title: Investigation of the mechanism of dural arteriovenous fistula formation induced by high intracranial venous pressure in a rabbit model.
abstract: 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.
authors.affiliation: Department of Neurosurgery, Fuzhou General Hospital, Fujian Medical University, 156 Road Xi'erhuanbei, Fuzhou 350025, Fujian, China. wshsen@126.com.
authors.forename: Shou-Sen
authors.initials: SS
authors.lastname: Wang
authors.forename: Chang-Hua
authors.initials: CH
authors.lastname: Li
authors.forename: Xiao-Jun
authors.initials: XJ
authors.lastname: Zhang
authors.forename: Ru-Mi
authors.initials: RM
authors.lastname: Wang
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002545:Brain Ischemia / Q000150:complications / Q000503:physiopathology; D020785:Central Nervous System Vascular Malformations / Q000209:etiology* / Q000503:physiopathology*; D002561:Cerebrovascular Disorders / Q000150:complications* / Q000503:physiopathology*; D004195:Disease Models, Animal; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D011817:Rabbits; D011897:Random Allocation; D013997:Time Factors; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D014690:Venous Pressure
chemical_list: D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D042461:Vascular Endothelial Growth Factor A