Abstract
The genesis of edema in the central nervous system (CNS) parallels changes in the blood-brain barrier (BBB). The anatomical seat of the BBB is located in the endothelium of the CNS. The presence of interendothelial tight junctions and the low rate of pinocytotic (vesicular) activity constitute the main features of the BBB. Based on the fate of intravascular horseradish peroxidase (HRP), mechanisms of edema genesis have been elucidated. A vesicular mechanism appears to play a role in the formation of edema in the injured (compression) spinal cord.Following spinal cord compression injury (200 gm/cm2-5 min), circulating HRP traversed the endothelium and entered extracellular spaces of the cord parenchyma (Fig. 1). Most microvessels in the injured and adjacent areas exhibited an intensified endothelial vesicular uptake of HRP (Figs. 1, 3). In areas of intense endothelial vesicular activity, the frequency of microtubules (MT) appeared to be increased (Figs. 2, 3).
Published Version
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