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原发性周期性麻痹系一组遗传性疾病。根据发病时的血K~+改变,分为低钾性和高钾性两种类型。而所谓正钾性周期性麻痹相当少见,可能与高钾性周期性麻痹密切相关或同属一类。低钾性周期性麻痹根据Nernst方程,细胞外K~+浓度〔K〕e的下降,产生超极化。因此早期推测麻痹是由于超极化致神经肌肉传递阻滞,在玻璃微电极引用到电生理不久,Creutzfeldt等测定了病人发作期膜电位,发现膜电位是下降而不是升高。他解释麻痹是去极化引起无兴奋性造成的。鉴于碳水化合物饮食和胰岛素可以诱发麻痹,有人提出碳水化合物代谢缺陷可能是K~+内流过度的原因。这种缺陷可能增加不能透过膜的阴离子的数目,从而被动地引起水和阳离子的内流。
Primary periodic paralysis is a group of inherited diseases. According to the onset of blood K ~ + change, divided into two types of hypokalemia and potassium. The so-called positive potassium periodic paralysis is relatively rare, may be closely related to high potassium periodic paralysis or belong to the same category. Hypokalemic periodic paralysis According to the Nernst equation, a decrease in extracellular K ~ + concentration [K] e produces hyperpolarization. So early speculated that paralysis is due to hyperpolarization caused by neuromuscular blockade, shortly after the reference to the electrophysiological glass microelectrode, Creutzfeldt other determination of the patient during the onset of membrane potential and found that the membrane potential is decreased rather than increased. He explained that paralysis is caused by depolarization and excitability. Given that carbohydrate diets and insulin can induce paralysis, it has been suggested that carbohydrate metabolism defects may be the cause of K ~ + influx. Such defects may increase the number of anions that can not permeate through the membrane, thereby passively inducing influx of water and cations.