Nodal persistent Na+ currents in human diabetic nerves estimated by the technique of latent addition
Nodal persistent Na+ currents in human diabetic nerves estimated by the technique of latent addition
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DOI：
10.1016/j.clinph.2005.11.019
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发表时间：
2006-04-01
影响因子：
4.7
通讯作者：
Hattori, T
中科院分区：
文献类型：
--
作者：
Misawa, S;Kuwabara, S;Hattori, T
目的：探讨高血糖对人类糖尿病神经持续Na+电流的影响。消除了被动膜性能因素的影响。先前的研究表明，在高血糖情况下，神经的强度持续时间常数会缩短，这表明轴突持续 Na+ 电流减少。然而，时间常数也受到被动膜特性变化的影响。使用计算机阈值跟踪的潜加法是一种可以单独评估Na+电流和被动膜特性的新方法。方法：使用潜加法估计83名糖尿病患者正中运动轴突的节点Na+电流。传递短暂的超极化调节电流脉冲，并测量 0.2 ms 调节测试间隔的阈值变化，作为节点持续 Na+ 电流的指标。对 17 名患者在胰岛素治疗前后进行了检查。结果：糖化血红蛋白水平与 0.2 ms 阈值变化之间存在负线性关系（P=0.02）；较高的糖化血红蛋白水平与较小的阈值变化相关。胰岛素治疗后。神经传导速度显着改善，且 0.2 毫秒时阈值变化更大（P=0.03），表明持续 Na+ 电流增加。潜在添加的快速成分是被动膜特性的指标，不受血糖控制状态的影响。结论：高血糖可以抑制节点持续的 Na+ 电流，可能是因为跨轴突 Na+ 梯度减少或 Na+ 通道受损，并且这可以通过血糖控制快速恢复。意义：减少的节点 Na+ 电流可能部分地 有助于人类糖尿病神经病变的病理生理学。 (c) 2006 年国际临床神经生理学联合会。由爱思唯尔爱尔兰有限公司出版。保留所有权利。
Objective: To investigate the effects of hyperglycemia on persistent Na+ currents in human diabetic nerves. eliminating the factors of passive membrane properties as a factor. Previous studies show that strength-duration time constant of a nerve is shortened under hyperglycemia, suggesting reduced axonal persistent Na+ currents. However, the time constant is also affected by changes in passive membrane properties. Latent addition using computerized threshold tracking is a new method that can separately evaluate Na+ currents and passive membrane properties.Methods: Latent addition was used to estimate nodal Na+ currents in median motor axons of 83 diabetic patients. Brief hyperpolarizing conditioning current pulses were delivered, and threshold changes at the conditioning-test interval of 0.2 ms were measured as an indicator of nodal persistent Na+ currents. Seventeen patients were examined before and after insulin treatment.Results: There was an inverse linear relationship between hemoglobin A1c levels and threshold changes at 0.2 ms (P=0.02); the higher hemoglobin A1c levels were associated with smaller threshold changes. After insulin treatment. there was a significant improvement in nerve conduction velocities associated with greater threshold changes at 0.2 ms (P=0.03), suggesting an increase in persistent Na+ currents. The fast component of latent addition, an indicator of passive membrane properties, was not affected by the state of glycemic control.Conclusions: Hyperglycemia could suppress nodal persistent Na+ currents, presumably because of reduced trans-axonal Na+ gradient or impaired Na+ channels, and this can be rapidly restored by glycemic control.Significance: Reduced nodal Na+ currents may partly contribute to the pathophysiology of human diabetic neuropathy. (c) 2006 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.