计算结果表明，体外反搏可以明显有效地改变血管壁剪切应力。
The computation results show that the external counterpulsation can effectively change the blood vessel pipe_wall shear stress.
建立剪切应力和动脉粥样硬化之间关系的主要机制是血管壁剪切应力基因表达的控制机制。
A central mechanism establishing the relation between shear stress and atherosclerosis is the control of gene expression by wall shear stress.
结论低血管壁面剪切应力，是动脉粥样硬化的危险性血流动力学因素。
Conclusion Low wall shear stress is a risk hemodynamic factor in the development of atherosclerotic plaque.
结论低血管壁面剪切应力，是动脉粥样硬化的危险性血流动力学因素。
Conclusion Low wall shear stress is a risk hemodynamic factor in the development of atherosclerotic plaque.
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