title: Blood-brain barrier function in intracerebral hemorrhage.
abstract: In this paper, we review current knowledge on blood-brain barrier (BBB) dysfunction following intracerebral hemorrhage (ICH). BBB disruption is a hallmark of ICH-induced brain injury. Such disruption contributes to edema formation, the influx of leukocytes, and the entry of potentially neuroactive agents into the perihematomal brain, all of which may contribute to brain injury. A range of factors have been implicated in inducing BBB disruption, including inflammatory mediators (e.g., cytokines and chemokines), thrombin, hemoglobin breakdown products, oxidative stress, complement, and matrix metalloproteinases. While there is interaction between some of these mediators, it is probable that prevention of ICH-induced BBB disruption will involve blocking multiple pathways or blocking a common end pathway (e.g., by stabilizing tight junction structure). While the effects of ICH on BBB passive permeability have been extensively examined, effects on other 'barrier' properties (metabolic and transport functions) have been less well-studied. However, recent data suggests that ICH can affect transport and that this may help protect the BBB and the brain. Indeed, it is possible in small bleeds that BBB disruption may be beneficial, and it is only in the presence of larger bleeds that disruption has detrimental effects.
authors.affiliation: Department of Neurosurgery, University of Michigan Medical School, Ann Arbor, MI 48109-2200, USA. rkeep@umich.edu
authors.forename: R F
authors.initials: RF
authors.lastname: Keep
authors.forename: J
authors.initials: J
authors.lastname: Xiang
authors.forename: S R
authors.initials: SR
authors.lastname: Ennis
authors.forename: A
authors.initials: A
authors.lastname: Andjelkovic
authors.forename: Y
authors.initials: Y
authors.lastname: Hua
authors.forename: G
authors.initials: G
authors.lastname: Xi
authors.forename: J T
authors.initials: JT
authors.lastname: Hoff
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects / Q000503:physiopathology*; D002543:Cerebral Hemorrhage / Q000188:drug therapy / Q000473:pathology*; D006801:Humans