Mechanical properties of oxygenated red blood cells in sickle cell (HbSS) disease.

Mechanical properties of oxygenated red blood cells in sickle cell (HbSS) disease.
复制标题

DOI:
10.1182/blood.v63.1.73.bloodjournal63173
复制
发表时间:
1984
期刊:
影响因子:
20.3
通讯作者:
G. Nash;C. Johnson;H. Meiselman
G. Nash;C. Johnson;H. Meiselman
中科院分区:
医学1区
文献类型:
--
作者:
G. Nash;C. Johnson;H. Meiselman

文献摘要

被引文献

相似文献

个别不可逆或可逆镰状细胞(ISC和RSC,分别)的机械性能的数据很少,也不是ISC形成的过程很好地理解。对于含氧ISC和密度分级RSC,我们使用微量移液管技术测量细胞表面积(SA)和体积(V)、膜剪切弹性模量(μ)、粘弹性形状恢复时间常数(tc),并因此计算膜表面粘度(η = μ X tc)。与细胞密度增加相关的体积损失伴随着成比例的较小的表面积减少;因此,SA/V比对于密度更高的细胞增加,ISC具有最高值。因此,由碎片化引起的膜面积损失必然伴随着细胞体积的加速减少。ISC膜较硬(mu比正常对照高130%),tc接近正常值,有效膜粘度比正常对照高一倍以上。RSC具有接近对照的粘弹性,但在镰状细胞供体之间和样品内显示出更宽的变化。对密度分离的RSC的测量表明,平均而言,mu几乎是恒定的,但对于密度分离的细胞,tc较长,其eta接近ISC水平。发现RSC的一个小亚群具有接近ISC值的mu。低渗肿胀的ISC(内部血红蛋白浓度降至正常水平)保持其增加的膜刚度,但显着降低tc,使其eta接近正常值。结果表明,血红蛋白浓度的升高会影响ISC和RSC的粘弹性行为,但ISC的膜弹性也会发生不可逆的变化。这些数据表明,ISC形成通过两个阶段的过程发生:(1)加速体积损失,导致细胞质和有效膜粘度增加;(2)膜刚度急剧上升,推测与膜结构改变有关。
Little data exist for the mechanical properties of individual irreversible or reversible sickle cells (ISC and RSC, respectively), nor is the process of ISC formation well understood. For oxygenated ISC and density-fractionated RSC, we have used micropipette techniques to measure cell surface area (SA) and volume (V), membrane shear elastic modulus (mu), time constant for viscoelastic shape recovery (tc), and hence to calculate membrane surface viscosity (eta = mu X tc). Volume loss associated with increasing cell density was accompanied by a proportionately smaller surface area decrease; SA/V ratio thus increased for denser cells, with ISC having the highest values. Membrane area loss by fragmentation must thus be accompanied by an accelerated decrease in cell volume. ISC had relatively rigid membranes (mu 130% above normal controls) and tc close to normal values, so that their effective membrane viscosity was more than double control. RSC had viscoelastic properties close to control, but showed wider variation between sickle cell donors and within samples. Measurements on density-separated RSC showed that, on average, mu was nearly constant, but that tc was longer for the densest cells, with their eta approaching ISC levels. A small subpopulation of RSC were found that had mu close to ISC values. Hypotonically swollen ISC (with internal hemoglobin concentration decreased to normal levels) retained their increased membrane stiffness but had markedly decreased tc, so that their eta approached normal values. The results show that elevated hemoglobin concentration influences the viscoelastic behavior of ISC and RSC, but that an irreversible change in membrane elasticity also occurs for ISC. These data suggest that ISC formation occurs via a two-stage process: (1) accelerated volume loss leading to increased cytoplasmic and effective membrane viscosity; (2) a sharp rise in membrane rigidity, presumably linked to membrane structural alteration.