Mathematical Model of the formation of the microvascular tree based on IVM-data in vivo.
Our working group uses the microfluidic dynamics module and Computational Fluid Dynamics (CFD) of the COMSOL Multiphysics software to create dynamical model on the base of comparative analysis between Intravital Microscopy data, microcirculatory blood flow velocity data and vasomotion in order to assess the influence of biomechanical factors such as microfluid dynamics on the processes of restructuration and changes of structural integrity and stability of the microvascular wall in early stages of neo-angiogenesis. Creation of a mathematical model based on in vivo data provides a more realistic way to interpret physiological processes underlying normal or pathological conditions. With the power of computer calculations, we can try to predict some risk factor coincidences, and if it is possible to try to avoid them, we can simulate relatively impossible processes for direct observations by means of intravital microscopy or other methods for screening of microcirculation, because the life span or vitality of already implanted dorsal skin fold chambers is limited in time up to 3 months or less. For more than two decades, our working group has been studying the molecular mechanisms by which biomechanical and electromagnetic signals at different frequencies are translated into spatial structural changes (affecting the 3D branching of microvascular vessels and changes in elasticity, etc.). The first results from our working group's experiments were obtained using Intravital Microscopy (IVM). Data on microvascular vasomotion, blood flow velocity, and angiogenesis tree formation were obtained from IVM and subsequently approximated to a numerical mathematical model using the specialized module - Computational Fluid Dynamics (CFD) of the COMSOL Multiphysics software: Computational Fluid Dynamics (CFD) and nonlinear microfluidic dynamics are powerful bioengineering tools for modeling hypo-/hyper-proteinemia, erythrocytosis, or other pathological changes in viscosity that disrupt microcirculation. CFD assesses altered hemodynamics, such as impaired wall shear stress (WSS), while nonlinear dynamics capture complex, chaotic fluctuations in blood flow. Together, they explain why lipid accumulation causes endothelial dysfunction and vascular resistance. How CFD analyzes hypo-/hyper-proteinemia and erythrocytosis. CFD uses advanced physics and mathematical simulations to model fluid dynamics within microvessels. In hyperlipidemic states, the following key variables are quantified: Non-Newtonian blood viscosity: Hyperlipidemia (elevated LDL and triglycerides) thickens the blood, turning it into a hyperviscous, shear-thinning fluid. CFD models show how this slows blood flow velocity and increases resistance. Wall shear stress (WSS): CFD simulations reveal a highly non-uniform distribution of WSS at microvascular bifurcations. Abnormal stress levels trigger endothelial cells to release pro-inflammatory and prothrombotic markers, fueling microvascular dysfunction. Red blood cell (RBC) dynamics: CFD models often use multiphase frameworks to track RBC aggregation (clumping) and altered deformability, which physically occlude narrow capillaries.
