Excision of human cerebral arteriovenous malformations (AVMs) can be c
omplicated by postoperative edema and hemorrhage in adjacent brain tis
sue, despite the complete excision of the malformation. Various theori
es have pur ported to explain the hemodynamic basis for this predispos
ition, including disordered autoregulation causing ''normal perfusion
pressure breakthrough'' and obstruction of venous drainage leading to
''occlusive hyperemia.'' This study did not evaluate the arterial or v
enous circulations in this scenario, but rather examined the capillari
es in adjacent brain parenchyma for any structural deficiencies that w
ould predispose the brain to the postoperative formation of edema and
hemorrhage. Arteriovenous fistulas (AVFs) were created surgically in t
he necks of 10 male Sprague-Dawley rats, which caused chronic cerebral
hypoperfusion with a reduction in cerebral blood flow of between 25%
and 50%. Ten age-matched animals were used as controls. Twenty-six wee
ks after AVF formation the animals were killed and perfusion fixed. Th
eir brain tissue was prepared for light microscopic studies by stainin
g for glial fibrillary acidic protein or for transmission electron mic
roscopy. In the CAI pyramidal cell region of the hippocampus, it was f
ound that in the animals with AVFs there was increased capillary densi
ty and absent astrocytic foot processes in some of these vessels. It w
as concluded that these vessels had developed as a result of neovascul
arization in response to chronic cerebral ischemia and that their anat
omical configuration made them prone to mechanical weakness and instab
ility following the increase in perfusion pressure that occurs in adja
cent brain parenchyma after AVM excision. The authors believe that thi
s study pinpoints a structural accompaniment to the hemodynamic change
s that occur in brain tissue in the vicinity of cerebral AVMs that pre
dispose these areas to the formation of edema and hemorrhage after AVM
excision.