title: Normal perfusion pressure breakthrough: the role of capillaries.
abstract: Excision of human cerebral arteriovenous malformations (AVMs) can be complicated by postoperative edema and hemorrhage in adjacent brain tissue, despite the complete excision of the malformation. Various theories have purported to explain the hemodynamic basis for this predisposition, 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 venous circulations in this scenario, but rather examined the capillaries in adjacent brain parenchyma for any structural deficiencies that would predispose the brain to the postoperative formation of edema and hemorrhage. Arteriovenous fistulas (AVFs) were created surgically in the 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 weeks after AVF formation the animals were killed and perfusion fixed. Their brain tissue was prepared for light microscopic studies by staining for glial fibrillary acidic protein or for transmission electron microscopy. In the CA1 pyramidal cell region of the hippocampus, it was found that in the animals with AVFs there was increased capillary density and absent astrocytic foot processes in some of these vessels. It was concluded that these vessels had developed as a result of neovascularization in response to chronic cerebral ischemia and that their anatomical configuration made them prone to mechanical weakness and instability following the increase in perfusion pressure that occurs in adjacent brain parenchyma after AVM excision. The authors believe that this study pinpoints a structural accompaniment to the hemodynamic changes that occur in brain tissue in the vicinity of cerebral AVMs that predispose these areas to the formation of edema and hemorrhage after AVM excision.
authors.affiliation: Department of Surgery, University of Sydney, New South Wales, Australia.
authors.forename: L H
authors.initials: LH
authors.lastname: Sekhon
authors.forename: M K
authors.initials: MK
authors.lastname: Morgan
authors.forename: I
authors.initials: I
authors.lastname: Spence
mesh_terms: D000818:Animals; D001164:Arteriovenous Fistula / Q000150:complications; D001253:Astrocytes / Q000648:ultrastructure; D001921:Brain / Q000098:blood supply*; D001929:Brain Edema / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D002545:Brain Ischemia / Q000209:etiology / Q000473:pathology; D002196:Capillaries / Q000473:pathology / Q000503:physiopathology; D016022:Case-Control Studies; D002543:Cerebral Hemorrhage / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D002550:Cerebral Veins / Q000473:pathology / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D002908:Chronic Disease; D004396:Coloring Agents; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D006624:Hippocampus / Q000098:blood supply / Q000473:pathology; D006940:Hyperemia / Q000209:etiology / Q000473:pathology; D002538:Intracranial Arteriovenous Malformations / Q000601:surgery*; D007427:Intracranial Pressure; D008297:Male; D008854:Microscopy, Electron; D009333:Neck / Q000098:blood supply; D009389:Neovascularization, Pathologic / Q000209:etiology / Q000473:pathology; D011183:Postoperative Complications; D017966:Pyramidal Cells / Q000648:ultrastructure; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D004396:Coloring Agents; D005904:Glial Fibrillary Acidic Protein