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Mechanics of shear stress transmission to endothelial cells in blood vessels lined with an endothelial surface layer

机译:内皮表面层内衬血管内皮细胞的剪切应力传递的力学

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Interior surfaces of blood vessels are lined with a layer of bound or adsorbed macromolecules, known as the endothelial surface layer (ESL). In vivo investigations of blood flow in capillaries have shown that this layer is of order 1 μm thick. The presence of the ESL is believed to be a major factor causing low tube hematocrit in capillaries [1], and higher flow resistance in microvessels than in glass tubes with corresponding diameters [2]. Disruption of the ESL by a light-dye treatment [3] increases the widths of columns of red blood cells and labeled dectran-70 in capillaries, without observable changes in capillaries' anatomical diameters, implying that the ESL restricts the space available for red blood cell motion and plasma flow in capillaries. The ability of the ESL to impede plasma flow is accounted for by assuming that it is a porous medium with a hydraulic resistivity of at least 10{sup}8 dyn≌s/cm{sup}4 [4]. To describe the ability of the layer to exclude flowing red cells, Damiano et al. [5] modeled the layer as an elastic solid, while Pries et al. [2] hypothesized that the layer resists flattening because of colloid osmotic pressures generated by plasma proteins adsorbed to the ESL. According to the latter hypothesis, the colloid osmotic pressure within the ESL is increased by an amount )B{sub}p above that of free plasma, and this additional pressure is balanced by tension in membrane-bound glycoprotein chains or strands [6]. An applied force sufficient to compress the ESL must exceed )B{sub}p in order to relieve the tension in the strands.
机译:血管的内表面衬有一层结合或吸附的大分子,称为内皮表面层(ESL)。在体内调查毛细血管中的血流已经表明,该层厚度为1μm。 ESL的存在被认为是导致毛细管中低管血细胞比容的主要因素[1],并且微血管中的较高流动性比具有相应直径的玻璃管[2]。通过轻染料处理破坏ESL [3]增加红细胞柱的宽度和毛细血管中标记的DECTRAN-70,没有可观察到的毛细管解剖直径的变化,这意味着ESL限制了红色血液的空间细胞运动和毛细血管中的等离子体流动。通过假设它是具有至少10 {sup} 8dyn≌/ cm {sup} 4的液压电阻率的多孔介质,所占抵消等离子体流动的能力。描述该层排除流动的红细胞的能力,Damiano等。 [5]将该层建模为弹性固体,而PRIES等。 [2]假设该层由于血浆蛋白质产生的胶体渗透压被吸附到ESL而产生的胶体渗透压。根据后一种假设,ESL内的胶体渗透压增加量增加了量的量)上方的量,并且这种额外的压力通过膜结合的糖蛋白链或股线的张力平衡[6]。足以压缩ESL的施加力必须超过)B {Sub} P以便缓解股线中的张力。

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