Arachidonate-induced experimental nerve infarction

Gareth J. Parry, Mark J. Brown

Research output: Contribution to journalArticle

48 Scopus citations


Despite the clinical importance of ischemia in the pathogenesis of many human neuropathies, little is known about the effect of circulatory compromise on the structure of peripheral nerves. This results in part from the lack of an entirely satisfactory model in which to study ischemic neuropathy. We therefore injected arachidonic acid, a potent stimulus to platelet aggregation and vasoconstriction, into the femoral artery of normal rats. This resulted in the rapid onset of focal infarction of the proximal posterior tibial nerve in all animals. Distally there was evidence of Wallerian degeneration but not of primary ischemic damage. The site and nature of the infarct and the temporal sequence of the pathological changes were highly consistent. This new method is a simple and highly reproducible means of producing experimental nerve infarction.

Original languageEnglish (US)
Pages (from-to)123-133
Number of pages11
JournalJournal of the Neurological Sciences
Issue number1
StatePublished - Apr 1981

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