在存在轴向扩散的情况下对肌红蛋白功能的评估。

Gardner J D, Schubert R W

Biomedical Engineering Department, Louisiana Tech University, Ruston 71272, USA.

Adv Exp Med Biol. 1997;411:157-69. doi: 10.1007/978-1-4615-5865-1_20.

Facilitation of oxygen transport by myoglobin has been assessed by many researchers. Yet, the models used in these studies often assume that radial diffusion is the primary transport mechanism in tissue. Axial diffusion is typically neglected. In this study, oxygen transport by myoglobin facilitation is added to a proven cardiac tissue model which contains axial diffusion in the tissue and capillary regions, the Radially-Averaged, Axially-Distributed (RAAD) model. Previous research has shown that the axial diffusion in the capillary and tissue regions becomes coupled, causing a reduction in the pO2 at the capillary inlet. The objective is to determine if this coupling effect increases the facilitation of oxygen transport by myoglobin. The RAAD model consists of non-interacting cylinders of tissue (Krogh cylinders), with each perfused by a central capillary. Derivation of the equations describing the RAAD model yields a stiff, fourth-order, non-linear, ODE, BVP. The equation set is solved numerically. Parameters for myoglobin concentration and diffusion coefficient are chosen to maximize myoglobin facilitation. The effect of myoglobin is assessed by observing changes in the pO2 profiles for the model with and without myoglobin. Also, the RAAD model is compared to experimental pO2 data to determine if the inclusion of myoglobin improves the model prediction. The computer simulations show that myoglobin does facilitate diffusion, but only to a small extent. The changes in the capillary pO2 profiles for the model with and without myoglobin are not significant, pO2 reductions are 0.8% at the inlet and 2% at the outlet. The model prediction is not substantially improved with the addition of myoglobin. The sum of squared error is reduced by 0.1%, from 5.6834 without myoglobin, to 5.6779 with myoglobin. The steady state solution of the RAAD model with myoglobin suggests that, in the presence of axial diffusion, facilitation of oxygen diffusion to tissue is not myoglobin's primary function. No conclusion can be made about the transient function of myoglobin.

许多研究人员已对肌红蛋白促进氧运输的作用进行了评估。然而，这些研究中使用的模型通常假定径向扩散是组织中的主要运输机制。轴向扩散通常被忽略。在本研究中，将肌红蛋白促进氧运输的作用添加到一个经过验证的心脏组织模型中，该模型包含组织和毛细血管区域中的轴向扩散，即径向平均、轴向分布（RAAD）模型。先前的研究表明，毛细血管和组织区域中的轴向扩散相互耦合，导致毛细血管入口处的pO2降低。目的是确定这种耦合效应是否会增加肌红蛋白对氧运输的促进作用。RAAD模型由不相互作用的组织圆柱体（克罗格圆柱体）组成，每个圆柱体由中央毛细血管灌注。描述RAAD模型的方程推导得出一个刚性的、四阶的、非线性的常微分方程边值问题（ODE，BVP）。该方程组通过数值求解。选择肌红蛋白浓度和扩散系数的参数以使肌红蛋白的促进作用最大化。通过观察有无肌红蛋白时模型的pO2分布变化来评估肌红蛋白的作用。此外，将RAAD模型与实验pO2数据进行比较，以确定添加肌红蛋白是否能改善模型预测。计算机模拟表明，肌红蛋白确实能促进扩散，但程度较小。有无肌红蛋白时模型的毛细血管pO2分布变化不显著，入口处pO2降低0.8%，出口处降低2%。添加肌红蛋白后模型预测没有得到实质性改善。均方误差总和降低了0.1%，从无肌红蛋白时的5.6834降至有肌红蛋白时的5.6779。含有肌红蛋白的RAAD模型的稳态解表明，在存在轴向扩散的情况下向组织促进氧扩散并非肌红蛋白的主要功能。关于肌红蛋白的瞬态功能无法得出结论。