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

摘要: It is well-known that ischemia causes disruption of the blood-brain barrier (BBB), which leads to formation vasogenic brain edema. One major mechanism BBB opening enhanced pinocytotic vesicle may be induced after transient focal by several mechanisms, including nitric oxide production, release neurotransmitters, inflammatory mediators and hemodynamic alterations. In present study we sought characterize extent pinocytosis in cerebral endothelium during both ischemia/reperfusion (I/R) elevated intravascular pressure. Transient was for 1 hour with 24 hours reperfusion using filament occlusion model male Wistar rats, occluded middle arteries (MCAs) were dissected mounted on glass cannulas an arteriograph chamber. This system allowed control over pressure, measurement lumen diameter perfusion various tracers (Lucifer Yellow horseradish peroxidase) transcellular transport quantification transmission electron microscopy. I/R found increase 166% basolaterally without a change apically compared non-ischemic MCAs at 75 mmHg (p less than 0.01). Similarly, acute pressure 200 caused 78% apical 0.05) non-significant 42% basolaterally. These results confirmed permeability measurements Lucifer demonstrate elevations enhance endothelial cell pinocytosis. The basolateral suggests efflux mechanisms transporting substances from blood. addition, since occurred isolated vitro influence metabolic or neuronal factors, these findings primary stimulus cells.