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人红细胞膜对脉冲拉伸的屈服强度。

Yield strength of human erythrocyte membranes to impulsive stretching.

机构信息

School of Physical and Mathematical Sciences, Nanyang Technological University, Singapore.

出版信息

Biophys J. 2013 Aug 20;105(4):872-9. doi: 10.1016/j.bpj.2013.06.045.

DOI:10.1016/j.bpj.2013.06.045
PMID:23972839
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3752135/
Abstract

Deformability while remaining viable is an important mechanical property of cells. Red blood cells (RBCs) deform considerably while flowing through small capillaries. The RBC membrane can withstand a finite strain, beyond which it ruptures. The classical yield areal strain of 2-4% for RBCs is generally accepted for a quasi-static strain. It has been noted previously that this threshold strain may be much larger with shorter exposure duration. Here we employ an impulse-like forcing to quantify this yield strain of RBC membranes. In the experiments, RBCs are stretched within tens of microseconds by a strong shear flow generated from a laser-induced cavitation bubble. The deformation of the cells in the strongly confined geometry is captured with a high-speed camera and viability is successively monitored with fluorescence microscopy. We find that the probability of cell survival is strongly dependent on the maximum strain. Above a critical areal strain of ∼40%, permanent membrane damage is observed for 50% of the cells. Interestingly, many of the cells do not rupture immediately and exhibit ghosting, but slowly obtain a round shape before they burst. This observation is explained with structural membrane damage leading to subnanometer-sized pores. The cells finally lyse from the colloidal osmotic pressure imbalance.

摘要

变形能力同时保持存活是细胞的一个重要力学性质。红细胞(RBCs)在流经小毛细血管时会发生相当大的变形。红细胞膜可以承受有限的应变,超过这个应变就会破裂。对于准静态应变,通常接受的经典屈服面应变是 2-4%。之前已经注意到,对于较短的暴露时间,这个阈值应变可能会大得多。在这里,我们采用脉冲式强迫来量化红细胞膜的这种屈服应变。在实验中,通过激光诱导空化泡产生的强剪切流在数十微秒内拉伸 RBC。使用高速摄像机捕获细胞在强约束几何形状中的变形,并通过荧光显微镜连续监测细胞活力。我们发现细胞存活率强烈依赖于最大应变。超过约 40%的临界面应变时,50%的细胞会发生永久性的膜损伤。有趣的是,许多细胞不会立即破裂,而是出现鬼影,但在破裂之前会缓慢地变成圆形。这一观察结果可以用结构膜损伤导致亚纳米大小的孔来解释。细胞最终会因胶体渗透压失衡而裂解。

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