Stephanova D I, Daskalova M
Institute of Biophysics and Biomedical Engineering, Bulgarian Academy of Sciences, Acad., G. Bontchev Str., Bl. 21, Sofia 1113, Bulgaria.
J Integr Neurosci. 2015 Jun;14(2):235-52. doi: 10.1142/S0219635215500119. Epub 2015 Apr 27.
Threshold electrotonus changes have been studied following warming to 37°C and cooling to 25°C in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). To extend the tracking of these changes also during hypothermia (≤ 25°C) and hyperthermia (≥ 40°C), and to explain their mechanisms, we investigate the effects of temperature (from 20°C to 42°C) on polarizing nodal and internodal electrotonic potentials and their current kinetics in previously simulated case of 70% CIDP. The computations use our temperature-dependent multi-layered model of the myelinated human motor nerve fiber. While the changes of electrotonic potentials and their current kinetics are largely similar for the physiological range of 28-37°C, they are altered during hypothermia and hyperthermia in the normal and CIDP cases. The normal (at 37°C) resting membrane potential is further depolarized or hyperpolarized during hypothermia or hyperthermia, respectively, and the internodal current types defining these changes are the same for both cases. Unexpectedly, our results show that in the CIDP case, the lowest and highest critical temperatures for blocking of electrotonic potentials are 20°C and 39°C, while in the normal case the highest critical temperature for blocking of these potentials is 42°C. In the temperature range of 20-39°C, the relevant potentials in the CIDP case, except for the lesser value (at 39°C) in hyperpolarized resting membrane potential, are modified: (i) polarizing nodal and depolarizing internodal electrotonic potentials and their defining currents are increased in magnitude; (ii) inward rectifier (I IR ) and leakage (I Lk ) currents, defining the hyperpolarizing internodal electrotonic potential, are gradually increased with the rise of temperature from 20°C to 39°C, and (iii) the accommodation to long-lasting hyperpolarization is greater than to depolarization. The present results suggest that the electrotonic potentials in patients with CIDP are in high risk for blocking not only during hypothermia and hyperthermia, but they are also in risk for worsening at the temperature range of 37-39°C.
我们研究了慢性炎症性脱髓鞘性多发性神经病（CIDP）患者体温升至37°C和降至25°C后的阈下电紧张变化。为了在体温过低（≤25°C）和体温过高（≥40°C）期间也能追踪这些变化，并解释其机制，我们在先前模拟的70%CIDP病例中，研究了温度（从20°C到42°C）对极化节段和节间电紧张电位及其电流动力学的影响。计算使用了我们基于温度的有髓人运动神经纤维多层模型。虽然在28-37°C的生理范围内，电紧张电位及其电流动力学的变化在很大程度上相似，但在正常和CIDP病例中，体温过低和过高时这些变化都会改变。正常情况下（37°C时）的静息膜电位在体温过低或过高时分别进一步去极化或超极化，并且定义这些变化的节间电流类型在两种情况下是相同的。出乎意料的是，我们的结果表明，在CIDP病例中，电紧张电位阻断的最低和最高临界温度分别为20°C和39°C，而在正常情况下，这些电位阻断的最高临界温度为42°C。在20-39°C的温度范围内，CIDP病例中的相关电位，除了超极化静息膜电位在39°C时较小的值外，均有改变：（i）极化节段和去极化节间电紧张电位及其定义电流的幅度增加；（ii）定义超极化节间电紧张电位的内向整流（IIR）和泄漏（ILk）电流随着温度从20°C升至39°C逐渐增加，以及（iii）对长时间超极化的适应性大于对去极化的适应性。目前的结果表明，CIDP患者的电紧张电位不仅在体温过低和过高时存在阻断的高风险，而且在37-39°C的温度范围内也有恶化的风险。
