Berkowitz L R, Orringer E P
Am J Hematol. 1984 Oct;17(3):217-23. doi: 10.1002/ajh.2830170302.
Energy depletion in the human erythrocyte causes a rise in intracellular calcium. This in turn accelerates the transmembrane movement of potassium and chloride, resulting in cell dehydration. This process, known as the Gardos phenomenon, is inhibited by cetiedil. The present study examines the mechanism by which cetiedil inhibits the Gardos phenomenon. The ability of cetiedil to retard the initial step in the Gardos phenomenon, a rise in intracellular calcium, was first tested. Cetiedil did not prevent calcium accumulation. Cetiedil's ability to inhibit anion movement was next evaluated, as cetiedil could appear to be blocking K movement when in fact it was preventing the movement of its accompanying anion. No inhibitory effect on anion movement was seen. Since cetiedil prevented neither calcium accumulation nor anion movement, it must inhibit the Gardos phenomenon by preventing the opening of the K-specific gate in the erythrocyte membrane. The fact that cetiedil's effect on the Gardos phenomenon could not be removed with repeated cell washing indicates that this effect is irreversible.
人体红细胞中的能量消耗会导致细胞内钙含量升高。这进而加速钾和氯的跨膜移动，导致细胞脱水。这一过程被称为加尔多斯现象，可被西替地尔抑制。本研究探讨了西替地尔抑制加尔多斯现象的机制。首先测试了西替地尔延缓加尔多斯现象初始步骤（细胞内钙含量升高）的能力。西替地尔并未阻止钙的积累。接下来评估了西替地尔抑制阴离子移动的能力，因为西替地尔看似在阻止钾移动时，实际上可能是在阻止其伴随阴离子的移动。未观察到对阴离子移动的抑制作用。由于西替地尔既未阻止钙的积累，也未阻止阴离子移动，它必定是通过阻止红细胞膜上钾特异性通道的开放来抑制加尔多斯现象。反复冲洗细胞后西替地尔对加尔多斯现象的影响仍无法消除，这一事实表明该作用是不可逆的。
