title: Intracranial pressure elevation reduces flow through collateral vessels and the penetrating arterioles they supply. A possible explanation for 'collateral failure' and infarct expansion after ischemic stroke.
abstract: Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite stable arterial occlusion. The cause for 'collateral failure' is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by >450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for 'collateral failure' in stroke-in-progression.
authors: School of Biomedical Sciences and Pharmacy, University of Newcastle and Hunter Medical Research Institute, Callaghan, New South Wales, Australia.
authors: Daniel J
authors: DJ
authors: Beard
authors: School of Biomedical Sciences and Pharmacy, University of Newcastle and Hunter Medical Research Institute, Callaghan, New South Wales, Australia.
authors: Damian D
authors: DD
authors: McLeod
authors: School of Biomedical Sciences and Pharmacy, University of Newcastle and Hunter Medical Research Institute, Callaghan, New South Wales, Australia.
authors: Caitlin L
authors: CL
authors: Logan
authors: School of Biomedical Sciences and Pharmacy, University of Newcastle and Hunter Medical Research Institute, Callaghan, New South Wales, Australia.
authors: Lucy A
authors: LA
authors: Murtha
authors: 1] School of Biomedical Sciences and Pharmacy, University of Newcastle and Hunter Medical Research Institute, Callaghan, New South Wales, Australia [2] Computational Cardiology Laboratory, Victor Chang Cardiac Research Institute, Darlinghurst, New South Wales, Australia.
authors: Mohammad S
authors: MS
authors: Imtiaz
authors: School of Biomedical Sciences and Pharmacy, University of Newcastle and Hunter Medical Research Institute, Callaghan, New South Wales, Australia.
authors: Dirk F
authors: DF
authors: van Helden
authors: 1] School of Biomedical Sciences and Pharmacy, University of Newcastle and Hunter Medical Research Institute, Callaghan, New South Wales, Australia [2] Department of Neurology, John Hunter Hospital, Hunter New England Local Health District, New Lambton Heights, New South Wales, Australia.
authors: Neil J
authors: NJ
authors: Spratt
mesh_terms: D000818:Animals; D001160:Arterioles / Q000473:pathology / Q000503:physiopathology; D001783:Blood Flow Velocity; D002545:Brain Ischemia / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D004195:Disease Models, Animal; D006801:Humans; D019586:Intracranial Hypertension / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D051381:Rats; D020521:Stroke / Q000150:complications / Q000473:pathology / Q000503:physiopathology*