Abstract
Human blood is a shear-thinning fluid with a complex response that strongly depends on the red blood cell’s (RBC’s) ability to form aggregates, called rouleaux. Despite numerous investigations, microscopic understanding of the break up of RBC aggregates has not been fully elucidated. Here, we present a study of breaking up aggregates consisting of two RBCs (a doublet) during shear flow. We introduce the filamentous fd bacteriophage as a rod-like depletant agent with a very long-range interaction force, which can be tuned by the rod’s concentration. We visualize the structures while shearing by combining a home-build counter-rotating cone-plate shear cell with microscopy imaging. A diagram of dynamic states for shear rates versus depletant concentration shows regions of different flow responses and separation stages for the RBCs doublets. With increasing interaction forces, the full-contact flow states dominate, such as rolling and tumbling. We argue that the RBC doublets can only undergo separation during tumbling motion when the angle between the normal of the doublets with the flow direction is within a critical range. However, at sufficiently high shear rates, the time spent in the critical range becomes too short, such that the cells continue to tumble without separating.
Highlights
Blood is a shear-thinning fluid with a complex response that strongly depends on the red blood cells (RBCs) ability to form aggregates in the form of stacks, as has been shown by experiments [1,2,3,4,5] and simulations [6]
To establish that fd does not interact with the red blood cells in a non-trivial manner, we observed the mixture of RBCs and fluorescently labeled fd to qualitatively access any interaction
At times the viruses can be seen bouncing on the surface of the RBCs
Summary
Blood is a shear-thinning fluid with a complex response that strongly depends on the red blood cells (RBCs) ability to form aggregates in the form of stacks, as has been shown by experiments [1,2,3,4,5] and simulations [6]. Two red blood cells stack face-to-face, resulting in a doublet which grows linearly as more cells aggregate onto the stack [8]. This initial process takes a couple of seconds. After an cardiac event [11], the concentration of fibrinogen is increased which can lead to an enhanced tendency of the RBCs to aggregate [10]. Pathological conditions such as sickle cell anemia [12], diabetes [13] and others contribute to an increased RBCs aggregability
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