High-flow angiopathy: cerebral blood vessel changes in experimental chronic arteriovenous fistula.
Profound vascular damage secondary to high-flow extracranial states has been well characterized. However, changes in cerebral vasculature secondary to high-flow states have not been studied. To determine changes related to high-flow states in cerebral vessels, a rabbit model was developed in which torrential flow was created in the vertebrals, carotids, basilar, and vessels of the circle of Willis by means of a carotid-jugular shunt after ligation of the proximal carotid. The clinical, angiographic, and histologic changes noted in the animal model include: abrupt clinical deterioration after a variable interval with some animals developing ptosis, afferent vessel dilatation and the development of prominent anastomotic channels, variable cerebral vessel histopathology--related to duration and relative proximity to the shunt--affecting all three vessel layers, plump, irregular, and clumped endothelium, denuded with adherent platelets, irregular, duplicated, and thinned internal elastic membrane, frayed with invasion of the intima by mesenchymal cells, vacuolization and necrosis of the media muscle, and invasion of adventitia by foreign cells and small blood vessels. The high-flow angiopathy seen in this model may help explain vascular changes associated with high-flow cerebral vascular lesions, as well as other types of vascular damage.
D000818:Animals; D001164:Arteriovenous Fistula / Q000503:physiopathology; D001783:Blood Flow Velocity; D002196:Capillaries / Q000473:pathology; D002339:Carotid Arteries; D002533:Cerebral Angiography; D002536:Cerebral Arteries / Q000473:pathology / Q000503:physiopathology*; D004727:Endothelium / Q000473:pathology; D007601:Jugular Veins; D011817:Rabbits