Arachidonate-induced experimental nerve infarction

Gareth J. Parry; Mark J. Brown

doi:10.1016/0022-510X(81)90047-2

Arachidonate-induced experimental nerve infarction

Gareth J. Parry, Mark J. Brown

Neurology

Research output: Contribution to journal › Article › peer-review

50 Scopus citations

Abstract

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 language	English (US)
Pages (from-to)	123-133
Number of pages	11
Journal	Journal of the Neurological Sciences
Volume	50
Issue number	1
DOIs	https://doi.org/10.1016/0022-510X(81)90047-2
State	Published - Apr 1981

Bibliographical note

Funding 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.

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title = "Arachidonate-induced experimental nerve infarction",

abstract = "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.",

author = "Parry, {Gareth J.} and Brown, {Mark J.}",

note = "Funding 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.",

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AU - Brown, Mark J.

N1 - Funding 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.

PY - 1981/4

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N2 - 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.

AB - 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.

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Arachidonate-induced experimental nerve infarction

Abstract

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