PDF(Pubmed)
Abstract：
BACKGROUND: Aqueous humor outflow resistance in the trabecular meshwork (TM), juxtacanalicular connective tissue (JCT), and Schlemm\'s canal (SC) endothelium of the conventional outflow pathway actively contribute to intraocular pressure (IOP) regulation. Outflow resistance is actively affected by the dynamic outflow pressure gradient across the TM, JCT, and SC inner wall tissues. The resistance effect implies the presence of a fluid-structure interaction (FSI) coupling between the outflow tissues and the aqueous humor. However, the biomechanical interactions between viscoelastic outflow tissues and aqueous humor dynamics are largely unknown.
METHODS: A 3D microstructural finite element (FE) model of a healthy human eye TM/JCT/SC complex was constructed with elastic and viscoelastic material properties for the bulk extracellular matrix and embedded elastic cable elements. The FE models were subjected to both idealized and a physiologic IOP load boundary using the FSI method.
RESULTS: The elastic material model for both the idealized and physiologic IOP load boundary at equal IOPs showed similar stresses and strains in the outflow tissues as well as pressure in the aqueous humor. However, outflow tissues with viscoelastic material properties were sensitive to the IOP load rate, resulting in different mechanical and hydrodynamic responses in the tissues and aqueous humor.
CONCLUSIONS: Transient IOP fluctuations may cause a relatively large IOP difference of ~20 mmHg in a very short time frame of ~0.1 s, resulting in a rate stiffening in the outflow tissues. Rate stiffening reduces strains and causes a rate-dependent pressure gradient across the outflow tissues. Thus, the results suggest it is necessary to use a viscoelastic material model in outflow tissues that includes the important role of IOP load rate.
METHODS: A 3D microstructural finite element (FE) model of a healthy human eye TM/JCT/SC complex was constructed with elastic and viscoelastic material properties for the bulk extracellular matrix and embedded elastic cable elements. The FE models were subjected to both idealized and a physiologic IOP load boundary using the FSI method.
RESULTS: The elastic material model for both the idealized and physiologic IOP load boundary at equal IOPs showed similar stresses and strains in the outflow tissues as well as pressure in the aqueous humor. However, outflow tissues with viscoelastic material properties were sensitive to the IOP load rate, resulting in different mechanical and hydrodynamic responses in the tissues and aqueous humor.
CONCLUSIONS: Transient IOP fluctuations may cause a relatively large IOP difference of ~20 mmHg in a very short time frame of ~0.1 s, resulting in a rate stiffening in the outflow tissues. Rate stiffening reduces strains and causes a rate-dependent pressure gradient across the outflow tissues. Thus, the results suggest it is necessary to use a viscoelastic material model in outflow tissues that includes the important role of IOP load rate.
摘要：
背景：小梁网（TM）中的房水流出阻力，结膜结缔组织（JCT），常规流出途径的Schlemm管（SC）内皮积极促进眼内压（IOP）调节。流出阻力受跨TM的动态流出压力梯度的影响。JCT,和SC内壁组织。阻力效应意味着流出组织和房水之间存在流体-结构相互作用（FSI）耦合。然而,粘弹性流出组织和房水动力学之间的生物力学相互作用在很大程度上是未知的。
方法：构建了健康人眼TM/JCT/SC复合物的3D微结构有限元（FE）模型，该模型具有弹性和粘弹性材料特性，用于大块细胞外基质和嵌入的弹性索元件。使用FSI方法对FE模型进行理想化和生理IOP负荷边界。
结果：在相同IOP下，理想化和生理性IOP负荷边界的弹性材料模型显示，流出组织中的应力和应变以及房水中的压力相似。然而,具有粘弹性材料特性的流出组织对IOP负荷率敏感，导致组织和房水不同的机械和流体动力学响应。
结论：瞬时眼压波动可能会在〜0.1s的非常短的时间范围内导致〜20mmHg的相对较大的眼压差异，导致流出组织的速率变硬。速率硬化可减少应变，并导致整个流出组织的速率依赖性压力梯度。因此，结果表明，有必要在流出组织中使用粘弹性材料模型，其中包括IOP负荷率的重要作用。
方法：构建了健康人眼TM/JCT/SC复合物的3D微结构有限元（FE）模型，该模型具有弹性和粘弹性材料特性，用于大块细胞外基质和嵌入的弹性索元件。使用FSI方法对FE模型进行理想化和生理IOP负荷边界。
结果：在相同IOP下，理想化和生理性IOP负荷边界的弹性材料模型显示，流出组织中的应力和应变以及房水中的压力相似。然而,具有粘弹性材料特性的流出组织对IOP负荷率敏感，导致组织和房水不同的机械和流体动力学响应。
结论：瞬时眼压波动可能会在〜0.1s的非常短的时间范围内导致〜20mmHg的相对较大的眼压差异，导致流出组织的速率变硬。速率硬化可减少应变，并导致整个流出组织的速率依赖性压力梯度。因此，结果表明，有必要在流出组织中使用粘弹性材料模型，其中包括IOP负荷率的重要作用。
