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Effect of Antioxidant Treatment of Streptozotocin-Induced Diabetic Rats on Endoneurial Blood Flow, Motor Nerve Conduction Veloci

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Effect of Antioxidant Treatment of Streptozotocin-Induced Diabetic Rats on Endoneurial Blood Flow, Motor Nerve Conduction Veloci Effect of Antioxidant Treatment of Streptozotocin-Induced Diabetic Rats on Endoneurial Blood Flow, Motor Nerve Conduction Velocity, and Vascular Reactivity of Epineurial Arterioles of the Sciatic Nerve Lawrence J. Coppey, Jill S. Gellett, Eric P. Davidson, Joyce A. Dunlap, Donald D. Lund, and Mark A. Yorek We have shown that diabetes-induced reduction in en- vascular and neural complications. Diabetes 50: doneurial blood flow (EBF) and impaired endothelium- 1927–1937, 2001 dependent vascular relaxation precede slowing of motor nerve conduction velocity (MNCV) and decreased sci- -atic nerve Na؉/K؉ ATPase activity. Furthermore, vascu lar dysfunction was accompanied by an accumulation of xidative stress has been defined as a distur- superoxide in arterioles that provide circulation to the bance in the balance between the production of sciatic nerve. In the present study, we examined the reactive oxygen species—oxygen-free radicals, effect that treatment of streptozotocin-induced diabetic i.e., hydroxyl radical (OH•), superoxide anion rats with antioxidants has on vascular and neural func- O• (O 2–), and H2O2—and antioxidant defenses, which may tion. Diabetic rats were treated with 0.5% ␣-lipoic acid lead to tissue injury (1). Oxidative stress and the damage as a diet supplement or with hydroxyethyl starch defer- that it causes have been implicated in a wide variety of oxamine (HES-DFO) by weekly intravenous injections natural and pathological processes, including aging, can- at a dose of 75 mg/kg. The treatments significantly improved diabetes-induced decrease in EBF, acetylcho- cer, diabetes, atherosclerosis, neurological degeneration, line-mediated vascular relaxation in arterioles that pro- schizophrenia, and autoimmune disorders, such as arthri- vide circulation to the region of the sciatic nerve, and tis (2). Oxidative stress can be derived from a variety of MNCV. The treatments also reduced the production of sources and includes events such as the production of superoxide by the aorta and superoxide and peroxyni- reactive oxygen species by mitochondrial oxidative phos- trite by arterioles that provide circulation to the region phorylation, ionizing radiation exposure, and metabolism of the sciatic nerve. Treating diabetic rats with ␣-lipoic of exogenous compounds (2). In addition to these sources acid prevented the diabetes-induced increase in thio- of oxidative stress, a decrease in the activity of antioxidant barbituric acid–reactive substances in serum and signif- enzymes, such as superoxide dismutase, glutathione per- icantly improved lens glutathione levels. In contrast, oxidase, and catalase, may contribute to oxidative stress treating diabetic rats with HES-DFO did not prevent diabetes-induced changes of either of these markers of in some disease states (3). oxidative stress. Diabetes-induced increase in sciatic There is substantial evidence that oxidative stress oc- nerve conjugated diene levels was not improved by curs during the course of diabetes and is believed to be a treatment with either ␣-lipoic acid or HES-DFO. Treat- contributing factor in the development of endothelial ing diabetic rats with ␣-lipoic acid but not HES-DFO dysfunction and vascular disease (4–9). Studies using -partially improved sciatic nerve Na؉/K؉ ATPase activity several types of diabetic rodent models have demon and myo-inositol content. The increase in sciatic nerve strated impaired endothelial-dependent relaxation in both sorbitol levels in diabetic rats was unchanged by either conduit and resistance arteries (4). Various factors have treatment. These studies suggest that diabetes-induced been proposed to contribute to this defect, including oxidative stress and the generation of superoxide may increased release of an endothelium-derived constricting be partially responsible for the development of diabetic factor, increased protein kinase C activity, inhibition of Naϩ/Kϩ ATPase activity, a deficiency of substrate or cofactors for nitric oxide synthase, increased quenching of From the Diabetes Endocrinology Research Center, Veterans Affairs Medical nitric oxide by advanced glycosylation end products, de- Center, and the Department of Internal Medicine, University of Iowa, Iowa City, Iowa. creased nitric oxide release and decreased nitric oxide Address correspondence and reprint requests to Dr. Mark A. Yorek, 3 E. 17 availability caused by increased quenching by superoxide, Veterans Affairs Medical Center, Iowa City, IA 52246. E-mail: [email protected]. Received for publication 25 October 2000 and accepted in revised form 2 and subsequent formation of peroxynitrite (4). Studies