Williamson Blake K, Hawkey Nathan M, Blake Diane A, Frenkel Joshua W, McDaniel Kevin P, Davis Justin K, Satija Celine, Beazer Alex, Dhungana Suraj, Carlson James, McRitchie Susan, Ayyala Ramesh S
Department of Ophthalmology, Tulane University School of Medicine, New Orleans, LA, USA.
Department of Biochemistry and Molecular Biology, Tulane University School of Medicine, New Orleans, LA, USA.
Transl Vis Sci Technol. 2018 Feb 2;7(1):14. doi: 10.1167/tvst.7.1.14. eCollection 2018 Feb.
Glaucoma drainage device (GDD) implantation can lead to corneal decompensation. We evaluated changes over time in oxygen tension and in the metabolic environment of the aqueous humor after GDD implantation in the rabbit eye.
Ahmed Glaucoma Valves were implanted in the left eyes of eight male New Zealand white rabbits. Right eyes were used as a control. Oxygen tension was measured immediately before surgery and at 1 and 2 months postoperation. Aqueous humor was collected from the surgical and control eyes at 1, 2, and 5 months postoperation. Aqueous humor samples collected at 1 and 5 months postoperation were selected for broad-spectrum metabolomics analysis using ultra-performance liquid chromatography-time of flight-mass spectrometry (UPLC TOF-MS). Multivariate analysis methods were used to identify metabolite profiles that separated the surgical and control eye at 1 and 5 months.
There was a significant decrease in oxygen tension in aqueous humor of the surgical eyes (9 mm Hg, 95% confidence interval [CI]: -14.7 to -3.5). Differences in the metabolic profiles between the surgical and control eye at 1 and 5 months were observed, as were differences for the surgical eye at 1 and 5 months. In addition, a metabolite profile was identified that differentiated the surgical eyes at 1 and 5 months.
Changes in the oxygen tension and metabolic intermediates occur within the aqueous humor as early as 1 month after GDD implantation.
Corneal decompensation following GDD implantation could be secondary to disruption of the normal aqueous circulation, resulting in hypoxia and an altered metabolic profile. Alterations to the GDD design might minimize aqueous disruption and prevent corneal decompensation.
青光眼引流装置（GDD）植入可导致角膜失代偿。我们评估了兔眼植入GDD后房水氧张力和代谢环境随时间的变化。
将艾哈迈德青光眼阀植入8只雄性新西兰白兔的左眼。右眼作为对照。在手术前以及术后1个月和2个月测量氧张力。在术后1、2和5个月从手术眼和对照眼中采集房水。选择术后1个月和5个月采集的房水样本，使用超高效液相色谱-飞行时间质谱（UPLC TOF-MS）进行广谱代谢组学分析。采用多变量分析方法确定在1个月和5个月时区分手术眼和对照眼的代谢物谱。
手术眼房水中的氧张力显著降低（9 mmHg，95%置信区间[CI]：-14.7至-3.5）。观察到手术眼和对照眼在1个月和5个月时代谢谱的差异，以及手术眼在1个月和5个月时的差异。此外，还确定了一种能区分手术眼在1个月和5个月时的代谢物谱。
GDD植入后最早在1个月内房水中的氧张力和代谢中间体就会发生变化。
GDD植入后角膜失代偿可能继发于正常房水循环的破坏，导致缺氧和代谢谱改变。对GDD设计的改变可能会使房水干扰最小化并预防角膜失代偿。
