Premium
Impaired Motor Nerve Conduction Velocity (MNCV), Endoneurial Blood Flow (EBF), AND Acetylcholine‐Induced Vasodilation In Arterioles That Overlie The Sciatic Nerve In Diabetic Rats Is Prevented By Antioxidant Therapy
Author(s) -
Yorek M,
Coppey L,
Davidson E,
Dunlap J,
Lund D.
Publication year - 2000
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1046/j.1529-8027.2000abstracts-23.x
Subject(s) - vasodilation , diabetes mellitus , diabetic neuropathy , endocrinology , medicine , sciatic nerve , acetylcholine , nerve conduction velocity , streptozotocin
Diabetes mellitus produces marked abnormalities in motor nerve conduction, but the mechanism is not clear. In the present study we hypothesized that in the streptozotocin‐induced diabetic rat impaired vasodilator function in arterioles that provide circulation to the sciatic nerve is associated with reduced EBF and that these defects precede slowing of MNCV, and thereby may contribute to nerve dysfunction. Three days after the induction of diabetes, EBF was reduced in the diabetic rat. After 1 week of diabetes, acetylcholine‐induced vasodilation was found to be impaired and was accompanied by an increase in the superoxide level in these arterioles. These changes preceded the slowing of MNCV. Treating diabetic rats weekly with hydroxyethyl starch‐conjugated deferoxamine (Biomedical Frontiers, MPLS, MN), an iron chelator and inhibitor of hydroxyl radical formation, partially prevented the formation of superoxide in these arterioles and reduced the diabetes‐induced deficits in MNCV, EBF and acetylcholine‐induced vasodilation. We conclude that the development of diabetic neuropathy in this rat model is due in part to the production of oxygen free radicals and impairment of vascular function.