Meram Ece, Yilmaz Bahar D, Bas Ceren, Atac Nazlı, Yalcin O, Meiselman Herbert J, Baskurt Oguz K
Koç University School of Medicine, Sariyer, Istanbul, Turkey.
Biorheology. 2013;50(3-4):165-76. doi: 10.3233/BIR-130637.
Classically, it is known that red blood cell (RBC) deformability is determined by the geometric and material properties of these cells. Experimental evidence accumulated during the last decade has introduced the concept of active regulation of RBC deformability. This regulation is mainly related to altered associations between membrane skeletal proteins and integral proteins, with the latter serving to anchor the skeleton to the lipid matrix. It has been hypothesized that shear stress induces alterations of RBC deformability: the current study investigated the dynamics of the transient improvement in deformability induced by shear stress at physiologically-relevant levels. RBC were exposed to various levels of shear stress (SS) in a Couette type shearing system that is part of an ektacytometer, thus permitting the changes in RBC deformability during the application of SS to be monitored. Initial studies showed that there is an increase in deformability of the RBC subjected to SS in the range of 5-20 Pa, with kinetics characterized by time constants of a few seconds. Such improvement in deformability, expressed by an elongation index (EI), was faster with higher levels of SS and hence yielded shorter time constants: absolute values of EI increased by 3-8% of the starting level. Upon the removal of the shear stress, this response by RBC was reversible with a slower time course compared to the increase in EI during application of SS. Increased calcium concentration in the RBC suspending medium prevented the improvement of deformability. It is suggested that the improvement of RBC deformability by shear forces may have significant effects on blood flow dynamics, at least in tissues supplied by blood vessels with impaired vasomotor reserve, and may therefore serve as a compensating mechanism for the maintenance of adequate microcirculatory perfusion.
传统上，已知红细胞（RBC）的可变形性由这些细胞的几何和材料特性决定。过去十年积累的实验证据引入了红细胞可变形性主动调节的概念。这种调节主要与膜骨架蛋白和整合蛋白之间改变的关联有关，后者用于将骨架锚定到脂质基质上。据推测，剪切应力会引起红细胞可变形性的改变：当前的研究调查了生理相关水平的剪切应力诱导的可变形性瞬时改善的动态过程。在作为血细胞变形仪一部分的库埃特型剪切系统中，将红细胞暴露于不同水平的剪切应力（SS）下，从而可以监测施加SS期间红细胞可变形性的变化。初步研究表明，在5 - 20 Pa范围内受到SS作用的红细胞的可变形性增加，其动力学特征是时间常数为几秒。这种由伸长指数（EI）表示的可变形性改善，在较高水平的SS作用下更快，因此产生的时间常数更短：EI的绝对值增加了起始水平的3 - 8%。去除剪切应力后，与施加SS期间EI的增加相比，红细胞的这种反应是可逆的，但时间进程较慢。红细胞悬浮介质中钙浓度的增加阻止了可变形性的改善。有人认为，剪切力引起的红细胞可变形性改善可能对血流动力学有显著影响，至少在血管运动储备受损的血管所供应的组织中是这样，因此可能作为维持足够微循环灌注的一种补偿机制。
