Layzer R B
Ann Neurol. 1982 Jun;11(6):547-52. doi: 10.1002/ana.410110602.
Analysis of the pathophysiology of hypokalemic paralysis, as it occurs in barium poisoning, chronic potassium deficiency, and thyrotoxicosis, suggests that these disorders may have a similar mechanism. An increased ratio of muscle sodium permeability to potassium permeability reduces the ionic diffusion potential, while the resting membrane potential is sustained by an increase of Na-K pump electrogenesis. The result is that potassium entry (the sum of active and passive influx) exceeds potassium efflux; this causes a large shift of extracellular potassium into muscle until the Na-K pump turns off, leading to depolarization and paralysis. The primary defect in familial hypokalemic periodic paralysis, as in the example of barium poisoning, may be a marked reduction of muscle permeability to potassium.
对钡中毒、慢性钾缺乏和甲状腺毒症中发生的低钾性麻痹的病理生理学分析表明，这些疾病可能具有相似的机制。肌肉钠通透性与钾通透性的比值增加会降低离子扩散电位，而静息膜电位则通过钠钾泵电生成的增加得以维持。结果是钾的进入（主动和被动内流之和）超过钾的外流；这会导致细胞外钾大量转移到肌肉中，直到钠钾泵关闭，从而导致去极化和麻痹。家族性低钾性周期性麻痹的主要缺陷，就像钡中毒的例子一样，可能是肌肉对钾的通透性显著降低。
