Noji S, Taniguchi S, Kon H
Laboratory of Chemical Physics, National Institute of Diabetes, and Digestive and Kidney Diseases, Bethesda, Maryland 20892.
Biophys J. 1987 Aug;52(2):221-7. doi: 10.1016/S0006-3495(87)83209-5.
The Ca2+-induced loss of deformability in human erythrocytes and the recovery of the lost deformability by stomatocytogenic reagents were investigated by means of a new flow electron paramagnetic resonance (EPR) spin label method, which provides information on deformation and orientation characteristics of spin labeled erythrocytes in shear flow. The Ca2+-induced loss of deformability is attributed mainly to the increase in intracellular viscosity resulting from efflux of intracellular potassium ions and water (Gardos effect). Partial recovery of the lost deformability is demonstrated in the presence of stomatocytogenic reagents, such as chlorpromazine, trifluoperazine, W-7, and calmidazolium (R24571). The recovery can not be explained solely by suppression of the Gardos effect due to the reagents. Incorporation of an optimal amount of the reagents into the membrane appears to compensate for the membrane modification due to Ca2+ ions to restore a part of the lost deformability.
采用一种新的流动电子顺磁共振(EPR)自旋标记方法,研究了钙离子诱导的人红细胞变形性丧失以及口形红细胞生成试剂对丧失的变形性的恢复作用。该方法可提供关于自旋标记红细胞在剪切流中的变形和取向特性的信息。钙离子诱导的变形性丧失主要归因于细胞内钾离子和水外流导致的细胞内粘度增加(加尔多斯效应)。在存在口形红细胞生成试剂(如氯丙嗪、三氟拉嗪、W-7和氯米帕明(R24571))的情况下,丧失的变形性有部分恢复。这种恢复不能仅用试剂对加尔多斯效应的抑制来解释。将最佳量的试剂掺入膜中似乎可以补偿钙离子对膜的修饰,从而恢复部分丧失的变形性。