Mukundakrishnan K, Ayyaswamy P S, Eckmann D M
Department of Mechanical Engineering, University of Pennsylvania, 220 South 33rd Street, Philadelphia, PA 19104, USA.
J Biomech Eng. 2009 Jul;131(7):074516. doi: 10.1115/1.3153310.
Mechanisms governing endothelial cell (EC) injury during arterial gas embolism have been investigated. Such mechanisms involve multiple scales. We have numerically investigated the macroscale flow dynamics due to the motion of a nearly occluding finite-sized air bubble in blood vessels of various sizes. Non-Newtonian behavior due to both the shear-thinning rheology of the blood and the Fahraeus-Lindqvist effect has been considered. The occluding bubble dynamics lends itself for an axisymmetric treatment. The numerical solutions have revealed several hydrodynamic features in the vicinity of the bubble. Large temporal and spatial shear stress gradients occur on the EC surface. The stress variations manifest in the form of a traveling wave. The gradients are accompanied by rapid sign changes. These features are ascribable to the development of a region of recirculation (vortex ring) in the proximity of the bubble. The shear stress gradients together with sign reversals may partially act as potential causes in the disruption of endothelial cell membrane integrity and functionality.
动脉气体栓塞期间内皮细胞(EC)损伤的调控机制已得到研究。此类机制涉及多个尺度。我们通过数值模拟研究了不同尺寸血管中近乎阻塞的有限大小气泡运动所导致的宏观流动动力学。同时考虑了血液的剪切变稀流变学和法厄斯 - 林德奎斯特效应所引起的非牛顿行为。阻塞气泡动力学适合进行轴对称处理。数值解揭示了气泡附近的几个流体动力学特征。内皮细胞表面出现了较大的时空剪切应力梯度。应力变化以行波的形式表现出来。这些梯度伴随着快速的符号变化。这些特征可归因于气泡附近再循环区域(涡环)的形成。剪切应力梯度以及符号反转可能部分地成为破坏内皮细胞膜完整性和功能的潜在原因。