ABSTRACT
Little is known about the characteristics of the hemostatic system responses to injury in the
central nervous system (CNS); however, hemostatic responses in the brain have been
posited to differ significantly from other vascular beds. Differences relate, at least in
part, to the uniqueness of the brain and spinal cord in terms of tissue architecture, cellular
composition, and function (1). The microvascular beds of the CNS are unique. Brain
capillaries are ternary vascular complexes consisting of an endothelial cell lining that is
separated from the astrocyte end-feet, which are also components of capillaries, by the
basal lamina or extracellular matrix (ECM). Astrocytes communicate with and support
neurons that are subserved by the microvasculature. Arterioles have a myointimal layer
that can regulate blood flow. Pericytes are located around or are embedded in the myoin-
timal layer and are near the matrix (2,3). The two permeability barriers of the microvas-
culature are represented by the interendothelial tight junctions (blood-brain barrier) and
the subtending ECM/basal lamina. Both barriers derive from the interaction of the endothelial cells and astrocytes during development and require these cells for their integrity
(4-8). The basal lamina consists of laminins, collagen type IV, fibronectin, heparan
sulfate proteoglycans, nidogen, entactin, and other glycoproteins (GPs). These cellular
and matrix relations are important for CNS vascular function, although their relation to
hemostasis is not well understood.
