Dreher K L, Eaton J W, Kuettner J F, Breslawec K P, Blackshear P L, White J G
Am J Pathol. 1978 Jul;92(1):215-25.
Modest increases in intracellular calcium concentrations, in association with ATP depletion, cause the appearance of pathologic changes in erthrocyte shape and deformability. The loss of erythrocyte ATP and simultaneous increase in cellular calcium have previously been considered the sole requisites for the appearance of erythrocyte membrane rigidity. We report that red cells suspended in high-potassium buffers may be simultaneously loaded with calcium (through exposure to the divalent cation ionophore A23187) and depleted of ATP without incurring drastic changes in shape or in membrane stiffness. Incubation of erythrocytes under these conditions effectively blocks both water and potassium loss normally caused by calcium accumulation. However, the high external potassium has no influence on either the ionophore-induced accumulation of calcium or on the the concomitant hydrolysis of cellular ATP. These results suggest the involvement of at least one further parameter, ie, changes in cell water and cation content, in the development of calcium-induced erythrocyte rigidity.
细胞内钙浓度的适度升高，与ATP耗竭相关联，会导致红细胞形状和可变形性出现病理变化。红细胞ATP的丧失以及细胞内钙的同时增加，此前一直被认为是红细胞膜刚性出现的唯一必要条件。我们报告称，悬浮在高钾缓冲液中的红细胞可能会同时加载钙（通过暴露于二价阳离子载体A23187）并耗尽ATP，而不会在形状或膜硬度上发生剧烈变化。在这些条件下孵育红细胞可有效阻止通常由钙积累引起的水和钾的流失。然而，高细胞外钾对载体诱导的钙积累或细胞ATP的伴随水解均无影响。这些结果表明，至少还有一个参数参与了钙诱导的红细胞刚性的发展，即细胞内水和阳离子含量的变化。
