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高血糖会改变人类糖尿病性神经病变中的不应期。

Hyperglycemia alters refractory periods in human diabetic neuropathy.

作者信息

Misawa Sonoko, Kuwabara Satoshi, Ogawara Kazue, Kitano Yukiko, Yagui Kazuo, Hattori Takamichi

机构信息

Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.

出版信息

Clin Neurophysiol. 2004 Nov;115(11):2525-9. doi: 10.1016/j.clinph.2004.06.008.

DOI:10.1016/j.clinph.2004.06.008
PMID:15465442
Abstract

OBJECTIVE

To investigate the effects of hyperglycemia on axonal excitability in human diabetics. Diabetic nerve dysfunction is partly associated with the altered polyol pathway and Na+-K+ ATPase activity, probably resulting in a decrease in the trans-axonal Na+ gradient and reduced nodal Na+ currents.

METHODS

Threshold tracking was used to measure the relative refractory periods (RPs) of median motor axons in 58 diabetic patients, 45 normal subjects, and 12 patients with non-diabetic axonal neuropathy. In diabetic patients, the relationship of RPs with hemoglobin A1c (HbA1c) levels was analyzed.

RESULTS

The mean RP was similar for diabetics and normal controls as a group, but was longer in patients with non-diabetic neuropathy than in normal controls (P=0.02). Diabetic patients with good glycemic control (HbA1c levels <7%) had longer RPs than patients with poorer glycemic control and normal controls (P=0.01). RP was longest at the HbA1c level of 6%, gradually decreasing and reaching a plateau at the HbA1c level of 8-9%.

CONCLUSIONS

Hyperglycemia shortens RPs, possibly because metabolic abnormalities lead to reduced nodal Na+ currents, and thereby to a lower inactivation of Na+ channels when generating an action potential.

SIGNIFICANCE

RP measurements could provide new insights into the ionic pathophysiology of human diabetic neuropathy.

摘要

目的

研究高血糖对糖尿病患者轴突兴奋性的影响。糖尿病神经功能障碍部分与多元醇途径改变及钠钾ATP酶活性有关,这可能导致轴突跨膜钠梯度降低和结区钠电流减少。

方法

采用阈值跟踪法测量58例糖尿病患者、45例正常受试者和12例非糖尿病性轴索性神经病患者正中运动轴突的相对不应期(RP)。分析糖尿病患者中RP与糖化血红蛋白(HbA1c)水平的关系。

结果

糖尿病患者组和正常对照组的平均RP相似,但非糖尿病性神经病患者的RP比正常对照组更长(P = 0.02)。血糖控制良好(HbA1c水平<7%)的糖尿病患者的RP比血糖控制较差的患者和正常对照组更长(P = 0.01)。RP在HbA1c水平为6%时最长,随后逐渐下降,在HbA1c水平为8 - 9%时达到平台期。

结论

高血糖会缩短RP,可能是因为代谢异常导致结区钠电流减少,从而在产生动作电位时钠通道失活降低。

意义

RP测量可为人类糖尿病性神经病的离子病理生理学提供新的见解。

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