Effects of hypoxia and hypercapnia on contact lens-induced corneal acidosis.
Effects of hypoxia and hypercapnia on contact lens-induced corneal acidosis.
复制标题
缺氧和高碳酸血症对隐形眼镜引起的角膜酸中毒的影响。
DOI：
10.1097/00006324-199603000-00009
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Polse,KA
中科院分区：
文献类型：
--
作者：
Rivera,RK;Polse,KA
角膜接触透镜配戴（CLW）可能会引起角膜基质酸中毒，这是角膜缺氧和泪液-透镜界面CO2蓄积（高碳酸血症）的结果。然而，它还没有直接显示是否缺氧和高碳酸血症是CL诱导的角膜酸化的唯一原因。在这项研究中，我们提供了初步的数据，高碳酸血症和缺氧的相对贡献CL诱导的基质酸化通过监测pH值，而角膜暴露于高压氧气氛。该范例最小化（如果没有消除）了除一名受试者之外的所有受试者的镜片诱导缺氧的pH效应，而不改变高碳酸血症的pH效应。7名受试者配戴水凝胶镜片; 5名为低O2透过率（Dk/LO 2 = 14.0 × 10-9（cm/s）（ml 02/[ml x mm Hg]））镜片，2名为中等O2透过率（Dk/LO 2= 17.2 × 10-9（cm/s）（ml 02/[ml x mm Hg]））镜片。在透镜植入后，安装改良的护目镜，通过将一只眼睛暴露于20%O2和80%N2（空气），对侧眼睛暴露于80%O2和20%N2（高压O2）来控制角膜环境。在CL插入前和配戴120分钟后测量角膜厚度（CT）。我们假设，如果在测试期间CT增加，则存在角膜缺氧。在透镜植入前，使用裂隙灯荧光光度计测量基质pH值，每隔20分钟测量一次，共80分钟。在高压暴露下配戴低Dk/L透镜80分钟后，5名受试者中有4名显示pH值降低（平均ApH= 0.23±0.05），CT无增加，表明仅高碳酸血症导致酸中毒。对于相同的透镜，但暴露于空气中，5名受试者中有4名显示pH值下降较大（平均ApH= 0.62±0.48），表明低氧和高碳酸血症均降低pH。佩戴中等Dk/L透镜的受试者在空气和高压条件下均显示出较小但相等的pH下降，而CT无变化，表明只有高碳酸血症才能导致酸中毒。这些初步结果表明，这两种机制都有助于伴随CLW的pH值变化，高碳酸血症的贡献约为30%。最后，高碳酸血症和缺氧的影响取决于个人的代谢要求和传递的透镜0 2和C 0 2。
It has been assumed that contact lens wear (CLW) may induce stromal acidosis, which is a result of corneal hypoxia and the accumulation of CO 2 (hypercapnia) at the tear-lens interface. However, it has not been directly shown whether hypoxia and hypercapnia are the only causes of CL-induced corneal acidification. In this study, we provide preliminary data about the relative contributions of hypercapnia and hypoxia to CL-induced stromal acidification by monitoring pH while the cornea was exposed to a hyperbaric oxygen atmosphere. This paradigm minimized if not eliminated the pH effects of lens-induced hypoxia on all but one subject without altering the pH effect of hypercapnia. Seven subjects were fitted with hydrogel lenses; 5 with low 0 2 transmissibility (Dk/LO 2—14.0 x 10-9 (cm/s)(ml 02/[ml x mm Hg])), and 2 with medium O 2 transmissibility (Dk/LO 2= 17.2 x 10-9 (cm/s)(ml 0 2/[ml x mm Hg])) lenses. After lens insertion, modified goggles were fitted to control the corneal environment by exposing 1 eye to 20% O 2 and 80% N 2 (air), and the contralateral eye to 80% O 2 and 20% N 2 (hyperbaric O 2. Corneal thickness (CT) was measured before CL insertion and over 120 min of wear. We assumed that corneal hypoxia was present if CT increased during the test period. Stromal pH was measured using a slitlamp fluorophotometer before lens insertion and at 20-min intervals for a total of 80 min. After 80 min of wearing the low Dk/L lens under hyperbaric exposure, 4 of 5 subjects showed reduced pH (mean ApH= 0.23±0.05) and no increase in CT, suggesting that only hypercapnia was contributing to acidosis. For the same lens, but with exposure to air, 4 of 5 subjects showed a larger drop in pH (mean ApH= 0.62±0.48) compared to hyperbaric exposure and an increase in CT, indicating that both hypoxia and hypercapnia reduced pH. Subjects wearing the medium Dk/L lens showed a small but equal drop in pH under both air and hyperbaric conditions without changes in CT, suggesting that only hypercapnia was contributing to acidosis. These preliminary results suggest that both mechanisms contribute to the pH shift accompanying CLW and that the contribution of hypercapnia is approximately 30%. Finally, the effects of hypercapnia and hypoxia are dependent on individual metabolic requirements and the transmissibility of the lens to 0 2 and C0 2.