Publication: Cellular mechanisms of the blood-brain barrier (BBB) opening to albumin-gold complex
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Date
1993
Authors
Vorbrodt, A.W. ; Lossinsky, A.S. ; Dobrogowska, D.H. ; Wisniewski, H.M.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Cold lesion injury applied to mouse brain
and infusion of hyperosmolar L(+) arabinose solution
into rat carotid artery were used as extravascular and
intravascular insults, respectively, leading to blood-brain
barrier (BBB) disruption. To study the cellular
mechanisms of the BBB opening, heterologous (bovine)
and homologous (mouse and rat) albumin-gold
complexes were used as a macromolecular tracer. Both
insults rapidly induce the leakage of the blood-borne
tracer, although the mechanisms of their action appear to
be different. Cold lesion injury (cryoinjury) leads to the
opening of interendothelial junctions and concomitantly
to an endothelial-platelet reaction. This insult is followed
by irreversible changes such as desquamation,
degeneration and necrosis of the endothelial lining,
formation of thromboses, and disruption of the basement
membrane. Osmotic opening occurs through at least the
four mechanisms (presumably temporal and reversible)
that follow: 1) opening of a part of the junctional
complexes; 2) the formation of transendothelial openings
(interendothelial gaps or penetrating, crater-like
excavations); 3) the uncontrolled passage of tracer
particles through the cytoplasm of the injured
endothelial cells; and 4) segmental denudation of the
endothelial lining. The basement membrane appears to
represent one of the main obstacles in the passage of
blood-borne albumin-gold complexes to the extracellular
space in the brain parenchyma.
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