Artikel
An experimental model of chronic cerebral ischemia in C57/BL6 mice
Suche in Medline nach
Autoren
Veröffentlicht: | 20. Mai 2009 |
---|
Gliederung
Text
Objective: In ordr to investigate alternative strategies of artificial vessel growth, there has been an increased interest in experimental models of chronic cerebral ischemia in transgenic mice. Therefore, we evaluated a reproducible model of chronic cerebral ischemia in C57/BL6 mice.
Methods: 30 male C57/BL6 mice, aged 4 to 6 weeks (20g–22g bw) were anaesthetized with Ketamine/Xylazin. To induce chronic cerebral ischemia in n=10 mice, the right internal carotid artery (ICA) was permanently ligated with a 7.0 silk suture. To quantify the hemodynamic compromise compared to sham (n=10; vessel manipulation but no occlusion) and control groups (n=10; no vessel manipulation and no occlusion) we performed a bihemispheric and transcranial Laser Speckle Flowmetry analysis with and without acetazolamide stimulation on day 0, 3, 7, 14 and 21 after right sided ICA-occlusion (ICAO). To evaluate potential collateral vessel growth, mice were perfused with a latex/carbon black solution at day 21.
Results: Following right ICAO at day 0, we observed a statistically significant reduction of the right and left hemispheric cerebrovascular reserve capacity (CVRC) to 16±9% and 28,4±13% (p<0.05 right vs. left), compared to sham (right: 44,3±12%; left: 43,5±10%) and control (right: 45,3±11; left: 42,9±13%) groups (2-WAY ANOVA, p<0.05). After 21 days, the right- and left-sided CVRC in the ICAO group was reduced to 6,2±7% and 19,4±13%, whereas the bilateral CVRC in sham and control groups remained above 30% and 40% throughout the entire measurement period. 21 days after ICAO the basal collateral vessel diameters were significantly increased compared to sham and control groups.
Conclusions: By unilateral occlusion of the ICAO we were able to reliably establish chronic cerebral ischemia in a C57/BL6 mouse model. This finding was combined with spontaneous growth of the basal collateral vessels of the Circle of Willis and therefore provides a promising model for further investigation of arteriogenic factors in transgenic mice.