title: Microvascular shunts in the pathogenesis of high intracranial pressure.
abstract: Hyperemia in the infarcted brain has been -suggested for years by "red veins" reported by neurosurgeons, shunt peaks in radioactive blood flow clearance curves, and quantitative cerebral blood flow using stable xenon CT. Histological characterization of infarcted brain revealed capillary rarefaction with prominent microvascular shunts (MVS). Despite abundant histological evidence, the presence of cerebrovascular shunts have been largely ignored, perhaps because of a lack of physiological evidence demonstrating the transition from capillary flow to MVS flow. Our studies have shown that high intracranial pressure induces a transition from capillary to microvascular shunt flow resulting in cerebral hypoperfusion, tissue hypoxia and brain edema, which could be delayed by increasing cerebral perfusion pressure. The transition from capillary to microvascular shunt flow provides for the first time a physiological basis for evaluating the optimal cerebral perfusion pressure with increased intracranial pressure. It also provides a physiological basis for evaluating the effectiveness of various drugs and therapies in reducing intracranial pressure and the development of brain edema and tissue hypoxia after brain injury and ischemia. In summary, the clear-cut demonstration of the transition from capillary to MVS flow provides an important method for evaluating various therapies for the treatment of brain edema and loss of autoregulation.
authors.affiliation: Department of Neurosurgery, University of New Mexico, Albuquerque, NM, USA. enemoto@salud.unm.edu
authors.forename: Edwin M
authors.initials: EM
authors.lastname: Nemoto
authors.forename: Denis
authors.initials: D
authors.lastname: Bragin
authors.forename: Martina
authors.initials: M
authors.lastname: Stippler
authors.forename: Suguna
authors.initials: S
authors.lastname: Pappu
authors.forename: Jessica
authors.initials: J
authors.lastname: Kraynik
authors.forename: Tracey
authors.initials: T
authors.lastname: Berlin
authors.forename: Howard
authors.initials: H
authors.lastname: Yonas
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D004195:Disease Models, Animal; D004906:Erythrocyte Count; D007839:Functional Laterality; D019586:Intracranial Hypertension / Q000503:physiopathology*; D007427:Intracranial Pressure / Q000502:physiology*; D017078:Laser-Doppler Flowmetry; D008297:Male; D008833:Microcirculation / Q000502:physiology*; D009249:NADP; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D009249:NADP
references.citation: Neurocrit Care. 2006;4(1):8-13
references.pmid: 16498188
references.citation: Neurosurg Focus. 2003 Dec 15;15(6):E5
references.pmid: 15305841
references.citation: J Neurotrauma. 2007;24 Suppl 1:S59-64
references.pmid: 17511547
references.citation: J Neurotrauma. 2011 May;28(5):775-85
references.pmid: 21395499
references.citation: J Trauma. 1990 Aug;30(8):933-40; discussion 940-1
references.pmid: 2117669
references.citation: J Neurosurg. 1975 Oct;43(4):385-98
references.pmid: 808593
references.citation: Acta Anaesthesiol Scand. 2002 Sep;46(8):929-41
references.pmid: 12190792
references.citation: Prog Brain Res. 1972;35:411-32
references.pmid: 5009562
references.citation: Acta Neurochir Suppl. 2008;101:131-6
references.pmid: 18642647