May 2001. showing that treatment with antioxidants prevents diabe- EBF, endoneurial blood flow; EDHF, endothelium-derived hyperpolarizing tes and hyperglycemia-induced impairment of endotheli- factor; GSH, glutathione; HES-DFO, hydroxyethyl starch deferoxamine; MNCV, motor nerve conduction velocity; PSS, physiological saline solution; um-dependent relaxation suggest that oxidative stress is a RLU, relative light unit; TBARS, thiobarbituric acid–reactive substance. major factor in the development of diabetic vascular DIABETES, VOL. 50, AUGUST 2001 1927 VASCULAR DYSFUNCTION IN DIABETIC NEUROPATHY disease (4,10–23). In addition, treatment of streptozotocin- starch at the same concentration as in the HES-DFO solution. Analysis of induced diabetic rats with antioxidants has demonstrated these experiments revealed that hydroxyethyl starch treatment alone had no effect on any of the evaluations made in these studies (data not shown). All that oxidative stress and vascular dysfunction may be a studies using HES-DFO treatments were conducted 3–5 days after the final major factor in the development of diabetic neuropathy injection. (13,15,22,24–26). Previously, we showed that acetylcho- On the day of the experiment, rats were anesthetized with Nembutal line-induced vasodilation by arterioles that provide circu- administered intraperitoneally (50 mg/kg; Abbott Laboratories, North Chi- lation to the region of the sciatic nerve is impaired early in cago, IL). After the determination of MNCV and EBF, the abdominal aorta was diabetes and is accompanied by a reduction of endoneurial isolated and occluded 1–2 cm above the branch of the common iliac artery. Distal to the occlusion, a solution containing India ink with 2% gelatin (27,30) blood flow (EBF) and an increase in superoxide levels in was injected to facilitate the identification of the superior gluteal and internal these vessels (27,28). These changes preceded the slowing pudendal arteries, which arise from the common iliac artery. The rat was then of motor nerve conduction velocity (MNCV) and the killed by exsanguination, and body temperature was lowered with topical ice. reduction in Naϩ/Kϩ ATPase activity in the sciatic nerve, Samples of the left sciatic nerve were then taken for determination of Naϩ/Kϩ suggesting that vascular dysfunction rather than hypergly- ATPase activity, sorbitol and myo-inositol content, and conjugated diene level. Conjugated diene level was also determined in liver samples. The lens cemia-induced metabolic abnormalities of the nerve is was collected for determination of glutathione (GSH) levels. Levels of responsible for the nerve disorders associated with the thiobarbituric acid–reactive substances (TBARSs) in the serum and liver and early onset of diabetes. the lactate-to-pyruvate ratio in the aorta were also determined. A segment of In the present study, we sought to determine the role of the aorta was used to determine superoxide level using lucigenin. Serum diabetes-induced oxidative stress on vascular function in samples were also taken for determination of free fatty acids and triglycerides. Samples for blood glucose measurements were taken on the day of the arterioles that provide circulation to the region of the experiment. sciatic nerve as well as the relationship to EBF and nerve MNCV. MNCV was determined as previously described using a noninvasive activity, as determined by measuring nerve conduction procedure in the sciatic-posterior tibial conducting system in a temperature- velocity. In these studies, we demonstrate that treating controlled environment (27,31). The left sciatic nerve was stimulated first at streptozotocin-induced diabetic rats with ␣-lipoic acid or the sciatic notch and then at the Achilles tendon. Stimulation consisted of single 0.2-ms supramaximal (8 V) pulses through a bipolar electrode (Grass hydroxyethyl starch deferoxamine (HES-DFO) prevents S44 Stimulator; Grass Medical Instruments, Quincy, MA). The evoked poten- the impairment of vascular function and the accumulation tials were recorded from the interosseous muscle with a unipolar platinum of superoxide and peroxynitrite induced by diabetes in electrode and displayed on a digital storage oscilloscope (model 54600A; arterioles that provide circulation to the region of the Hewlett-Packard, Rolling Meadows, IL). MNCV was calculated by subtracting sciatic nerve and it also prevents the reduction in EBF and the distal from the proximal latency (measured in milliseconds) from the stimulus artifact of the take-off of the evoked potential, and the difference was the slowing of MNCV. divided into the distance between the two stimulating electrodes (measured in millimeters using a Vernier caliper). The MNCV was reported in meters per second. RESEARCH DESIGN AND METHODS EBF. Immediately after determination of MNCV, sciatic nerve endoneurial Materials. Unless stated otherwise, all chemicals used in these studies were
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