FRACTURE FACES OF CELL-JUNCTIONS IN CEREBRAL ENDOTHELIUM DURING NORMAL AND HYPEROSMOTIC CONDITIONS

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  • 1 January 1984
    • journal article
    • research article
    • Vol. 50  (3) , 313-322
Abstract
Infusion of hyperosmolar solutions into the internal carotid artery causes opening of blood-brain barrier to macromolecules. Ultrastructural tracer studies indicate that extravasation of macro-molecules takes place primarily in segments of large penetrating cortical blood vessels. Fracture faces of cerebral endothelium in normal and hyperosmolar mannitol-treated rat brains were examined to elucidate: the organization of endothelial cell junctions in various segments of the cerebral vascular bed and the structural basis of blood-brain barrier opening in hyperosmotic conditions. In control rat brains: capillary endothelium is provided with complex networks of continuous multistranded tight junctions; continuous capillary-type tight junctions extend, although in a simpler beltlike fashion, into the endothelium of postcapillary venules; the endothelium of collecting veins possess widely discontinuous single- or double-stranded tight junctions associated with gap junctions and arteries have endothelial tight junctions containing focal discontinuities associated with gap junctions. In hyperosmolar mannitol-treated rat brains, there appeared focal distensions of compartments but no definitive structural discontinuities in capillary-type tight junctions. The blood-brain barrier consists of: an extended tight region (comprising both capillaries and postcapillary venules) and focal, potentially leaky regions (restricted to collecting veins and possibly arteries). No direct evidence for the structural basis of blood-brain barrier opening in hyperosmolar mannitol-treated rat brains was furnished.