Blood-brain barrier breakdown in XXXX and @entity1313 .

@entity7202 @entity2162 @entity295 @entity19642 @entity1313 @entity75 @entity4 @entity11177 @entity7 @entity816 @entity3951 @entity420 @entity528
@entity75 is associated with breakdown of the blood-brain barrier and @entity4 . These features are also common properties of @entity1313 . Perimicrovessel @entity4 , disruption of associated astrocyte end feet and @entity528 occur in a porcine model of acute @entity75 . The adrenergic system has been implicated in the inflammatory response to @entity295 and may play a role in controlling blood-brain barrier permeability, since the @entity2162 agonist @entity19642 inhibits perimicrovessel @entity4 formation whereas the alpha1-adrenoceptor agonist @entity7202 provokes it. Electron microscopy revealed tight junction opening in high-grade @entity816 microvessels. Expression of the tight junction protein @entity11177 is reduced in these microvessels and this reduction is inversely correlated with the degree of @entity4 . Normal astrocytes secrete factors that induce barrier properties in endothelial cells, whereas high-grade @entity816 secrete @entity7 , which stimulates angiogenesis, down regulates @entity11177 and increases endothelial cell permeability. The water channel protein @entity3951 is normally expressed in astrocyte foot processes around cerebral microvessels. Its expression is massively up-regulated in high-grade @entity816 and around @entity420 . There is a significant correlation between @entity3951 expression and the degree of @entity4 , but it is not clear whether increased @entity3951 expression enhances @entity4 formation or clearance. These results suggest that the pathophysiology of @entity4 is multifactorial, but that there may be common processes operating regardless of the aetiology.
