Boërio Delphine, Bostock Hugh, Spescha Romana, Z'Graggen Werner J
Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.
Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland; Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London, United Kingdom.
PLoS One. 2014 Jun 3;9(6):e98262. doi: 10.1371/journal.pone.0098262. eCollection 2014.
Hyperkalemia is an important cause of membrane depolarization in renal failure. A recent theoretical model of axonal excitability explains the effects of potassium on threshold electrotonus, but predicts changes in superexcitability in the opposite direction to those observed. To resolve this contradiction we assessed the relationship between serum potassium and motor axon excitability properties in 38 volunteers with normal potassium levels. Most threshold electrotonus measures were strongly correlated with potassium, and superexcitability decreased at higher potassium levels (P = 0.016), contrary to the existing model. Improved modelling of potassium effects was achieved by making the potassium currents obey the constant-field theory, and by making the potassium permeabilities proportional to external potassium, as has been observed in vitro. This new model also accounted well for the changes in superexcitability and other excitability measures previously reported in renal failure. These results demonstrate the importance of taking potassium levels into account when assessing axonal membrane dysfunction by excitability testing, and provide evidence that potassium currents are activated by external potassium in vivo.
高钾血症是肾衰竭时膜去极化的一个重要原因。最近一个关于轴突兴奋性的理论模型解释了钾对阈下电紧张的影响，但预测的超兴奋性变化方向与观察到的相反。为了解决这一矛盾，我们评估了38名血钾水平正常的志愿者血清钾与运动轴突兴奋性特性之间的关系。大多数阈下电紧张测量值与钾密切相关，并且在血钾水平较高时超兴奋性降低（P = 0.016），这与现有模型相反。通过使钾电流遵循恒场理论，并使钾通透性与细胞外钾成比例（正如在体外观察到的那样），实现了对钾效应的改进建模。这个新模型也很好地解释了先前在肾衰竭中报道的超兴奋性和其他兴奋性测量值的变化。这些结果证明了在通过兴奋性测试评估轴突膜功能障碍时考虑血钾水平的重要性，并提供了证据表明钾电流在体内被细胞外钾激活。
