Abstract
The endothelium of cerebral microvessels with tight junctions (zonula occludentes), sparce pinocytosis and absent pores or fenestrations, is an essential component of the blood-brain barrier (1,2). Freeze-injury has been one of several methods used to disrupt this barrier and to study the passage of tracer substances from the vascular to the extravascular compartment (3–10). With injury, egress of tracer is associated with disruption of endothelial membranes within the lesion and increased pinocytosis and/or canaliculus formation in viable cells at the edge of the lesion (1–3). Rarely, opening of tight junctions has been demonstrated in this and other types of injury (3).
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