ARACHIDONATE-INDUCED EXPERIMENTAL NERVE INFARCTION

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 partly from the lack of an entirely satisfactory model in which to study ischemic neuropathy. Arachidonic acid, a potent stimulus to platelet aggregation and vasoconstriction, was injected into the femoral artery of normal rats, resulting 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.