Masella Benjamin D, Hunter Jennifer J, Williams David R
The Institute of Optics, University of Rochester, Rochester, New York, United States Center for Visual Science, University of Rochester, Rochester, New York, United States.
Center for Visual Science, University of Rochester, Rochester, New York, United States Flaum Eye Institute, University of Rochester, Rochester, New York, United States.
Invest Ophthalmol Vis Sci. 2014 Oct 14;55(11):7535-44. doi: 10.1167/iovs.13-13796.
Advances in retinal imaging have led to the discovery of long-lasting retinal changes caused by light exposures below published safety limits, including disruption of the RPE. To investigate the functional consequences of RPE disruption, we combined adaptive optics ophthalmoscopy with retinal densitometry.
A modified adaptive optics scanning light ophthalmoscope (AOSLO) measured the apparent density and regeneration rate of rhodopsin in two macaques before and after four different 568-nm retinal radiant exposures (RREs; 400-3200 J/cm(2)). Optical coherence tomography (OCT) was used to measure the optical path length through the photoreceptor outer segments before and after RPE disruption.
All tested RREs caused visible RPE disruption. Apparent rhodopsin density was significantly reduced following 1600 (P = 0.01) and 3200 J/cm(2) (P = 0.007) exposures. No significant change in apparent density was observed in response to 800 J/cm(2). Surprisingly, exposure to 400 J/cm(2) showed a significant increase in apparent density (P = 0.047). Rhodopsin recovery rate was not significantly affected by these RREs. Optical coherence tomography measurements showed a significant decrease in the optical path length through the photoreceptor outer segments for RREs above 800 J/cm(2) (P < 0.001).
At higher RREs, optical path length through the outer segments was reduced. However, the rate of photopigment regeneration was unchanged. While some ambiguity remains as to the correlation between measured reflectivity and absolute rhodopsin density; at the lowest RREs, RPE disruption appears not to be accompanied by a loss of apparent rhodopsin density, which would have been indicative of functional loss.
视网膜成像技术的进步促使人们发现,低于已公布安全限值的光暴露会导致视网膜发生长期变化,包括视网膜色素上皮(RPE)的破坏。为了研究RPE破坏的功能后果,我们将自适应光学检眼镜与视网膜密度测量相结合。
使用改良的自适应光学扫描激光检眼镜(AOSLO)测量了两只猕猴在四次不同的568纳米视网膜辐射暴露(RRE;400 - 3200 J/cm²)前后视紫红质的表观密度和再生率。光学相干断层扫描(OCT)用于测量RPE破坏前后通过光感受器外段的光程长度。
所有测试的RRE均导致可见的RPE破坏。在1600(P = 0.01)和3200 J/cm²(P = 0.007)暴露后,视紫红质的表观密度显著降低。在800 J/cm²暴露后,未观察到表观密度的显著变化。令人惊讶的是,400 J/cm²暴露显示表观密度显著增加(P = 0.047)。这些RRE对视紫红质的恢复率没有显著影响。光学相干断层扫描测量显示,对于高于800 J/cm²的RRE,通过光感受器外段的光程长度显著减少(P < 0.001)。
在较高的RRE下,通过外段的光程长度减少。然而,光色素的再生速率未改变。虽然测量的反射率与视紫红质绝对密度之间的相关性仍存在一些不确定性;在最低的RRE下,RPE破坏似乎并未伴随着视紫红质表观密度的损失,而视紫红质表观密度的损失本可表明功能丧失。