title: Expression of angiogenic growth factor in the rat DAVF model.
abstract: OBJECTIVE
  The precise mechanisms responsible for the development and growth of dural arteriovenous fistula (DAVF) remain unclear, but it has been hypothesized that vascular endothelial growth factor (VEGF) might be involved in the pathogenesis. The aim of this study was to examine the expression of VEGF in the rat DAVF model.
  
  
  METHODS
  Forty-five Sprague-Dawley rats were used in two experiments. In Experiment 1 (n = 20, including sham-operated controls), VEGF expression was analysed by Western blots in three different rat DAVF models: model I: common carotid artery-external jugular vein (CCA-EJV) anastomosis (n = 5); model II: sagittal sinus thrombosis and bipolar coagulation of the vein draining the transverse sinus (n = 5); model III: CCA-EJV anastomosis and bipolar coagulation of the vein draining the transverse sinus and sagittal sinus thrombosis to induce venous hypertension (n = 5). Based on the results of Experiment 1, Western blots were performed at weekly intervals 1, 2 and 3 weeks in Experiment 2 following induction of venous hypertension in model III (n = 5 at each time point and n = 5 sham controls); in addition, VEGF expression was immunohistochemically examined in the dura and the brain near the occluded sinus in five model III animals after 1 week.
  
  
  RESULTS
  In Experiment 1, Western blot analysis showed barely detectable bands with molecular weights of 45 kD, corresponding to VEGF, in the sham group, but the highest level of VEGF was induced in model III, followed by models I and II (model III>model I>model II). In Experiment 2, the expression of VEGF peaked 1 week after induction of venous hypertension in model III, decreasing in a linear fashion over 2 and 3 weeks (week 1>weeks 2 and 3). The expression of immunoreactive VEGF was restricted in the connective tissue and the endothelial layer of the dura matter, cerebral cortical tissue and neurons of the basal ganglia.
  
  
  CONCLUSIONS
  Our results strongly suggest a possible contribution of an angiogenic factor to the growth of DAVF. Venous ischemia by venous hypertension might be a mechanism for inducing up-regulation of angiogenic factor expression.
authors.affiliation: Department of Neurosurgery, Nara Medical University School of Medicine, Kashihara, Nara, Japan.
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Shin
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Nakase
authors.forename: Mitsutoshi
authors.initials: M
authors.lastname: Nakamura
authors.forename: Keiji
authors.initials: K
authors.lastname: Shimada
authors.forename: Noboru
authors.initials: N
authors.lastname: Konishi
authors.forename: Toshisuke
authors.initials: T
authors.lastname: Sakaki
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D002545:Brain Ischemia / Q000378:metabolism / Q000503:physiopathology; D020785:Central Nervous System Vascular Malformations / Q000378:metabolism* / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D003392:Cranial Sinuses / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000378:metabolism; D008297:Male; D008576:Meningeal Arteries / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015854:Up-Regulation; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*; D014690:Venous Pressure
chemical_list: D042461:Vascular Endothelial Growth Factor A