Increased endoneurial fluid pressure in experimental lead neuropathy

Abstract

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.

Access options

Rent or Buy article

Get time limited or full article access on ReadCube.

from$8.99

All prices are NET prices.

References

  1. 1

    Shanthaveerappa, T. R. & Bourne, G. H. J. Anat. 96, 527–537 1962.

    CAS  PubMed  PubMed Central  Google Scholar 

  2. 2

    Olsson, Y. Peripheral Neuropathy, 190–212 (Saunders, Philadelphia, 1975).

    Google Scholar 

  3. 3

    Low, P., Marchard, P., Knox, F. & Dyck, P. J. Brain Res. 122, 373–377 (1977).

    CAS  Article  Google Scholar 

  4. 4

    Guyton, A. C., Granger, H. J. & Taylor, A. E. Physiol. Rev. 51, 527–563 (1971).

    CAS  Article  Google Scholar 

  5. 5

    Haymaker, W. & Kernohan, J. W. Medicine 28, 59–141 (1949).

    CAS  Article  Google Scholar 

  6. 6

    Thomas, P. K. & Lascelles, R. G. Q. J. Med. 35, 489–509 (1966).

    Google Scholar 

  7. 7

    Woltman, H. W. Arch. Neurol. Psychiat. 45, 680–682 (1941).

    Article  Google Scholar 

  8. 8

    Ohnishi, A. et al. J. Neuropath. exp. Neurol. (in the press).

  9. 9

    Gabbay, K. H. & Snider, J. J. Diabetes 21, 295–300 (1972).

    CAS  Article  Google Scholar 

  10. 10

    Sharma, A. K., Thomas, P. K. & Baker, R. W. R. J. Neurol. Neurosurg. Psychiat. 39, 794–802 (1976).

    CAS  Article  Google Scholar 

  11. 11

    Dyck, P. J. Arch. Neurol. 21, 73–95 (1969).

    CAS  Article  Google Scholar 

  12. 12

    Wiederhielm, C. A., Woodbury, J. W., Kirk, S. & Rushmer, R. F. Am. J. Physiol. 207, 173–176 (1964).

    CAS  Article  Google Scholar 

  13. 13

    Fowler, T. J., Danta, G. & Gilliatt, R. W. J. Neurol. Neurosurg. Psychiat. 35, 638–647 (1972).

    CAS  Article  Google Scholar 

  14. 14

    Ochoa, J., Fowler, T. J. & Gilliatt, R. W. J. Anat. 113, 433–455 (1972).

    CAS  PubMed  PubMed Central  Google Scholar 

  15. 15

    Zweifach, B. W. Circulat. Res. 34, 858–866 (1974).

    CAS  Article  Google Scholar 

  16. 16

    Sunderland, S. J. Neurol. Neurosurg. Psychiat. 39, 615–626 (1976).

    CAS  Article  Google Scholar 

Download references

Author information

Affiliations

Authors

Rights and permissions

Reprints and Permissions

About this article

Cite this article

LOW, P., DYCK, P. Increased endoneurial fluid pressure in experimental lead neuropathy. Nature 269, 427–428 (1977). https://doi.org/10.1038/269427a0

Download citation

Further reading

Comments

By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.