Prolonged ischemic conduction failure after reperfusion in diabetic nerve

Baba, Masayuki; Nukada, Hitoshi; McMorran, Denise; Takahashi, Kazunori; Wada, Ryuichi; Yagihashi, Soroku

doi:10.1002/mus.20474

Cited by 11 publications

(12 citation statements)

References 22 publications

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“…However, the concentration of insulin released after the meal could not prevent a further increase of glycaemia. It is well known that hyperglycaemia causes changes of functional parameters in the peripheral nerves, particularly a reduction in NCV and an increase in RICF in rats (Low et al 1985;Bíró et al 1997;Baba et al 2006). The results of our experiment confirmed these findings.…”

Section: Discussionsupporting

confidence: 90%

Neuropathy in a rat model of mild diabetes induced by multiple low doses of streptozotocin: effects of the antioxidant stobadine in comparison with a high-dose α-lipoic acid treatment

Skalska¹,

Kucera²,

Goldenberg³

et al. 2010

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Hyperglycaemia-induced oxidative stress makes an important contribution to the aetiology of diabetic neuropathy. The aim of our study was to evaluate the effect of the antioxidant stobadine (STB) in comparison with a treatment by a high-dose of α-lipoic acid (ALA), on the neurological consequences of chronic hyperglycaemia in an animal model of diabetes in Wistar rats (16 weeks old), made diabetic by streptozotocin (STZ 3 × 20 mg i.v.). Neuropathy was evaluated electrophysiologically by measuring motor nerve conduction velocity (NCV) in the 4 th and 8 th week in vivo and motor NCV and resistance to ischaemic conduction failure (RICF) of the sciatic nerve in the 10 th week of the experiment in vitro. The therapy with ALA (100 mg/kg i.p., 5 times a week) and STB (25 mg/kg i.p., 5 times a week) had a significant effect on NCV in vivo in the 8 th week of the experiment and no effect in the 10 th week in vitro. The RICF elevated in diabetic animals was significantly modified by ALA. The effect of the antioxidant STB on NCV was comparable with that of ALA, while RICF was affected only by ALA. We conclude that treatment with appropriate antioxidants might partially prevent nerve dysfunction in diabetic rats.

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Section: Discussionsupporting

confidence: 90%

Neuropathy in a rat model of mild diabetes induced by multiple low doses of streptozotocin: effects of the antioxidant stobadine in comparison with a high-dose α-lipoic acid treatment

Skalska¹,

Kucera²,

Goldenberg³

et al. 2010

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“…We demonstrated electrophysiologic evidence that, in contrast to RICF, STZ-diabetic nerves cause prolonged ischemic conduction failure after transient ischemia (Baba et al, 2006). In diabetic nerve, there was delayed recovery or persistent failure of impulse transmission upon reperfusion following 60-120 minutes of ischemia, in contrast to immediate recovery in control nerve.…”

Section: Physiologic and Morphologic Vulnerability To Reperfusion Nermentioning

confidence: 77%

Ischemia and diabetic neuropathy

Nukada

2014

Handbook of Clinical Neurology

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“…This fact is supported by our finding that aging was the most significant explanatory variable in multiple regression for CAVI. Loss of vascular elasticity causes impairment of regulated continuous blood supply to the periphery and leads to ischemia and reperfusion-induced injury to neural tissues [15, 43]. This injury causes failure of autonomic drive and leads to further arteriosclerotic changes [15, 44].…”

Section: Discussionmentioning

confidence: 99%

Cardio-Ankle Vascular Index and Indices of Diabetic Polyneuropathy in Patients with Type 2 Diabetes

Ando

Miyamoto

Kotani

et al. 2017

Journal of Diabetes Research

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The cardio-ankle vascular index (CAVI) is used to test vascular function and is an arterial stiffness marker and potential predictor of cardiovascular events. This study aimed to analyze the relation between objective indices of diabetic polyneuropathy (DPN) and the CAVI. One hundred sixty-six patients with type 2 diabetes mellitus were included in this study. We used nerve conduction studies (NCSs) and the coefficient of variation of the R-R interval to evaluate DPN. We estimated arteriosclerosis by the CAVI. Simple and multiple linear regression analyses were performed between neuropathy indices and the CAVI. In univariate analysis, the CAVI showed significant associations with sural sensory nerve conduction velocity and median F-wave conduction velocity. Multiple linear regression analysis for the CAVI showed that sural nerve conduction velocity and median F-wave conduction velocity were significant explanatory variables second only to age. In multiple linear regression analysis for sural nerve conduction velocity among neuropathy indices, the CAVI remained the most significant explanatory variable. In multiple linear regression analysis for median nerve F-wave conduction velocity among neuropathy indices, the CAVI remained the second most significant explanatory variable following HbA1c. These results suggest a close relationship between macroangiopathy and DPN.

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Prolonged ischemic conduction failure after reperfusion in diabetic nerve

Cited by 11 publications

References 22 publications

Neuropathy in a rat model of mild diabetes induced by multiple low doses of streptozotocin: effects of the antioxidant stobadine in comparison with a high-dose α-lipoic acid treatment

Neuropathy in a rat model of mild diabetes induced by multiple low doses of streptozotocin: effects of the antioxidant stobadine in comparison with a high-dose α-lipoic acid treatment

Ischemia and diabetic neuropathy

Cardio-Ankle Vascular Index and Indices of Diabetic Polyneuropathy in Patients with Type 2 Diabetes

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