RELATIONSHIP OF CEREBRAL BLOOD-FLOW DISTURBANCES WITH BRAIN EDEMA FORMATION

Brain oedema is an important factor which compromises maintenance of t he cerebral blood flow. Conversely, primary blood flow disturbances ar e leading to brain oedema. The mechanisms underlying blood flow impair ment by brain oedema are associated with an increased regional tissue pressure in proportion to the degree of water accumulation in the pare nchyma. The release of vasoactive mediator compounds might be consider ed in addition. Primary disturbances of the cerebral blood flow, such as focal or global cerebral ischaemia are leading to an increased cere bral water content. A decrease of the cerebral blood flow to ca. 40% o f 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 ischae mia oedema formation is a function of the severity of the flow decreas e, it is a pathophysiological hallmark of early postischaemic recircul ation in global cerebral ischaemia. Nevertheless, during complete inte rruption of cerebral blood flow translocation of interstitial fluid in to 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 respo nse attributable to the uptake of excitotoxic transmitters, such as gl utamate, and of K+-ions which are excessively released at the onset of ischaemia into the extracellular space. Purpose of the swelling proce ss, thus, is clearance of extracellular fluid from this material to re -establish homeostasis. Brain oedema in focal cerebral ischaemia is in itially of cytotoxic nature, whereas disruption of the blood-brain bar rier evolves with a delay of few days. On the other hand, opening of t he blood-brain barrier in global cerebral ischaemia is characteristic of the postischaemic recirculation phase and, probably a function of s everity of the reactive hyperaemia. Treatment of cerebral ischaemia, i .e., reestablishment of a normal blood flow to the brain must consider the specific significance of the various pathophysiological phenomena of ischaemic brain oedema, such as cell swelling and opening of the b lood-brain barrier.