Cheng Xiaopo, Caruso Christina, Lam Wilbur A, Graham Michael D
Department of Chemical and Biological Engineering, University of Wisconsin-Madison, Madison, WI 53706.
Aflac Cancer and Blood Disorders Center of Children's Healthcare of Atlanta, Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30307.
bioRxiv. 2023 May 18:2023.05.16.541016. doi: 10.1101/2023.05.16.541016.
Red blood cell (RBC) disorders affect billions worldwide. While alterations in the physical properties of aberrant RBCs and associated hemodynamic changes are readily observed, in conditions such as sickle cell disease and iron deficiency, RBC disorders can also be associated with vascular dysfunction. The mechanisms of vasculopathy in those diseases remain unclear and scant research has explored whether biophysical alterations of RBCs can directly affect vascular function. Here we hypothesize that the purely physical interactions between aberrant RBCs and endothelial cells, due to the margination of stiff aberrant RBCs, play a key role in this phenomenon for a range of disorders. This hypothesis is tested by direct simulations of a cellular scale computational model of blood flow in sickle cell disease, iron deficiency anemia, COVID-19, and spherocytosis. We characterize cell distributions for normal and aberrant RBC mixtures in straight and curved tubes, the latter to address issues of geometric complexity that arise in the microcirculation. In all cases aberrant RBCs strongly localize near the vessel walls (margination) due to contrasts in cell size, shape, and deformability from the normal cells. In the curved channel, the distribution of marginated cells is very heterogeneous, indicating a key role for vascular geometry. Finally, we characterize the shear stresses on the vessel walls; consistent with our hypothesis, the marginated aberrant cells generate large transient stress fluctuations due to the high velocity gradients induced by their near-wall motions. The anomalous stress fluctuations experienced by endothelial cells may be responsible for the observed vascular inflammation.
红细胞(RBC)疾病影响着全球数十亿人。虽然异常红细胞的物理特性改变及相关血液动力学变化很容易观察到,但在镰状细胞病和缺铁等情况下,红细胞疾病也可能与血管功能障碍有关。这些疾病中的血管病变机制尚不清楚,很少有研究探讨红细胞的生物物理改变是否能直接影响血管功能。在此,我们假设,由于僵硬的异常红细胞的边缘化,异常红细胞与内皮细胞之间的纯物理相互作用在一系列疾病的这一现象中起关键作用。通过对镰状细胞病、缺铁性贫血、新冠肺炎和球形红细胞增多症血流的细胞尺度计算模型进行直接模拟来检验这一假设。我们对直管和弯管中正常和异常红细胞混合物的细胞分布进行了表征,后者是为了解决微循环中出现的几何复杂性问题。在所有情况下,由于异常红细胞与正常细胞在大小、形状和可变形性方面存在差异,异常红细胞强烈地定位在血管壁附近(边缘化)。在弯曲通道中,边缘化细胞的分布非常不均匀,表明血管几何形状起关键作用。最后,我们对血管壁上的剪切应力进行了表征;与我们的假设一致,边缘化的异常细胞由于其近壁运动引起的高速梯度而产生大的瞬态应力波动。内皮细胞经历的异常应力波动可能是观察到的血管炎症的原因。