Transcellular transport as a mechanism of blood-brain barrier disruption during stroke.

It is well-known that ischemia causes disruption of the blood-brain barrier (BBB), which leads to the formation of vasogenic brain edema. One major mechanism of BBB opening is enhanced pinocytotic vesicle formation that may be induced after transient focal ischemia by several mechanisms, including nitric oxide production, release of neurotransmitters, inflammatory mediators and hemodynamic alterations. In the present study we sought to characterize the extent of pinocytosis in cerebral endothelium during both ischemia/reperfusion (I/R) and elevated intravascular pressure.