Orlov S N, Pokudin N I, El'-Rabi L S, Brusovanik V I, Kubatiev A A
Biokhimiia. 1993 Jun;58(6):866-73.
The activity of Na+, K(+)-ATPase (ouabain-inhibited 86Rb influx), Na+, K+ cotransport (ouabain-insensitive furosemide-inhibited 86Rb or 22Na influx), Na+/Na+ exchange (ouabain-insensitive phloretin-inhibited 22Na influx) and Na+/Li+ exchange (ouabain-insensitive Na0(+)-depended Li+ efflux) as well as the passive permeability of the erythrocyte membrane for Na+, K+ and Li+ have been studied in patients with primary (microspherocytosis, hemoglobinopathy) and secondary (autoimmune) hemolytic anemia. The activities of the Na+, K(+)-pump and Na+, K(+)-cotransport were increased in patients with microspherocytosis-by 45% and 70%, respectively. In patients with hemoglobinopathy the Na+/Li+ exchange and passive permeability for K+ were increased 2-3-fold in comparison with the control with the control group. The increased passive permeability for K+ may partly be due to the increased K+, Cl(-)-cotransport. In patients with autoimmune anemia the 3-fold increase in the passive permeability for monovalent cations and the 2-fold increased activity of Na+, K+ cotransport were found. There was no significant correlation between the Na+/Na+ and Na+/Li+ exchange which suggests that the cellular mechanisms of activity control in those ion transport systems differ essentially. No correlation was found between the passive permeability for Na+ and K+ either. These data indicate that simple diffusion (leakage) is not the only pathway for the passive permeability of the erythrocyte membrane for monovalent cations.
在原发性（球形红细胞增多症、血红蛋白病）和继发性（自身免疫性）溶血性贫血患者中，研究了钠钾ATP酶活性（哇巴因抑制的86Rb内流）、钠钾协同转运（哇巴因不敏感、呋塞米抑制的86Rb或22Na内流）、钠/钠交换（哇巴因不敏感、根皮素抑制的22Na内流）和钠/锂交换（哇巴因不敏感、钠依赖的锂外流），以及红细胞膜对钠、钾和锂的被动通透性。球形红细胞增多症患者的钠钾泵和钠钾协同转运活性分别增加了45%和70%。与对照组相比，血红蛋白病患者的钠/锂交换和钾的被动通透性增加了2至3倍。钾被动通透性增加可能部分归因于钾氯协同转运增加。在自身免疫性贫血患者中，发现单价阳离子的被动通透性增加了3倍，钠钾协同转运活性增加了2倍。钠/钠交换和钠/锂交换之间没有显著相关性，这表明这些离子转运系统中活性控制的细胞机制存在本质差异。钠和钾的被动通透性之间也没有相关性。这些数据表明，单纯扩散（渗漏）不是红细胞膜对单价阳离子被动通透性的唯一途径。
