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动脉狭窄处低密度脂蛋白及其分解产物释放速率的理论模型。

Theoretical modelling of the release rate of low-density lipoproteins and their breakdown products at arterial stenoses.

作者信息

Deng X, Stroman P W, Guidoin R

机构信息

Department of Surgery, Laval University, Quebec.

出版信息

Clin Invest Med. 1996 Apr;19(2):83-91.

PMID:8697674
Abstract

Arterial stenoses and luminal-surface irregularities at anastomoses cause blood-flow disturbances with slow recirculation. The authors created a computer simulation to study the rates of the release into blood of atherogenic substances such as low-density lipoproteins and their breakdown products from within the arterial walls at stenoses. Finite-difference methods were used to solve the Navier-Stokes equations (in the form of stream function and vorticity function) and the steady-state mass transfer equation for bell-shaped stenoses with two different degrees of constriction. This simulation indicated that the efflux rates of lipids and their breakdown products from the vessel walls were suppressed in the region of disturbed flow, with slow circulation distal to stenoses. The lowest efflux rate was found at the point of flow separation, and this rate was much lower than rates in regions of undisturbed flow. Therefore, this mathematical model predicts that locally disturbed blood flow at arterial stenoses and arterial anastomoses is responsible for two distinct phenomena: first, it provides favourable conditions for lipid infiltration into vessel walls; and, second, it impairs the release into the blood of atherogenic substances accumulated in the vessel wall. Such mass transfer abnormalities may account for atherogenesis and the late failures of arterial reconstructions at these sites.

摘要

吻合处的动脉狭窄和管腔表面不规则会导致血流紊乱以及血液缓慢再循环。作者创建了一个计算机模拟,以研究动脉壁狭窄处诸如低密度脂蛋白及其分解产物等致动脉粥样硬化物质向血液中的释放速率。采用有限差分法求解具有两种不同收缩程度的钟形狭窄的纳维-斯托克斯方程(以流函数和涡度函数的形式)以及稳态传质方程。该模拟表明,在血流紊乱区域,脂质及其分解产物从血管壁的流出速率受到抑制,狭窄远端血流缓慢。在血流分离点发现最低流出速率,且该速率远低于未受干扰血流区域的速率。因此,该数学模型预测,动脉狭窄和动脉吻合处局部血流紊乱会导致两种不同现象:第一,为脂质浸润血管壁提供了有利条件;第二,损害了血管壁中积累的致动脉粥样硬化物质向血液中的释放。这种传质异常可能是这些部位动脉粥样硬化形成以及动脉重建后期失败的原因。

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