Dreher K L, Eaton J W, Breslawec K P, Berger E, Blackshear P L, White J G
Am J Pathol. 1980 Dec;101(3):543-56.
Previous investigations have shown that incubation of human erythrocytes with the ionophore A23187 and calcium causes accumulation of the cation, losses in potassium, water, and cellular volume, hydrolysis of adenosine triphosphate (ATP), conversion of biconcave discocytes to echinocytes and spheroechinocytes, and marked increases in erythrocyte resistance to micropipette aspiration. Subsequent studies demonstrated that prevention of water and potassium loss blocked the influence of calcium loading on erythrocyte stiffness without affecting calcium uptake by the cells or hydrolysis of ATP. In the present study erythrocytes were exposed to conditions that permitted individual or coordinate manipulation of cellular ATP, water, potassium, and calcium in order to determine which factors developing as a result of calcium loading were responsible for the calcium-induced changes in erythrocyte viscoelastic properties. Results of the study demonstrate that volume loss, ATP hydrolysis, and potassium depletion do not individually or in combination cause increases in erythrocyte stiffness. However, all of these changes are essential and must develop in conjunction with calcium loading in order for erythrocytes to develop diminished deformability and elasticity.
先前的研究表明，将人红细胞与离子载体A23187和钙一起孵育会导致阳离子积累、钾、水和细胞体积的损失、三磷酸腺苷（ATP）水解、双凹圆盘状红细胞转变为棘状红细胞和球形棘状红细胞，以及红细胞对微量移液器抽吸的抵抗力显著增加。随后的研究表明，防止水和钾的流失可阻断钙负荷对红细胞硬度的影响，而不会影响细胞对钙的摄取或ATP的水解。在本研究中，将红细胞暴露于允许单独或协同操纵细胞内ATP、水、钾和钙的条件下，以确定钙负荷导致的哪些因素是钙诱导的红细胞粘弹性特性变化的原因。研究结果表明，体积损失、ATP水解和钾耗竭单独或共同作用都不会导致红细胞硬度增加。然而，所有这些变化都是必不可少的，并且必须与钙负荷同时发生，以便红细胞的变形性和弹性降低。
