Dataset Information

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-1? 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-1? expression and then increased vascular endothelial growth factor expression.

SUBMITTER: Wang SS

PROVIDER: S-EPMC4152575 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature

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Publications

Investigation of the mechanism of dural arteriovenous fistula formation induced by high intracranial venous pressure in a rabbit model.

Wang Shou-Sen SS Li Chang-Hua CH Zhang Xiao-Jun XJ Wang Ru-Mi RM

BMC neuroscience 20140827

<h4>Background</h4>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.<h4>Results</h4>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 facia ...[more]

PMID: 25160131

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Project description:Object: Spinal dural arteriovenous fistula (SDAVF) is the most common spinal vascular shunt lesion. Although pathological changes in the SDAVF draining vein (SDAVF-DV) have been elucidated, protein changes remain enigmatic. We investigated the pathology and protein changes in the SDAVF-DV under sustained high vascular pressure. Methods: Three SDAVF-DV samples were compared with superficial temporal artery (STA) and superficial temporal vein (STV) samples as controls. Vascular structure was revealed by hematoxylin and eosin (H&E) and Masson staining; and cell distribution, extracellular matrix, and inflammation infiltration were observed by immunohistochemistry. Label-free quantitative proteomics was performed, and the peptide mixture was fractionated and analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) to identify differentially expressed proteins. Bioinformatics analysis of the differentially expressed proteins was performed using Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction (PPI) networks. Results: H&E and Masson staining showed an artery-like structure of the SDAVF-DV. Immunostaining showed that vWF+ cells were not continuous in the SDAVF-DV. Although α-SMA+ and AT1+ cells were more abundant in the STV than in the SDAVF-DV, piezo-1 expression was lower in the SDAVF-DV. The SDAVF-DV showed different distributions of elastin, COL I, and COL III. COL IV and COL VI were decreased in the SDAVF-DV, while CD45+ cells and COX-1 were increased compared with those in the controls. No differences in CD68 expression and COX-2 staining were observed between the SDAVF-DV and controls. Compared with the STA, 95 proteins were upregulated and 303 proteins were downregulated in the SDAVF-DV. The most differential GO terms in each category were the adenylate cyclase-modulating G protein-coupled receptor signaling pathway, U6 snRNP, and SH3 domain binding. The most differentially expressed KEGG protein pathway was focal adhesion. Compared with the STV, the SDAVF-DV had 158 upregulated proteins and 362 downregulated proteins. The most differential GO terms in each category were lamellipodium assembly, U6 snRNP, and SH3 domain binding; and the most differentially expressed KEGG protein pathway was dilated cardiomyopathy. PPI analysis revealed PPIs among the top 300 proteins. Conclusions: The SDAVF-DV exhibits specific pathology and protein expression changes under sustained high vascular pressure. The results of the present study provide insights into the pathogenesis of SDAVF formation at the protein level as well as a scientific foundation for further exploration of the pathophysiological mechanism of the SDAVF.

Dataset Information

Investigation of the mechanism of dural arteriovenous fistula formation induced by high intracranial venous pressure in a rabbit model.

Background

Results

Conclusions

Publications

Investigation of the mechanism of dural arteriovenous fistula formation induced by high intracranial venous pressure in a rabbit model.

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