Macromolecular transport in heart valves. II. Theoretical models.
Macromolecular transport in heart valves. II. Theoretical models.
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心脏瓣膜中的大分子运输。
DOI：
10.1152/ajpheart.00608.2006
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
Rumschitzki,DavidS
中科院分区：
文献类型：
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作者：
Zeng,Zhongqing;Yin,Yongyi;Jan,Kung-Ming;Rumschitzki,DavidS
本文基于本系列第一篇论文（第一部分；Zeng Z、Yin Y、Huang AL、Jan KM、Rumschitzki DS.Am J Physiol Heart Circ Physiol292：H2664–H2670，2007）中提出的基于大鼠辣根过氧化物酶（HRP）实验的心脏瓣膜大分子运输的二维对流扩散模型。实验需要两个瓣膜内膜，每个内皮下方各一个。汤普金斯等人。 (Tompkins RG, Schnitzer JJ, Yarmush ML.Circ Res64: 1213–1223, 1989) 在四只松鼠猴的相同实验中发现跨瓣125I标记的低密度脂蛋白(LDL)谱在形状和大小上存在很大差异。他们的一维、仅均匀介质扩散模型独立地拟合每个轮廓的三个参数；数据可变性导致参数分布较大。我们的理论旨在用一组参数来解释他们的数据。它使用测量参数和一些主动脉值，但拟合内皮传质系数（ka=kv= 1.63 × 10−8cm/s，其中下标 a 和 v 分别表示主动脉方面和心室方面）和中层渗透性（K\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(_{p_{2}}\) \end{document}= 2.28 × 10−16cm2) 和 LDL 扩散系数 [D2(LDL) = 5.93 × 10−9cm2/s]，使用 Tompkins 等人的配置文件之一，并在整个过程中修复它们。它准确地预测了第一部分在大鼠小叶中由于内膜稀疏的结构而导致的快速局部 HRP 渗漏点增长率，从而决定了其更大的传输参数 [K\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(_{p_{1}}\) \end{document}= 1.10 × 10−12cm2,D1(LDL/HRP) = 1.02/4.09 × 10−7cm2/s] 比中间层慢。这与具有类似大 HRP 点的大动脉形成对比，因为瓣膜没有内部弹性层。该模型定量地解释了汤普金斯等人使用这些相同参数的所有猴子特征。两个方面上不同数量和位置的孤立大分子泄漏以及不同的截面泄漏距离产生所有轮廓。
This paper proposes a new, two-dimensional convection-diffusion model for macromolecular transport in heart valves based on horseradish peroxidase (HRP) experiments on rats presented in the first of the papers in this series (Part I; Zeng Z, Yin Y, Huang AL, Jan KM, Rumschitzki DS.Am J Physiol Heart Circ Physiol292: H2664–H2670, 2007). Experiments require two valvular intimae, one underneath each endothelium. Tompkins et al. (Tompkins RG, Schnitzer JJ, Yarmush ML.Circ Res64: 1213–1223, 1989) found large variations in shape and magnitude in transvalvular125I-labeled low-density lipoprotein (LDL) profiles from identical experiments on four squirrel monkeys. Their one-dimensional, uniform-medium diffusion-only model fit three parameters independently for each profile; data variability resulted in large parameter spreads. Our theory aims to explain their data with one parameter set. It uses measured parameters and some aortic values but fits the endothelial mass transfer coefficient (ka=kv= 1.63 × 10−8cm/s, where subscripts a and v indicate aortic aspect and ventricular aspect, respectively) and middle layer permeability (K\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(_{p_{2}}\) \end{document}= 2.28 × 10−16cm2) and LDL diffusion coefficient [D2(LDL) = 5.93 × 10−9cm2/s], using one of Tompkins et al.'s profiles, and fixes them throughout. It accurately predicts Part I's rapid localized HRP leakage spot growth rate in rat leaflets that results from the intima's much sparser structure, dictating its far larger transport parameters [K\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(_{p_{1}}\) \end{document}= 1.10 × 10−12cm2,D1(LDL/HRP) = 1.02/4.09 × 10−7cm2/s] than the middle layer. This contrasts with large arteries with similarly large HRP spots, since the valve has no internal elastic lamina. The model quantitatively explains all of Tompkins et al.'s monkey profiles with these same parameters. Different numbers and locations of isolated macromolecular leaks on both aspects and different section-leak(s) distances yield all profiles.