OBJECTIVE: To investigate the cause of intracranial dural arteriovenous fistula, focusing on the role of angiogenic factors and local chronic brain hypoperfusion. METHODS: One hundred twenty rats were assigned to 4 groups: group A (n = 35), the venous hypertension group; group B (n = 35), the venous hypertension and sinus thrombosis group; group C (n = 25), the sham operation group; and group D (n = 25), the sagittal sinus thrombosis group. Mean arterial pressure, sinus pressure, cerebral perfusion pressure, and regional cerebral blood flow were monitored during the operation and 1, 2, 4, and 12 weeks after the operation. Immunohistological and Western blot analyses of vascular endothelial growth factor and matrix metalloproteinase-9 were performed, and perfusion magnetic resonance imaging of the brain was performed during the follow-up. RESULTS: In groups A and B, a decreased cerebral perfusion pressure from 98.25 +/- 5.83 to 69.35 +/- 6.87 mm Hg and from 99.32 +/- 4.19 to 64.79 +/- 6.71 mm Hg was detected, respectively. Concurrently, the cerebral blood flow obviously decreased. In the right occipital lobe only, the hypoperfusion state lasted for 12 weeks. Immunohistological staining of vascular endothelial growth factor was persistently positive in the right occipital lobe, arachnoid membrane, and nearby dura mater. Angiogenesis in the dura mater was prominent 12 weeks after the operation in groups A and B. Western blotting showed high expression of vascular endothelial growth factor and matrix metalloproteinase-9 in the dura mater in groups A and B. CONCLUSION: Chronic local hypoperfusion secondary to intracranial sinus high pressure seemed to be the main cause of angiogenesis in the dura mater, leading to the formation of intracranial dural arteriovenous fistula.
OBJECTIVE: To investigate the cause of intracranial dural arteriovenous fistula, focusing on the role of angiogenic factors and local chronic brain hypoperfusion. METHODS: One hundred twenty rats were assigned to 4 groups: group A (n = 35), the venous hypertension group; group B (n = 35), the venous hypertension and sinus thrombosis group; group C (n = 25), the sham operation group; and group D (n = 25), the sagittal sinus thrombosis group. Mean arterial pressure, sinus pressure, cerebral perfusion pressure, and regional cerebral blood flow were monitored during the operation and 1, 2, 4, and 12 weeks after the operation. Immunohistological and Western blot analyses of vascular endothelial growth factor and matrix metalloproteinase-9 were performed, and perfusion magnetic resonance imaging of the brain was performed during the follow-up. RESULTS: In groups A and B, a decreased cerebral perfusion pressure from 98.25 +/- 5.83 to 69.35 +/- 6.87 mm Hg and from 99.32 +/- 4.19 to 64.79 +/- 6.71 mm Hg was detected, respectively. Concurrently, the cerebral blood flow obviously decreased. In the right occipital lobe only, the hypoperfusion state lasted for 12 weeks. Immunohistological staining of vascular endothelial growth factor was persistently positive in the right occipital lobe, arachnoid membrane, and nearby dura mater. Angiogenesis in the dura mater was prominent 12 weeks after the operation in groups A and B. Western blotting showed high expression of vascular endothelial growth factor and matrix metalloproteinase-9 in the dura mater in groups A and B. CONCLUSION: Chronic local hypoperfusion secondary to intracranial sinus high pressure seemed to be the main cause of angiogenesis in the dura mater, leading to the formation of intracranial dural arteriovenous fistula.