Karimi Alireza, Razaghi Reza, Rahmati Seyed Mohammadali, Downs J Crawford, Acott Ted S, Kelley Mary J, Wang Ruikang K, Johnstone Murray
Department of Ophthalmology and Visual Sciences, University of Alabama at Birmingham, Birmingham, AL 35233, USA.
School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA 30332, USA.
Bioengineering (Basel). 2022 Nov 10;9(11):672. doi: 10.3390/bioengineering9110672.
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.
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.
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.
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.
传统房水流出途径中的小梁网（TM）、邻管结缔组织（JCT）和施莱姆管（SC）内皮的房水流出阻力对眼压（IOP）调节起着积极作用。流出阻力受到跨TM、JCT和SC内壁组织的动态流出压力梯度的积极影响。阻力效应意味着流出组织与房水之间存在流固耦合（FSI）。然而，粘弹性流出组织与房水动力学之间的生物力学相互作用在很大程度上尚不清楚。
构建了一个健康人眼TM/JCT/SC复合体的三维微观结构有限元（FE）模型，其细胞外基质主体具有弹性和粘弹性材料特性，并嵌入了弹性索单元。使用FSI方法对FE模型施加理想化和生理IOP负荷边界。
在相同IOP下，理想化和生理IOP负荷边界的弹性材料模型在流出组织中显示出相似的应力和应变，以及房水中的压力。然而，具有粘弹性材料特性的流出组织对IOP负荷率敏感，导致组织和房水中不同的力学和流体动力学响应。
短暂的IOP波动可能在约0.1 s的极短时间内导致约20 mmHg的相对较大IOP差异，从而导致流出组织的速率硬化。速率硬化会降低应变，并在流出组织中产生与速率相关的压力梯度。因此，结果表明有必要在流出组织中使用粘弹性材料模型，该模型应考虑IOP负荷率的重要作用。
