Abstract

The effect of spinal cord transection on the blood-spinal cord barrier was examined at both the light and electron microscopic levels using the vascular tracer, horseradish peroxidase (HRP). At the light microscopic level, the pattern of hemorrhage and distribution of reaction product were examined and quantified at 0.5, 1.0, and 2.0 cm proximal and distal to the transection. The morphometric data supports the hypothesis that regions of the cord that are distal to a transection, exhibit a more pronounced vascular disruption than at comparable sites proximal to the injury. This asymmetry is not apparent until 1 day after injury and is characterized by an increase in the areas of hemorrhage and reaction product at 1.0 and 2.0 cm distal to the transection as compared to similar sites proximal. In previous ultrastructural studies we demonstrate that the primary mechanism for barrier breakdown distal to a transection appeared to be transendothelial vasular transport of the tracer. In the present study, we extended these observations to sites proximal to a transection and confirmed that a similar mechanism of barrier breakdown occurs. There was no evidence for interendothelial passage of tracer across compromised tight junctions. Further studies are under differences in the intensity of this response contribute to the asymmetry in barrier permeability demonstrated by light microscopy.

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