Effects of volume replacement fluids on blood flow in-vitro and in-vivo

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Red blood cells (RBCs) are from a physical point of view highly deformable objects that can pass capillaries and constrictions smaller than their own diameter. They consist of a lipid bilayer membrane that is supported by a polymeric spectrin network, which encloses the inner fluid that contains hemoglobin. Due to their high deformability, RBCs interact strongly with the flow and depending on the type of flow many different shapes have been predicted and observed, both in simple shear and in Poiseuille flow. In this sense, RBCs serve as an excellent model system to study fluid with soft structure interaction. In physiological vascular flow most of the pressure drop occurs along capillaries, where only one single cell can pass at a time, but the interaction of the flow field with the wall induces an additional complexity. In such strong confinements a strong temporal dynamic of the cell shape ranging from simple oscillations up to chaos is observed, even in steady flow. Physiological flow is generally unstationary, either due to the pulsation of the heart or due to flow irregularities caused by the complexity of the capillary network, where local density fluctuations lead to severe pressure and flow rate fluctuations. The cells are suspended in an aqueous medium, the plasma, that contains about 8% of macromolecular proteins. They cause a strong attraction between RBCs leading to aggregates that are the cause of the pronounced shear thinning of blood. At least in elongational flow, the plasma has viscoelastic properties, as well. In the clinical situations of severe blood loss and the resulting shock, different solutions are used to substitute the blood volume. These include crystalloids that are basically ionic buffers and colloids (so-called plasma expanders), which consist of macromolecules and, thus, exhibit the capability to maintain a higher plasma oncotic pressure. We will experimentally study the temporal dynamics of single RBCs in pulsating flow in-vitro in a microfluidic geometry and in-vivo in a hamster model. Our goal is to understand the effect of different resuscitation fluids and viscoelastic model solutions on the fluid mechanics of blood. We are also interested in the effect of pathological RBCs on the flow properties, which has motivating clinical implication. In many blood diseases, RBCs change their shape and flexibility yielding highly altered rheological and fluid dynamical properties. Again, we want to study if the application of polymeric replacement fluids might lead to a, at least temporal, improvement of the volumetric flow rate in-vivo.