-03

DOI: 10.3205/09dgnc343, URN: urn:nbn:de:0183-09dgnc3439

Published: May 20, 2009

© 2009 Trabold et al.
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Outline

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Objective: The pharmacological inhibition of Arginine-Vasopressin (AVP) V1a receptor is able to reduce the brain edema, intracranial pressure (ICP), secondary brain damage and also improves therefore the neurological function after experimental brain injury. The aim of the study was to identify the optimal time of treatment in which the AVP V1 receptor antagonists are neuroprotective.

Methods: Male C57/BL6 were anesthetized, subjected to controlled cortical impact (CCI; 8m/s, 1mm) and received a intracerebroventricular injection of the specific AVP V1a antagonist SR49059 after 5 min, 1 h, 3 h or 6 h (n=7 each group). After 24 h ICP, contusion volume, brain water content and neurological function (beam walk and Neurological Severity Score) were analyzed. In further groups the neurological function and the volume of contusion were determined over seven days.

Results: The inhibition of V1a receptors 5 min and 3 h after trauma reduces the post-traumatic brain edema of 81,7 ± 0,2 % in controls to 80,6 ± 0,4% (p<0.05) respectively 80,8 ± 0,4% (p<0.05). Only the application immediately after trauma reduced the contusion volume of 35.3 ± 1.3 mm³ to 30.2 ± 1.2 mm³ (p<0.05) and improved the neurological function of the animals after 7 days.

Conclusions: The early central inhibition of AVP V1a receptors by the small molecule SR-49059 significantly reduced posttraumatic brain edema, intracranial pressure and secondary lesion expansion. These findings show that for the aggravation of TBI, AVP is most important in the early phase after trauma. Further experiments will have to clarify the mechanism of V1a receptor-induced neuroprotection and have to demonstrate, if a clinical examination of this new pathophysiological concept seems to be reasonable.