Defining the role of capillaries in “normal perfusion pressure breakthrough” and “occlusive hyperemia”

Introduction: Excision of human cerebral arteriovenous malformation (AVM) can be complicated by the formation of edema and hemorrhage in adjacent surrounding brain tissue, despite the complete excision of the malformation. Disordered autoregulation causing “normal perfusion pressure breakthrough” and obstructive of venous drainage leading to “occlusive hyperemia” have been suggested as potentially responsible. This study examined the capillaries in adjacent brain parenchyma for any structural deficiencies that would predispose to the postoperative formation of edema and hemorrhage. Methods: Ten male Sprague-Dawley rats had arteriovenous fistula created surgically in the neck which created a situation of 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 weeks after fistula formation the animals were killed and perfusion fixated with preparation for either light microscopic (stained for glial fibrillary acidic protein) or for transmission electron microscopic studies. Results: In the CA1 pyramidal cell region of the hippocampus, it was found that in the fistula animals there was an increased capillary density, with some of these vessels having absent astrocytic foot processes. Conclusions: It was concluded that these vessels had occurred as a result of neovascularization in response to chronic cerebral ischemia, and that their anatomical configuration made them prone to mechanical weakness and instability in a situation of an increase in perfusion pressure that occurs in adjacent brain parenchyma after AVM excision. We believe that this occurs in brain tissue in the vicinity of human cerebral AVMs and predisposes to the formation of edema and hemorrhage after AVM excision.