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肝流出道阻塞后肝窦灌注重塑的双相模型。

A biphasic model for sinusoidal liver perfusion remodeling after outflow obstruction.

机构信息

University of Duisburg-Essen, Essen, Germany.

出版信息

Biomech Model Mechanobiol. 2010 Aug;9(4):435-50. doi: 10.1007/s10237-009-0186-x. Epub 2010 Jan 12.

DOI:10.1007/s10237-009-0186-x
PMID:20066463
Abstract

Liver resection can lead to focal outflow obstruction due to transection of hepatic veins. Outflow obstruction may cause additional damage to the small remnant liver. Drainage of the obstructed territories is reestablished via dilatation of sinusoids. Subsequently, sinusoidal canals are formed draining the blood from the obstructed territory to the neighboring unobstructed territories. We raised the phenomenological hypothesis that the blood pressure gradient is the main driving force for the formation of sinusoidal vascular canals. We generated a biphasic mechanical model to describe this vascular remodeling process in relation to the variable pressure gradient. Therefore, we introduced a transverse isotropic permeability relation as well as an evolutional optimization rule to describe the relationship between pressure gradient and the direction of the sinusoidal blood flow in the fluid phase. As a next step, we developed a framework for the calculation concept including the representation of the governing weak formulations. Then, we examined a representative numerical example with simulation of the blood flow under both conditions, the physiological situation as well as after outflow obstruction. Doing so, we were able to reproduce numerically the experimentally observed process of reestablishing hepatic venous drainage via redirection of blood flow and formation of new vascular structures in respect to the fluid flow. The calculated results support the hypothesis that the reorientation of blood flow mainly depends on the pressure gradient. Further investigations are needed to determine the micromechanical influences on the reorientation of the sinusoids.

摘要

肝切除术可导致肝静脉横断后发生局部流出道阻塞。流出道阻塞可能会对残余的小肝组织造成额外的损伤。通过扩张窦状隙来重新建立阻塞区域的引流。随后,窦状隙通道形成,将血液从阻塞区域引流到邻近的未阻塞区域。我们提出了一个现象学假设,即血压梯度是窦状血管通道形成的主要驱动力。我们生成了一个双相力学模型,以描述与可变压力梯度相关的这种血管重塑过程。因此,我们引入了一个横向各向同性的渗透性关系以及一个进化优化规则,以描述压力梯度与血流方向之间的关系。在流体相中。接下来,我们为计算概念开发了一个框架,包括表示控制弱形式。然后,我们对一个有代表性的数值示例进行了检查,模拟了生理情况下以及流出道阻塞后的血流情况。这样,我们就能够在数值上重现通过重新引导血流和形成新的血管结构来重新建立肝静脉引流的实验观察过程。计算结果支持这样的假设,即血流的重新定向主要取决于压力梯度。需要进一步的研究来确定对窦状隙重新定向的微观力学影响。

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