title: Relationship of cerebral blood flow disturbances with brain oedema formation.
abstract: Brain oedema is an important factor which compromises maintenance of the cerebral blood flow. Conversely, primary blood flow disturbances are leading to brain oedema. The mechanisms underlying blood flow impairment by brain oedema are associated with an increased regional tissue pressure in proportion to the degree of water accumulation in the parenchyma. The release of vasoactive mediator compounds might be considered in addition. Primary disturbances of the cerebral blood flow, such as focal or global cerebral ischaemia are leading to an increased cerebral water content. A decrease of the cerebral blood flow to ca. 40% of normal or below has been found to result in the development of brain oedema. This flow threshold is in the neighbourhood of the ischaemic flow level causing irreversible tissue damage. Whereas in focal ischaemia oedema formation is a function of the severity of the flow decrease, it is a pathophysiological hallmark of early postischaemic recirculation in global cerebral ischaemia. Nevertheless, during complete interruption of cerebral blood flow translocation of interstitial fluid into the intracellular compartment occurs as manifestation of ischaemic cell swelling. Cell swelling under these conditions may, however, not necessarily indicate cell damage, but more likely a compensatory response attributable to the uptake of excitotoxic transmitters such as glutamate, and of K(+)-ions which are excessively released at the onset of ischaemia into the extracellular space. Purpose of the swelling process, thus, is clearance of extracellular fluid from this material to re-establish homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Institute of Anaesthesiology, Klinikum Grosshaden, Ludwig-Maximilians-University, München, Federal Republic of Germany.
authors.forename: R
authors.initials: R
authors.lastname: Murr
authors.forename: S
authors.initials: S
authors.lastname: Berger
authors.forename: L
authors.initials: L
authors.lastname: Schürer
authors.forename: O
authors.initials: O
authors.lastname: Kempski
authors.forename: F
authors.initials: F
authors.lastname: Staub
authors.forename: A
authors.initials: A
authors.lastname: Baethmann
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000502:physiology; D001921:Brain / Q000098:blood supply*; D001929:Brain Edema / Q000503:physiopathology*; D002545:Brain Ischemia / Q000503:physiopathology*; D005110:Extracellular Space / Q000502:physiology; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D007473:Ion Channels / Q000502:physiology
chemical_list: D007473:Ion Channels