Artikel
Role of vasopressor receptors for post-traumatic brain edema formation and secondary brain damage
Rolle von Arginin-Vasopressin V1- und V2-Rezeptoren auf den zerebralen Schaden nach experimentellem Schädel-Hirn-Trauma
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Autoren
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R. Trabold
- Neurochirurgische Universitätsklinik, Institut für Chirurgische Forschung, Klinikum Großhadern, Ludwig-Maximilians-Universität München
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N. Plesnila
- Neurochirurgische Universitätsklinik, Institut für Chirurgische Forschung, Klinikum Großhadern, Ludwig-Maximilians-Universität München
| Veröffentlicht: | 11. April 2007 |
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Gliederung
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Objective: Brain edema is still one of the most deleterious sequels of traumatic brain injury (TBI) and its pathophysiology is not well understood. The aim of the current study was to investigate the role of arginine-vasopressin (AVP, antidiuretic hormone, ADH), an important regulator of water homeostasis, for the formation of post-traumatic brain edema.
Methods: C57/Bl6 mice (n=59) were subjected to controlled cortical impact (CCI; 8m/s, 1mm). 3 min after the trauma, the animals received 500 ng of a AVP V1-receptor antogonist (deamino-Pen(1), O-Me-Tyr(2), Arg(8)]-Vasopressin) or 500 ng of an AVP V2-receptor antagonist (adamantaneacetyl(1), O-Et-D-Tyr(2),Val(4), Abu(6),Arg(8,9)]-Vasopressin) icv. 24 h after the trauma, the cerebral water content, ICP, and contusion volume were assessed.
Results: Post-traumatic inhibition of AVP V1 receptors reduced brain water content by 45% (p<0.05), intracranial pressure by 29% (p<0.05), and contusion volume by 18% (p<0.05), while inhibition of AVP V2 receptors had no effect.
Conclusions: The current results demonstrate that vasopressin V1 receptors are involved in the pathogenesis of post-traumatic brain edema and the subsequent formation of secondary brain damage. Although the underlying mechanisms of AVP-mediated brain edema formation remain to be elucidated, our study suggests that vasopressin V1 receptors may represent a novel pharmacological target for the treatment of post-traumatic brain edema.
