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首页> 外文会议>Engineering in Medicine and Biology Society, 1995., IEEE 17th Annual Conference >Theoretical analysis of human muscle membrane behavior in hypokalemic periodic paralysis
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Theoretical analysis of human muscle membrane behavior in hypokalemic periodic paralysis

机译：低钾性周期性麻痹中人肌肉膜行为的理论分析

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Computer simulations were performed to investigate the behavior of human muscle membrane with membrane defects supposed to be present in the muscular disease Hypokalemic Periodic Paralysis (HOPP). The model used for simulation was a Hodgkin-Huxley model. The T-tubular system was also incorporated. It was studied whether the membrane defects caused the following recorded HOPP phenomena: a slight depolarization of a HOPP muscle cell when serum potassium is normal and a strong depolarization to -50 mV when serum potassium is low. In the authors' model a constant small sodium leak conductance slightly depolarized the cell, whereas a small fraction of noninactivating sodium channels caused a strong depolarization. In the case of a dependency of this fraction on serum potassium according to a Boltzmann relation such a depolarization occurred only when serum potassium was low. In the authors' simulations, the resting membrane potential moved from -90 mV to -30 mV after a single action potential when 8%, or more of the sodium channels did not inactivate. The authors' results were qualitatively similar when the T-tubular system was decoupled.
机译：进行计算机模拟以调查人肌肉膜的行为，该行为可能与肌肉疾病低钾性周期性麻痹（HOPP）中存在的膜缺陷有关。用于仿真的模型是Hodgkin-Huxley模型。还合并了T管系统。研究了膜缺陷是否引起了以下记录的HOPP现象：当血清钾正常时，HOPP肌肉细胞略微去极化，而当血清钾低时，强烈去极化至-50 mV。在作者的模型中，恒定的较小的钠泄漏电导使细胞稍微去极化，而一小部分非灭活的钠通道引起强烈的去极化。在根据玻耳兹曼关系该分数依赖于血清钾的情况下，仅当血清钾低时才发生去极化。在作者的模拟中，当8％或更多的钠通道未失活时，单个动作电位后，静息膜电位从-90 mV移至-30 mV。当分离T管系统时，作者的结果在质量上相似。

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