The flow inside the perivascular space (PVS) is modeled using a first-principles approach in order to investigate how the cerebrospinal fluid (CSF) enters the brain through a permeable layer of glial cells. Lubrication theory is employed to deal with the flow in the thin annular gap of the perivascular space between an impermeable artery and the brain tissue. The artery has an imposed peristaltic deformation and the deformable brain tissue is modeled by means of an elastic Hooke’s law. The perivascular flow model is solved numerically, discovering that the peristaltic wave induces a steady streaming to/from the brain which strongly depends on the rigidity and the permeability of the brain tissue. A detailed quantification of the through flow across the glial boundary is obtained for a large parameter space of physiologically relevant conditions. The parameters include the elasticity and permeability of the brain, the curvature of the artery, its length and the amplitude of the peristaltic wave. A steady streaming component of the through flow due to the peristaltic wave is characterized by an in-depth physical analysis and the velocity across the glial layer is found to flow from and to the PVS, depending on the elasticity and permeability of the brain. The through CSF flow velocity is quantified to be of the order of micrometers per seconds.

Surfactant-laden liquid plug propagation and rupture occurring in lower lung airways are studied computationally using a front-tracking method. The plug is driven by an applied constant pressure in a rigid axisymmetric tube whose inner surface is coated by a thin liquid film. The evolution equations of the interfacial and bulk surfactant concentrations coupled with the incompressible Navier–Stokes equations are solved in the front-tracking framework. The numerical method is first validated for a surfactant-free case and the results are found to be in good agreement with the earlier simulations of Fujioka et al. (Phys. Fluids, vol. 20, 2008, 062104) and Hassan et al. (Intl J. Numer. Meth. Fluids, vol. 67, 2011, pp. 1373–1392). Then extensive simulations are performed to investigate the effects of surfactant on the mechanical stresses that could be injurious to epithelial cells, such as pressure and shear stress. It is found that the liquid plug ruptures violently to induce large pressure and shear stress on airway walls and even a tiny amount of surfactant significantly reduces the pressure and shear stress and thus improves cell survivability. However, addition of surfactant also delays the plug rupture and thus airway reopening.

The closure of a human lung airway is modeled as an instability of a two-phase flow in a pipe coated internally with a Newtonian liquid. For a thick enough coating, the Plateau-Rayleigh instability creates a liquid plug which blocks the airway, halting distal gas exchange. Owing to a bifrontal plug growth, this airway closure flow induces high stress levels on the wall, which is the location of airway epithelial cells. A parametric numerical study is carried out simulating relevant conditions for human lungs, in either ordinary or pathological situations. Our simulations can represent the physical process from pre- to postcoalescence phases. Previous studies have been limited to precoalescence only. The topological change during coalescence induces a high level of stress and stress gradients on the epithelial cells, which are large enough to damage them, causing sublethal or lethal responses. We find that postcoalescence wall stresses can be in the range of 300% to 600% greater than precoalescence values and so introduce an important source of mechanical perturbation to the cells.

Airway mucus is a complex material with both viscoelastic and viscoplastic properties that vary with healthy and pathological conditions of the lung. In this study, the effects of these conditions on airway closure are examined in a model problem, where an elastoviscoplastic (EVP) single liquid layer lines the inner wall of a rigid pipe and surrounds the air core. The EVP liquid layer is modelled using the Saramito-HB model. The parameters for the model are obtained for the mucus in healthy, asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis (CF) conditions by fitting the rheological model to the experimental data. Then the liquid plug formation is studied by varying the Laplace number and undisturbed liquid film thickness. Airway closure is a surface-tension-driven phenomenon that occurs when the ratio of the pulmonary liquid layer thickness to the airway radius exceeds a certain threshold. In previous studies, it has been found that airway epithelial cells can be lethally or sublethally damaged due to the high peak of the wall stresses and stress gradients during the liquid plug formation. Here we demonstrate that these stresses are also related to the EVP features of the liquid layer. Yielded zones of the liquid layer are investigated for the different mucus conditions, and it is found that the liquid layer is in a chiefly unyielded state before the closure, which indicates that this phase is dominated by the elastic behavior and solvent viscosity. This is further confirmed by showing that the elastic coefficient is one of the most critical parameters determining whether the closure occurs. This parameter also largely affects the closure time. The wall stresses are also investigated for the pathological and healthy cases. Their peaks for COPD and CF are found to be the highest due to the viscoelastic extra stress contribution. Contrary to the Newtonian case, the wall stresses for COPD and CF do not smoothly relax after closure, as they rather remain effectively almost as high as the Newtonian peak. Moreover, the local normal wall stress gradients are smaller for the COPD and CF liquid layer due to their higher stiffness causing a smaller curvature at the capillary wave. The local tangential wall stress gradients are also shown to be smaller for these cases because of the slower accumulation of the liquid at the bulge.

The closure of a human lung airway is modelled as a pipe coated internally with a liquid that takes into account the viscoelastic properties of mucus. For a thick-enough coating, the Plateau–Rayleigh instability blocks the airway by the creation of a liquid plug, and the preclosure phase is dominated by the Newtonian behaviour of the liquid. Our previous study with a Newtonian-liquid model demonstrated that the bifrontal plug growth consequent to airway closure induces a high level of stress and stress gradients on the airway wall, which is large enough to damage the epithelial cells, causing sublethal or lethal responses. In this study, we explore the effect of the viscoelastic properties of mucus by means of the Oldroyd-B and FENE-CR model. Viscoelasticity is shown to be very relevant in the postcoalescence process, introducing a second peak of the wall shear stresses. This second peak is related to an elastic instability due to the presence of the polymeric extra stresses. For high-enough Weissenberg and Laplace numbers, this second shear stress peak is as severe as the first one. Consequently, a second lethal or sublethal response of the epithelial cells is induced.