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持续性压迫对椎间盘内氧代谢运输的影响随着退行性变化而降低。

The effect of sustained compression on oxygen metabolic transport in the intervertebral disc decreases with degenerative changes.

机构信息

Institute for Bioengineering of Catalonia, Barcelona, Spain.

出版信息

PLoS Comput Biol. 2011 Aug;7(8):e1002112. doi: 10.1371/journal.pcbi.1002112. Epub 2011 Aug 4.

DOI:10.1371/journal.pcbi.1002112
PMID:21829341
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3150290/
Abstract

Intervertebral disc metabolic transport is essential to the functional spine and provides the cells with the nutrients necessary to tissue maintenance. Disc degenerative changes alter the tissue mechanics, but interactions between mechanical loading and disc transport are still an open issue. A poromechanical finite element model of the human disc was coupled with oxygen and lactate transport models. Deformations and fluid flow were linked to transport predictions by including strain-dependent diffusion and advection. The two solute transport models were also coupled to account for cell metabolism. With this approach, the relevance of metabolic and mechano-transport couplings were assessed in the healthy disc under loading-recovery daily compression. Disc height, cell density and material degenerative changes were parametrically simulated to study their influence on the calculated solute concentrations. The effects of load frequency and amplitude were also studied in the healthy disc by considering short periods of cyclic compression. Results indicate that external loads influence the oxygen and lactate regional distributions within the disc when large volume changes modify diffusion distances and diffusivities, especially when healthy disc properties are simulated. Advection was negligible under both sustained and cyclic compression. Simulating degeneration, mechanical changes inhibited the mechanical effect on transport while disc height, fluid content, nucleus pressure and overall cell density reductions affected significantly transport predictions. For the healthy disc, nutrient concentration patterns depended mostly on the time of sustained compression and recovery. The relevant effect of cell density on the metabolic transport indicates the disturbance of cell number as a possible onset for disc degeneration via alteration of the metabolic balance. Results also suggest that healthy disc properties have a positive effect of loading on metabolic transport. Such relation, relevant to the maintenance of the tissue functional composition, would therefore link disc function with disc nutrition.

摘要

椎间盘代谢转运对于功能性脊柱至关重要,为细胞提供维持组织所需的营养物质。椎间盘退行性变化改变了组织力学,但机械负荷与椎间盘转运之间的相互作用仍然是一个悬而未决的问题。本文将人体椎间盘的渗透力学有限元模型与氧和乳酸转运模型相耦合。通过包括应变相关扩散和对流,将变形和流体流动与转运预测联系起来。还将两个溶质转运模型耦合起来,以考虑细胞代谢。通过这种方法,在每日加载-恢复压缩下,评估了健康椎间盘代谢和力学转运耦联的相关性。通过参数模拟椎间盘高度、细胞密度和材料退行性变化,研究它们对计算溶质浓度的影响。还通过考虑短周期循环压缩,研究了负载频率和幅度对健康椎间盘的影响。结果表明,当大体积变化改变扩散距离和扩散系数时,外部负载会影响椎间盘内氧气和乳酸的区域分布,尤其是在模拟健康椎间盘特性时。在持续和循环压缩下,对流可以忽略不计。模拟退变时,力学变化抑制了对转运的力学影响,而椎间盘高度、流体含量、核压和总体细胞密度的降低则显著影响转运预测。对于健康的椎间盘,营养物质浓度模式主要取决于持续压缩和恢复的时间。细胞密度对代谢转运的相关影响表明,细胞数量的减少可能会通过改变代谢平衡而引发椎间盘退变。结果还表明,健康椎间盘的特性对负荷代谢转运有积极影响。这种与组织功能成分维持相关的关系,将椎间盘功能与椎间盘营养联系起来。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/251014de30a3/pcbi.1002112.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/a2c09dde155e/pcbi.1002112.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/91c53d5529fc/pcbi.1002112.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/fb7f3e21fa1a/pcbi.1002112.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/4012b2cb43b0/pcbi.1002112.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/c325d2deb33d/pcbi.1002112.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/172fc34e4623/pcbi.1002112.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/631543b65f22/pcbi.1002112.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/251014de30a3/pcbi.1002112.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/a2c09dde155e/pcbi.1002112.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/91c53d5529fc/pcbi.1002112.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/fb7f3e21fa1a/pcbi.1002112.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/4012b2cb43b0/pcbi.1002112.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/c325d2deb33d/pcbi.1002112.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/172fc34e4623/pcbi.1002112.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/631543b65f22/pcbi.1002112.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d1/3150290/251014de30a3/pcbi.1002112.g008.jpg

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