Abstract
We have numerically investigated the axisymmetric motion of a finite-sized nearly occluding air bubble through a shear-thinning Casson fluid flowing in blood vessels of circular cross section. The numerical solution entails solving a two-layer fluid model--a cell-free layer and a non-Newtonian core together with the gas bubble. This problem is of interest to the field of rheology and for gas embolism studies in health sciences. The numerical method is based on a modified front-tracking method. The viscosity expression in the Casson model for blood (bulk fluid) includes the hematocrit [the volume fraction of red blood cells (RBCs)] as an explicit parameter. Three different flow Reynolds numbers, Reapp=rholUmaxdmicroapp , in the neighborhood of 0.2, 2, and 200 are investigated. Here, rhol is the density of blood, Umax is the centerline velocity of the inlet Casson profile, d is the diameter of the vessel, and microapp is the apparent viscosity of whole blood. Three different hematocrits have also been considered: 0.45, 0.4, and 0.335. The vessel sizes considered correspond to small arteries, and small and large arterioles in normal humans. The degree of bubble occlusion is characterized by the ratio of bubble to vessel radius (aspect ratio), lambda , in the range 0.9< or =lambda< or =1.05 . For arteriolar flow, where relevant, the Fahraeus-Lindqvist effects are taken into account. Both horizontal and vertical vessel geometries have been investigated. Many significant insights are revealed by our study: (i) bubble motion causes large temporal and spatial gradients of shear stress at the "endothelial cell" (EC) surface lining the blood vessel wall as the bubble approaches the cell, moves over it, and passes it by; (ii) rapid reversals occur in the sign of the shear stress (+ --> - --> +) imparted to the cell surface during bubble motion; (iii) large shear stress gradients together with sign reversals are ascribable to the development of a recirculation vortex at the rear of the bubble; (iv) computed magnitudes of shear stress gradients coupled with their sign reversals may correspond to levels that cause injury to the cell by membrane disruption through impulsive compression and stretching; and (v) for the vessel sizes and flow rates investigated, gravitational effects are negligible.