In silico biophysics and hemorheology of blood hyperviscosity syndrome

Abstract

Hyperviscosity syndrome (HVS) is characterized by an increase of the blood viscosity by up to seven times the normal blood viscosity, resulting in disturbances to the circulation in the vasculature system. HVS is commonly associated with an increase of large plasma proteins and abnormalities in the properties of red blood cells, such as cell interactions, cell stiffness, and increased hematocrit. Here, we perform a systematic study of the effect of each biophysical factor on the viscosity of blood by employing the dissipative particle dynamic method. Our in silico platform enables manipulation of each parameter in isolation, providing a unique scheme to quantify and accurately investigate the role of each factor in increasing the blood viscosity. To study the effect of these four factors independently, each factor was elevated more than its values for a healthy blood while the other factors remained constant, and viscosity measurement was performed for different hematocrits and flow rates. Although all four factors were found to increase the overall blood viscosity, these increases were highly dependent on the hematocrit and the flow rates imposed. The effect of cell aggregation and cell concentration on blood viscosity were predominantly observed at low shear rates, in contrast to the more magnified role of cell rigidity and plasma viscosity at high shear rates. Additionally, cell-related factors increase the whole blood viscosity at high hematocrits compared with the relative role of plasma-related factors at lower hematocrits. Our results, mapped onto the flow rates and hematocrits along the circulatory system, provide a correlation to underpinning mechanisms for HVS findings in different blood vessels.