RESUMO
Leukocyte recruitment is an essential stage of the inflammatory response and although the molecular mechanisms of this process are relatively well known, the influence of the hydrodynamic effects that govern the inflammatory response are still under study. In this paper we made use of the images and experimental parameters obtained by intravital microscopy in an in vivo animal model of inflammation to track the leukocytes trajectories and measure their velocities and diameters. Using a recent validated mathematical model describing the coupled deformation-flow of an individual leukocyte in a microchannel, numerical simulations of an individual and of two leukocytes under flow were performed. The results showed that velocity plays an important role in the motion, deformation and attraction of the cells during an inflammatory response. In fact, for higher inlet velocities the cell movement along the endothelial wall is accelerated and the attraction forces break faster. These results highlight the role of the mechanical properties of the blood, namely the ones influenced by the velocity field, in the case of inflammation.
Assuntos
Endotélio Vascular/fisiopatologia , Hemorreologia , Inflamação/fisiopatologia , Migração e Rolagem de Leucócitos , Leucócitos/imunologia , Animais , Velocidade do Fluxo Sanguíneo , Simulação por Computador , Modelos Animais de Doenças , Endotélio Vascular/imunologia , Análise de Elementos Finitos , Hidrodinâmica , Inflamação/sangue , Inflamação/imunologia , Microscopia Intravital , Masculino , Camundongos Transgênicos , Modelos Cardiovasculares , Análise Numérica Assistida por Computador , Fluxo Sanguíneo Regional , Fatores de TempoRESUMO
The inflammatory process of atherosclerosis leads to the formation of an atheromatous plaque in the intima of the blood vessel. The plaque rupture may result from the interaction between the blood and the plaque. In each cardiac cycle, blood interacts with the vessel, considered as a compliant nonlinear hyperelastic. A three dimensional idealized fluid-structure interaction (FSI) model is constructed to perform the blood-plaque and blood-vessel wall interaction studies. An absorbing boundary condition (BC) is imposed directly on the outflow in order to cope with the spurious reflexions due to the truncation of the computational domain. The difference between the Newtonian and non-Newtonian effects is highlighted. It is shown that the von Mises and wall shear stresses are significantly affected according to the rigidity of the wall. The numerical results have shown that the risk of plaque rupture is higher in the case of a moving wall, while in the case of a fixed wall the risk of progression of the atheromatous plaque is higher.