BMC Neuroscience | |
Investigation of the mechanism of dural arteriovenous fistula formation induced by high intracranial venous pressure in a rabbit model | |
Ru-Mi Wang1  Xiao-Jun Zhang1  Chang-Hua Li1  Shou-Sen Wang1  | |
[1] Department of Neurosurgery, Fuzhou General Hospital, Fujian Medical University, 156 Road Xi’erhuanbei, Fuzhou 350025, Fujian, China | |
关键词: Vascular endothelial growth factor; Hypoxia inducible factor-1α; High intracranial venous pressure; Rabbit model; Dural arteriovenous fistula; | |
Others : 1091275 DOI : 10.1186/1471-2202-15-101 |
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received in 2014-02-17, accepted in 2014-08-14, 发布年份 2014 | |
【 摘 要 】
Background
The causes of dural arteriovenous fistula have not been clearly defined. The aim of this study was to investigate the mechanism of dural arteriovenous fistula formation induced by high intracranial venous pressure using a rabbit model.
Results
By using rabbit model, dural arteriovenous fistula formation induced by high intracranial venous pressure could be produced by end-to-end and end-to-side anastomosis of the right side common carotid artery with the posterior facial vein plus ligation of the contralateral external jugular vein. As compared the post arteriovenous fistula formation among 1 week, 2 weeks, 3 weeks, and 90 days, the expression level of vascular endothelial growth factor in the 1- and 2-weeks groups was significantly higher compared with the control group, 3 weeks and 90 days groups (p ≤0.002). There was significantly higher hypoxia inducible factor-1α expression in the one week group compared with the control, 2 weeks, 3 weeks, and 90 days groups (p ≤0.002). The results of Western blotting showed that vascular endothelial growth factor expression level was highest in the 1 week group. The expression level of vascular endothelial growth factor was significantly different between all groups.
Conclusions
The results of the experiments in our rabbit model indicate that high intracranial venous pressure is a key for dural arteriovenous fistula formation. Cerebral ischemia caused by lack of cerebral perfusion pressure plays a key role in the process that leads from high intracranial venous pressure to increased hypoxia inducible factor-1α expression and then increased vascular endothelial growth factor expression.
【 授权许可】
2014 Wang et al.; licensee BioMed Central Ltd.
【 预 览 】
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