Artikel
Role of Bradykinin B2 receptors for secondary brain damage after traumatic brain injury in mice
Rolle von Bradykinin-B2-Rezeptoren für den sekundären Hirnschaden nach Schädel-Hirn-Trauma bei der Maus
Suche in Medline nach
Autoren
Veröffentlicht: | 23. April 2004 |
---|
Gliederung
Text
Objective
Bradykinin B2 receptors may be involved in the pathophysiology of traumatic brain injury (TBI). However, direct evidence is still missing. In the present study we have investigated contusion volume, brain edema and functional outcome of bradykinin B2 receptor knock out (B2 Ko) and wild type (WT) mice after experimental TBI.
Methods
B2 Ko and WT mice (n=7 each) were subjected to controlled cortical impact injury (CCI, 8 m/s, 1 mm indentation). Brain water content and contusion volume were assessed after 24 h and after 7 days, respectively. Hind paw misplacements during beam walking were counted daily 4 days before and 7 days after CCI. WT mice had a contusion volume of 7 days after CCI.
Results
Deletion of the B2 gene resulted in a reduction of contusion volume by 33% as compared to WT mice (9.1±1.4 mm3 vs. 13.5±4.5 mm3; p<0.02). In B2 Ko mice cerebral water content 24 h after trauma was reduced from 81.1±0.7% in WT mice to 79.6±0.4% (- 51%; p<0.05). Functional outcome was significantly better on day 5 post trauma in B2 Ko mice as compared to WT mice (6.7±3.2 and 12.2±5.8 foot misplacements, respectively. p<0.05).
Conclusions
Bradykinin B2 receptors mediate brain edema formation, loss of brain parenchyma, and loss of function after TBI. Therefore the bradykinin B2 receptor might represent a good target molecule for the development of drugs against secondary brain damage after TBI in man.