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视网膜神经节细胞内在感光(黑视素)在青光眼中的作用。

Intrinsically photosensitive (melanopsin) retinal ganglion cell function in glaucoma.

机构信息

Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Australia.

出版信息

Invest Ophthalmol Vis Sci. 2011 Jun 21;52(7):4362-7. doi: 10.1167/iovs.10-7069.

Abstract

PURPOSE

To determine whether glaucoma alters intrinsically photosensitive retinal ganglion cell (ipRGC) function.

METHODS

Forty-one patients (25 with glaucoma and 16 healthy age-matched control participants) were tested. Intrinsically photosensitive retinal ganglion cell function was directly measured by the sustained, postillumination pupil response (PIPR). Forty-one eyes of 41 participants were tested with 7°, 10-second, short-wavelength (488 nm; bluish) and long-wavelength (610 nm; reddish) stimuli (14.2 log photons · cm(-2) · s(-1)) presented to the right eye in Maxwellian view, and the consensual pupil response of the left eye was measured by infrared pupillometry. The difference between PIPR amplitude (percentage baseline pupil diameter), net PIPR (percentage change) and kinetics (time in mm · s(-1) to the PIPR plateau) for the blue and red stimuli in patients with early and advanced (moderate/severe) glaucoma was compared to that in age-matched control participants.

RESULTS

The blue PIPR was significantly smaller between normal participants and patients with advanced glaucoma, as well as between those with early and those with advanced glaucoma (P < 0.05). The kinetics of the red and blue PIPRs were not significantly different between any groups. Normal age-matched participants and patients with early-stage glaucoma were not significantly different on any parameter, and neither was the normal and glaucoma group (advanced and early combined).

CONCLUSIONS

Persons with moderate and severe glaucoma have a dysfunctional ipRGC-mediated PIPR. Intrinsically photosensitive retinal ganglion cell function measured directly with the PIPR may become a clinical indicator of progressive changes in glaucoma.

摘要

目的

确定青光眼是否会改变内在光敏性视网膜神经节细胞(ipRGC)的功能。

方法

共纳入 41 名患者(25 名青光眼患者和 16 名年龄匹配的健康对照者)。通过持续的光照后瞳孔反应(PIPR)直接测量内在光敏性视网膜神经节细胞功能。用 7°、10 秒、短波(488nm;蓝色)和长波(610nm;红色)刺激物(14.2log 光子·cm(-2)·s(-1))对右眼进行测试,采用麦克斯韦视野,对左眼进行共发性瞳孔反应的红外瞳孔测量。比较早期和晚期(中度/重度)青光眼患者与年龄匹配的对照组之间,蓝色和红色刺激物的 PIPR 振幅(相对于基础瞳孔直径的百分比)、净 PIPR(百分比变化)和动力学(达到 PIPR 平台的时间,mm·s(-1))的差异。

结果

与正常参与者和晚期青光眼患者相比,早期青光眼患者的蓝色 PIPR 明显较小(P < 0.05)。红色和蓝色 PIPR 的动力学在任何组之间均无显著差异。正常年龄匹配的参与者和早期青光眼患者在任何参数上均无显著差异,正常和青光眼组(晚期和早期合并)之间也无显著差异。

结论

中度和重度青光眼患者的 ipRGC 介导的 PIPR 功能障碍。直接通过 PIPR 测量的内在光敏性视网膜神经节细胞功能可能成为青光眼进行性变化的临床指标。

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