Department of Ophthalmology & Visual Sciences, Washington University School of Medicine, St. Louis, Missouri.
Invest Ophthalmol Vis Sci. 2013 Oct 15;54(10):6549-59. doi: 10.1167/iovs.13-12609.
Previous studies that measured liquefaction and oxygen content in human vitreous suggested that exposure of the lens to excess oxygen causes nuclear cataracts. Here, we developed a computational model that reproduced available experimental oxygen distributions for intact and degraded human vitreous in physiologic and environmentally perturbed conditions. After validation, the model was used to estimate how age-related changes in vitreous physiology and structure alter oxygen levels at the lens.
A finite-element model for oxygen transport and consumption in the human vitreous was created. Major inputs included ascorbate-mediated oxygen consumption in the vitreous, consumption at the posterior lens surface, and inflow from the retinal vasculature. Concentration-dependent relations were determined from experimental human data or estimated from animal studies, with the impact of all assumptions explored via parameter studies.
The model reproduced experimental data in humans, including oxygen partial pressure (Po2) gradients (≈15 mm Hg) across the anterior-posterior extent of the vitreous body, higher oxygen levels at the pars plana relative to the vitreous core, increases in Po2 near the lens after cataract surgery, and equilibration in the vitreous chamber following vitrectomy. Loss of the antioxidative capacity of ascorbate increases oxygen levels 3-fold at the lens surface. Homogeneous vitreous degeneration (liquefaction), but not partial posterior vitreous detachment, greatly increases oxygen exposure to the lens.
Ascorbate content and the structure of the vitreous gel are critical determinants of lens oxygen exposure. Minimally invasive surgery and restoration of vitreous structure warrant further attention as strategies for preventing nuclear cataracts.
先前研究表明，晶状体暴露于过量氧气中会导致核性白内障，这些研究通过测量人眼玻璃体的液化和氧含量得出。在此，我们开发了一个计算模型，重现了在生理和环境干扰条件下完整和降解的人眼玻璃体中可用的实验氧分布。模型验证后，用于估计与年龄相关的玻璃体生理学和结构变化如何改变晶状体的氧水平。
建立了一个人眼玻璃体中氧传输和消耗的有限元模型。主要输入包括玻璃体中抗坏血酸介导的氧消耗、后晶状体表面的消耗以及视网膜血管流入。浓度依赖性关系是从实验人体数据中确定的，或从动物研究中估计的，通过参数研究探讨了所有假设的影响。
模型重现了人类的实验数据，包括玻璃体体前后方向的氧分压（Po2）梯度（≈15mmHg）、相对于玻璃体核心，扁平部的氧水平更高、白内障手术后晶状体附近的 Po2 增加以及玻璃体切除术后玻璃体腔内的平衡。抗坏血酸抗氧化能力的丧失会使晶状体表面的氧水平增加 3 倍。均匀的玻璃体变性（液化），而不是部分后玻璃体脱离，会大大增加晶状体的氧气暴露。
抗坏血酸含量和玻璃体凝胶结构是晶状体氧气暴露的关键决定因素。微创手术和玻璃体结构的恢复作为预防核性白内障的策略值得进一步关注。
