Function and morphology of the retinal pigment epithelium after light-induced damage.

The purpose of this study was to determine the threshold energy for light-induced functional damage of the retinal pigment epithelium at various wavelengths. Retinas of 58 pigmented and 21 albino rabbits were exposed to low intensity broadband blue light (400-520 nm), yellow light (510-740 nm), and narrowband blue light (408, 417, 439, 455, 485, 501 nm, respectively; deltalambda = 10-13 nm). The intensity values were 50, 280, and 5 mW x cm (-2), respectively, and the illumination time was 0.5 up to 5 h. The cumulative dose of light energy was calculated from these data (J x cm(-2)). The blood-retinal barrier dysfunction was evaluated in vivo using fluorophotometry to measure the leakage of fluorescein into the vitreous after intravenous injection and in vitro using light and electron microscopy after an in vivo intraarterial injection of horseradish peroxidase (HRP). The threshold energy for fluorescein leakage was 50 J x cm (-2) for blue light and 1,600 J x cm(-2) for yellow light. After broadband blue light exposure, the HRP reaction product was seen in the cytoplasm of the retinal pigment epithelium (RPE) cells and in the subretinal space but only if fluorescein leakage had been observed. Threshold energy and fluorescein leakage as a function of light energy were similar for albino and pigmented rabbits (P > 0.5). Only after yellow light exposure in excess of 3,700 J x cm(-2) was fluorescein leakage found. In that case complete disruption of the RPE was seen, but no HRP was observed in the RPE cytoplasm. Of the narrow-band blue light exposures, only that at lambda = 418 nm caused a significant increase in fluorescein leakage; the threshold energy was 18 J x cm(- 2). Blue light was found to be at least 30 times more efficient than yellow light in causing dysfunction of the blood-retinal barrier. The most efficient wavelength was 418 nm, corresponding with the absorption spectrum of cytochrome c oxidase. Melanin seemed to play no role. The presence or absence of melanin in the RPE appeared to have no influence on the threshold energy.

Spectral sensitivity of the blood-retinal barrier at the pigment epithelium for blue light in the 400-500 nm range.

To specify the spectral sensitivity of the retinal pigment epithelium (RPE) for blue light damage, pigmented rabbits were exposed to light of 408, 418, 439, 455, 485, and 500 nm (half-peak bandwidth approximately 12 nm). The range of radiant exposure was 15-275 J cm-2 (1.7-19 mW cm-2 for 0.5-5 h). Vitreous fluorophotometry was used to functionally evaluate the blood-retinal barrier at the RPE in vivo, and electron microscopy to visualize RPE ultrastructure in vitro. A significant increase in permeability of the blood-retinal barrier was seen only after exposure to light of 418 nm. Radiant exposure at threshold for permeability increase was 18 J cm-2. Electron microscopy of the RPE demonstrated dispersion and clumping of melanin granules. The results suggest that the RPE is most sensitive to light in the range 412-425 nm, possibly due to damage-mediating chromophores such as cytochrome c oxidase and lipofuscin.

Blood-retinal barrier dysfunction at the pigment epithelium induced by blue light.

Exposure to low-intensity white light can induce dysfunction of the blood-retinal barrier (BRB) at the retinal pigment epithelium (RPE). To determine whether the shorter wavelengths white light are responsible for this dysfunction, rabbit retinas were exposed to blue light (400-520 nm) or yellow light (510-740 nm). The permeability of the BRB, a parameter for the integrity of the barrier, was quantified with vitreous fluorophotometry. Morphologically, the barrier at the RPE was visualized on light and electron microscopy using horseradish peroxidase (HRP) as a tracer. Seventeen pigmented rabbits were exposed to blue light and 11 were exposed to yellow light. Vitreous fluorescein leakage increased with the exposure energy according to a power function (correlation coefficient > 0.79). The threshold energy for an increase in BRB permeability was 50 J/cm2 (0.014 W/cm2 for 1 hr) after blue and 1600 J/cm2 after yellow light. HRP tracing demonstrated that after blue light exposure, a significant fluorescein leakage on fluorophotometry corresponded to the presence of HRP in the RPE cells and in the subretinal space. After yellow light exposures of < 3700 J/cm2 and in rabbits with no significant fluorescein leakage, the HRP was limited to the choroidal capillaries and Bruch's membrane. These results demonstrate that the blue component of white light causes dysfunction of the BRB at the RPE 30 times more effectively than the longer wavelength fraction of white light. As a result, a blue light blocking filter should be used in ocular surgery on humans when an operating microscope is being used (light power 0.1-0.9 W/cm2).

Dysfunction and repair of the blood-retina barrier following white light exposure: a fluorophotometric and histologic study.

The purpose of this study was to pinpoint the site of blood-retina barrier disruption after white light exposure and determine the course of barrier repair. The retinas of 25 anaesthetized pigmented rabbits were exposed for 1 hr to the light of a xenon arc lamp filtered to eliminate ultraviolet and infrared light. The light intensities selected were near the threshold intensity causing visible retinal lesions in order to evaluate the function of the blood-retina barrier (BRB) in this range. Functional assessment of the BRB was made with vitreous fluorophotometry (VF), and electron microscopy (EM) after intra-arterial administration of horseradish peroxidase (HRP) as tracer. In 11 of the 14 rabbits exposed to threshold intensity (90-110 mW cm-2; retinal field of illumination, 0.64 cm2), a breakdown of the BRB was demonstrated by a 2-40-fold increase in the permeability of the BRB for fluorescein and by transcellular passage of HRP through the retina pigment epithelium (RPE). All 11 rabbits developed oedematous fundus lesions. Within a week, pigmentary alterations of the fundus were seen on ophthalmoscopy, while the BRB permeability for fluorescein and HRP had returned to normal. EM of the retina showed slight swelling of RPE during the period of increased permeability but no alterations of the neuroretina. After functional barrier repair, the RPE cells demonstrated irregularity of the melanin pigment alignment and some loss of the monocellular arrangement. In six rabbits exposed to subthreshold light intensity (65-89 mW cm-2) no fundus lesion developed and EM evaluation of the BRB was normal.2+ remains altered.

Lateral feedback from monophasic horizontal cells to cones in carp retina. I. Experiments.

The spatial and color coding of the monophasic horizontal cells were studied in light- and dark-adapted retinae. Slit displacement experiments revealed differences in integration area for the different cone inputs of the monophasic horizontal cells. The integration area measured with a 670-nm stimulus was larger than that measured with a 570-nm stimulus. Experiments in which the diameter of the test spot was varied, however, revealed at high stimulus intensities a larger summation area for 520-nm stimuli than for 670-nm stimuli. The reverse was found for low stimulus intensities. To investigate whether these differences were due to interaction between the various cone inputs to the monophasic horizontal cell, adaptation experiments were performed. It was found that the various cone inputs were not independent. Finally, some mechanisms for the spatial and color coding will be discussed.

Computed tomography of an ancient Egyptian cat.

The use of CT in the documentation of ancient Egyptian mummified human remains has previously been described in this and other journals. We recently applied this technique to a collection of ancient Egyptian mummified fauna and sarcophagi. We selected an example to illustrate that CT is also uniquely suitable for the study of such specimens in a noninvasive way.