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Shenouda Yacoub, Quinn Sessums, Byron Li, Ganesh Prasanna; Ocular Hypertension-Induced Changes in the Anterior Segment of Cynomolgus Monkeys. Invest. Ophthalmol. Vis. Sci. 2013;54(15):1975.
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To compare the corneal thickness (CT), corneal curvature (CC), anterior chamber depth (ACD), iridocorneal angle (ICA), and corneal endothelial cell density (ECD), in naïve and chronic ocular hypertensive (OHT) cynomolgus monkeys.
Chronic OHT of various durations (0.7-12 y) was induced in the right eye (OD) of 52 cynomolgus monkeys by argon laser trabeculoplasty. The left eye (OS) with normal intraocular pressure (IOP) was untreated. An additional 23 naïve animals served as controls. The central corneal thickness (CCT), para-central corneal thickness (PCCT), peripheral corneal thickness (PCT), CC, ACD and ICA were evaluated with a Galilei Dual Scheimpflug Analyzer (GDSA, SIS, Switzerland). The ECD at central corneal area was evaluated with a SP2000 Specular microscope (Topcon).
In the 23 naïve 4-yo monkeys, there were no differences in CT, CC, ACD, ICA, and ECD between OD and OS. In 20 OHT 4-yo monkeys (OHT duration in OD = 0.7 y), the differences of CT, CC, ACD and ICA between OD and OS were insignificant. However, significant ECD reduction in OD (-17.2%, P < 0.01) was detected compared to the OS. In a second group of 32 OHT monkeys (age = 7-16 y; OHT duration = 2-12 y), the mean CCT of OD (490 ± 23 µm) was thicker (11 µm, 2.4%, p < 0.05) than the contralateral control eyes (479 ± 20 µm). The ECD of OD was reduced (-20%, p < 0.001) compared to OS. There was no significant difference in PCCT, PCT, ACD, and ICA between OD and OS.
Chronic OHT in monkeys caused a duration-dependent reduction in ECD in the central corneal area. Longer duration of IOP elevation correlated with a more severe reduction, concomitant with a small increase of CCT. There was no difference in CC, ACD, and ICA between OHT and normal eyes. The thickening of CCT and progressive decrease of ECD observed in monkey eyes with increased duration of OHT is similar to the disease progression in primary open angle glaucoma patients.
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