Endoneurial vascular permeability in degenerating and regenerating peripheral nerves.

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The endoneurial blood vessels of rodents are normally impermeable to proteins but they become permeable when the axons in the nerve have been severed. In this investigation, the increased permeability is examined in relation to the occurrence or absence of axonal regeneration. The sciatic and hypoglossal nerves of rats were either ligated and transected so that axons would not regenerate, or crushed and then allowed to regenerate. Changes in vascular permeability to fluorescently labelled albumin were examined in the endoneurium distal to the sites of both types of injury at postoperative intervals of 1–21 days. When axonal regeneration was prevented, the endoneurial vessels remained impermeable to the protein tracer until the 6th day. They then became permeable throughout the distal stump and remained so for the remainder of the experimental period. When axons regenerated, there was a considerably more intense exudation of the tracer in the distal segment of the nerve. The zone of greatly increased endoneurial vascular permeability advanced along the nerve at the same rate as that of the most rapidly regenerating axons, as observed in silver-stained sections. It is suggested that in the absence of regenerating axons, vascular permeability may be initiated by products of Wallerian degeneration. The greater permeability in regenerating nerves may be induced by vasoactive substances secreted by growth-cones. The results support a hypothesis in which it is maintained that the presence of plasma proteins around growth-cones is necessary for the occurrence of axonal regeneration. The further increase in permeability caused by the most rapidly elongating axons may assist the regenerative process by making larger quantities of plasma proteins available to other growing axons.