Polse K A, Brand R J, Cohen S R, Guillon M
School of Optometry, University of California, Berkeley 94720.
Invest Ophthalmol Vis Sci. 1990 Aug;31(8):1542-54.
Normal corneal metabolism depends on a critical level of oxygen, below which a series of acute corneal responses occur, including an increase in stromal lactate, a reduction in intercellular pH, and an increase in corneal hydration. These acute responses are reversible when normal oxygen is restored; however, it has been shown that chronic exposure to low oxygen levels can result in permanent morphologic changes in the corneal endothelium. Clinicians have expressed concern that these observed structural changes may also be accompanied by alterations in corneal physiology. Whether such effects occur is not known, since it has been difficult to assess human corneal function accurately. Recently, we have developed an in vivo test, able to measure overall corneal hydration control, that can be used to study the effects of hypoxia on corneal function. This test provides information on several characteristics of hydration control, one of which is the percent corneal thickness recovery per hour (PRPH) after inducing corneal swelling. In this study, we assumed that corneal hypoxia accompanies both extended and polymethylmethacrylate (PMMA) contact lens wear and that the dose received is related to the years of past lens wear. Using this paradigm, we explored the relationship of hypoxic dose to an endothelial polymegethism index (EPI), endothelial cell density (ECD), and PRPH in 36 subjects with varying contact lens wearing histories. Based on multiple regression analysis, the relative change (expressed as percent per year) associated with hypoxic dose (adjusted for age and gender) was found to be dose-dependent and corresponded to estimated changes of 1.70%/yr, -0.25%/yr, and -1.26%/yr, with 95% confidence limits of (-0.3, 3.7), (-1.4, 0.9), and (-2.6, 0.06) for EPI, ECD, and PRPH, respectively. These preliminary data suggest that hypoxic exposure alters endothelial morphology and reduces corneal function; however, it is important to indicate that this was a exploratory investigation with several limitations, and that therefore these results should be viewed as preliminary until more definitive studies are completed.
正常角膜代谢依赖于临界水平的氧气，低于此水平会发生一系列急性角膜反应，包括基质乳酸增加、细胞间pH值降低以及角膜水合作用增加。当恢复正常氧气供应时，这些急性反应是可逆的；然而，研究表明，长期暴露于低氧水平会导致角膜内皮出现永久性形态学改变。临床医生担心这些观察到的结构变化可能还伴有角膜生理功能的改变。由于难以准确评估人类角膜功能，尚不清楚是否会出现此类影响。最近，我们开发了一种体内测试方法，能够测量角膜整体水合作用控制情况，可用于研究缺氧对角膜功能的影响。该测试提供了有关水合作用控制的几个特征的信息，其中之一是诱导角膜肿胀后每小时角膜厚度恢复百分比（PRPH）。在本研究中，我们假设角膜缺氧与长期佩戴和聚甲基丙烯酸甲酯（PMMA）隐形眼镜有关，且所接受的剂量与过去佩戴镜片的年限相关。采用此模式，我们在36名有不同隐形眼镜佩戴史的受试者中探究了缺氧剂量与内皮多形性指数（EPI）、内皮细胞密度（ECD）和PRPH之间的关系。基于多元回归分析，发现与缺氧剂量相关的相对变化（以每年百分比表示）（根据年龄和性别进行调整）呈剂量依赖性，EPI、ECD和PRPH的估计变化分别为每年1.70%、-0.25%和-1.26%，95%置信区间分别为（-0.3, 3.7）、（-1.4, 0.9）和（-2.6, 0.06）。这些初步数据表明缺氧暴露会改变内皮形态并降低角膜功能；然而，必须指出这是一项存在若干局限性的探索性研究，因此在完成更具确定性的研究之前，这些结果应被视为初步结果。
