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.
Bibliographical noteFunding Information:
Ischemia has been implicated in the pathogenesis of many human neuropathies, including those associated with diabetes mellitus, the collagen vascular disorders and amyloidosis (Asbury and Johnson 1978). Common to these conditions is an abnormality of small blood vessels, including the vasa nervorum. Neuropathy also occurs in some patients with severe atherosclerotic vascular disease, particularly when there is occlusion of small arteries and arterioles (Hutchinson and Liversedge 1956; Eames and Lange 1967; Daube and Dyck 1975). Ischemia may also play a role This work was supported by the Muscular Dystrophy Association of America, Inc. and by USPHS Grant No. NS-08075. Address reprint requests and correspondence to Dr. G.J. Parry, Department of Neurology, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104, U.S.A. Dr. Parry was a Clinical Fellow of the Muscular Dystrophy Association.