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The Influence of Indomethacin and Guanethidine on Experimental Streptozotocin Diabetic Neuropathy

Published online by Cambridge University Press:  18 September 2015

Douglas W. Zochodne*
Affiliation:
Peripheral Nerve Research Laboratory, Queen’s University, Kingston (now at University of Calgary)
Lam T. Ho
Affiliation:
Peripheral Nerve Research Laboratory, Queen’s University, Kingston (now at University of Calgary)
*
Room 182-A, Heritage Medical Research Building, 3330 Hospital Drive N.W., Calgary, Alberta, Canada T2N 4N1
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Abstract:

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In diabetic animals, reduced endoneurial perfusion and oxygen content have been linked to neuropathic abnormalities and might be amenable to pharmacological manipulation. In streptozotocin-induced diabetic rats, we studied the influence of guanethidine adrenergic sympathectomy, indomethacin treatment and a combined strategy on: serial in vivo motor and sensory conduction, resistance to ischemic conduction failure, in vitro myelinated and unmyelinated conduction, endoneurial perfusion and endoneurial oxygen tension. Unlike previous work diabetic animals had normal endoneurial perfusion but lower endoneurial oxygen tensions after six months of hyperglycemia. Guanethidine worsened sensory conduction despite lower microvascular resistance and an improvement in endoneurial oxygen tension. In contrast, indomethacin improved motor and sensory conduction but not oxygen tension. These studies do not support a linkage between conduction deficits and early endoneurial microangiopathy in experimental diabetes. Indomethacin, or related agents may offer a new therapeutic approach toward diabetic neuropathy through a mechanism independent of the endoneurial microvasculature.

Type
Articles
Copyright
Copyright © Canadian Neurological Sciences Federation 1992

References

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