THE endoneurial compartment of peripheral nerve is relatively inaccessible because of its small size and is maintained in a specialised environment by means of a perineurial barrier1, a blood-nerve barrier2 and a cerebrospinal fluid barrier. We have gained access to the endoneurial compartment of mammalian peripheral nerve by means of small polyethylene matrix (PEM) capsules and have recorded endoneurial fluid pressure (EFP) using an active servo null system3. The solid PEM capsules have pores of approximately 60 μm which facilitate entry of fluid into the interstices and connecting polyethylene tubing, but unlike hollow capsules4, are not invaded by connective tissue. We have used PEM capsules to make serial measurements of EFP in control and lead-fed rats and watched the pathological changes. We did this because of the prominence of endoneurial oedema in, for example, inflammatory polyradiculoneuropathy5, diabetic neuropathy6, acromegalic neuropathy7 and experimental lead8 and galactose9,10 neuropathies, and because external pressure causes segmental demyelination and even axonal degeneration of peripheral nerve fibres11. We found that EFP increased progressively in lead-fed rats and preceded the onset of fibre pathology. The time course of the increase and of fibre pathology suggests that increased EFP is a cause of segmental demyelination in lead neuropathy.
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