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Structure, mechanical properties, and modeling of cyclically compressed pulmonary emboli.
Journal of the Mechanical Behavior of Biomedical Materials ( IF 3.3 ) Pub Date : 2020-02-19 , DOI: 10.1016/j.jmbbm.2020.103699
Irina N Chernysh 1 , Russell Spiewak 2 , Carolyn L Cambor 3 , Prashant K Purohit 2 , John W Weisel 1
Affiliation  

Pulmonary embolism occurs when blood flow to a part of the lungs is blocked by a venous thrombus that has traveled from the lower limbs. Little is known about the mechanical behavior of emboli under compressive forces from the surrounding musculature and blood pressure. We measured the stress-strain responses of human pulmonary emboli under cyclic compression, and showed that emboli exhibit a hysteretic stress-strain curve. The fibrin fibers and red blood cells (RBCs) are damaged during the compression process, causing irreversible changes in the structure of the emboli. We showed using electron and confocal microscopy that bundling of fibrin fibers occurs due to compression, and damage is accumulated as more cycles are applied. The stress-strain curves depend on embolus structure, such that variations in composition give quantitatively different responses. Emboli with a high fibrin component demonstrate higher normal stress compared to emboli that have a high RBC component. We compared the compression response of emboli to that of whole blood clots containing various volume fractions of RBCs, and found that RBCs rupture at a certain critical stress. We describe the hysteretic response characteristic of foams, using a model of phase transitions in which the compressed foam is segregated into coexisting rarefied and densified phases whose fractions change during compression. Our model takes account of the rupture of RBCs in the compressed emboli and stresses due to fluid flow through their small pores. Our results can help in classifying emboli as rich in fibrin or rich in red blood cells, and can help in understanding what responses to expect when stresses are applied to thrombi in vivo.



中文翻译:

循环压缩肺栓子的结构,力学性能和模型。

当从下肢流出的静脉血栓阻塞了流向一部分肺部的血液时,就会发生肺栓塞。关于栓子在来自周围肌肉组织和血压的压缩力下的机械行为知之甚少。我们测量了人肺栓塞在循环压缩下的应力应变响应,并表明栓塞表现出滞后应力应变曲线。纤维蛋白纤维和红细胞(RBC)在压缩过程中受损,导致栓子结构发生不可逆变化。我们使用电子显微镜和共聚焦显微镜表明,纤维蛋白纤维的束缚是由于压缩而发生的,并且随着施加更多的循环,损伤会累积。应力-应变曲线取决于栓子的结构,这样组成上的变化会在数量上产生不同的响应。与具有高RBC成分的栓子相比,具有高纤维蛋白成分的栓子表现出更高的法向应力。我们比较了栓子的压缩响应与包含不同体积分数的RBC的全血凝块的压缩响应,发现RBC在一定的临界应力下破裂。我们使用相变模型描述了泡沫的滞后响应特征,在该相变模型中,压缩的泡沫被隔离为稀薄和致密的共存相,其压缩过程中分数发生变化。我们的模型考虑了压缩栓塞中RBC的破裂以及由于流体流过小孔而引起的应力。我们的结果有助于将栓子分类为富含纤维蛋白或富含红血球,体内

更新日期:2020-02-19
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