title: Slowing of motor nerve conduction velocity in streptozotocin-induced diabetic rats is preceded by impaired vasodilation in arterioles that overlie the sciatic nerve.
abstract: 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 (STZ)-induced diabetic rat impaired vasodilator function in arterioles that provide circulation to the region of the sciatic nerve is associated with reduced endoneural blood flow (EBF) and that these defects precede slowing of motor nerve conduction velocity, and thereby may contribute to nerve dysfunction. As early as three days after the induction of diabetes endoneural blood flow was reduced in the STZ-induced diabetic rat. Furthermore, after 1 week of diabetes acetylcholine-induced vasodilation was found to be impaired. This was accompanied by an increase in the superoxide level in arterioles that provide circulation to the region of the sciatic nerve as well as changes in the level of other markers of oxidative stress including an increase in serum levels of thiobarbituric acid reactive substances and a decrease in lens glutathione level. In contrast to the vascular related changes that occur within 1 week of diabetes, motor nerve conduction velocity and sciatic nerve Na+/K+ ATPase activity were significantly reduced following 2 and 4 weeks of diabetes, respectively. These studies demonstrate that changes in vascular function in the STZ-induced diabetic rat precede the slowing of motor nerve conduction velocity (MNCV) and are accompanied by an increase in superoxide levels in arterioles that provide circulation to the region of the sciatic nerve.
authors.affiliation: Veterans Affairs Medical Center, Diabetes Endocrinology Research Center and Department of Internal Medicine, University of Iowa, Iowa City 52246, USA.
authors.forename: L J
authors.initials: LJ
authors.lastname: Coppey
authors.forename: E P
authors.initials: EP
authors.lastname: Davidson
authors.forename: J A
authors.initials: JA
authors.lastname: Dunlap
authors.forename: D D
authors.initials: DD
authors.lastname: Lund
authors.forename: M A
authors.initials: MA
authors.lastname: Yorek
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D015415:Biomarkers / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D003929:Diabetic Neuropathies / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology; D005632:Fructose / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D007294:Inositol / Q000378:metabolism; D008297:Male; D009046:Motor Neurons / Q000502:physiology*; D009431:Neural Conduction / Q000502:physiology*; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow; D012584:Sciatic Nerve / Q000098:blood supply* / Q000503:physiopathology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013012:Sorbitol / Q000378:metabolism; D013481:Superoxides / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D015415:Biomarkers; D017392:Thiobarbituric Acid Reactive Substances; D013481:Superoxides; D005632:Fructose; D007294:Inositol; D013012:Sorbitol; D000254:Sodium-Potassium-Exchanging ATPase; D005978:Glutathione; D000109:Acetylcholine