Steroidal and nonsteroidal antiinflammatory medications can improve photoreceptor survival after laser retinal photocoagulation.

OBJECTIVE: To determine whether methylprednisolone or indomethacin can enhance photoreceptor survival after laser retinal injury in an animal model. DESIGN: Experimental study. PARTICIPANTS: Twenty rhesus monkeys. METHODS: Twenty rhesus monkeys (Macaca mulatta) received a grid of argon green (514.5 nm, 10 ms) laser lesions in the macula of the right eye and a grid of neodymium:yttrium-aluminum-garnet (Nd:YAG; 1064 nm, 10 ns) lesions in the macula of the left eye, followed by randomization to 2 weeks of treatment in 1 of 4 treatment groups: high-dose methylprednisolone, moderate-dose methylprednisolone, indomethacin, or control. The lesions were assessed at day 1, day 14, 2 months, and 4 months. The authors were masked to the treatment group. This report discusses the histologic results of ocular tissue harvested at 4 months. MAIN OUTCOME MEASURE: The number of surviving photoreceptor cell nuclei within each lesion was compared with the number of photoreceptor nuclei in surrounding unaffected retina. The proportion of surviving photoreceptor nuclei was compared between each treatment group. RESULTS: Argon retinal lesions in the high-dose steroid treatment group and the indomethacin treatment group demonstrated improved photoreceptor survival compared with the control group (P = 0.004). Hemorrhagic Nd:YAG lesions demonstrated improved survivability with indomethacin treatment compared with controls (P = 0.003). In nonhemorrhagic Nd:YAG laser retinal lesions, the lesions treated with moderate-dose steroids demonstrated improved photoreceptor survival compared with the control group (P = 0.004). CONCLUSIONS: Based on histologic samples of retinal laser lesions 4 months after injury, treatment with indomethacin resulted in improved photoreceptor survival in argon laser lesions and hemorrhagic Nd:YAG laser lesions. Treatment with systemic methylprednisolone demonstrated improved photoreceptor survival in argon retinal lesions and in nonhemorrhagic Nd:YAG lesions.

Lecithin:retinol acyltransferase in ARPE-19.

The purpose of this study is to investigate if a readily available cell line (APRE-19) may be used to study in vitro function of visual cycle enzymes such as lecithin:retinol acyltransferase (LRAT). Cells incubated with exogenous retinol accumulated intracellular all-trans retinol and all-trans retinyl ester. Membrane proteins from ARPE-19 exhibited LRAT activity, which was inhibited by an LRAT inhibitor, retinyl bromoacetate (RBA). Gene microarray and Western blot results indicated that ARPE-19 cells expressed LRAT transcript and the LRAT protein. Therefore, our data show that ARPE-19 contains an active LRAT enzyme and suggest that it is an appropriate cell system to study visual cycle enzymes.

Laser-induced macular holes demonstrate impaired choroidal perfusion.

PURPOSE: To evaluate choroidal perfusion following creation of a laser-induced macular hole in a nonhuman primate model. METHODS: Six rhesus monkeys underwent macular exposures delivered by a Q-switched Nd:YAG laser. The lesions were evaluated with fluorescein angiography and indocyanine green angiography using scanning laser ophthalmoscopy. RESULTS: Each lesion produced vitreous hemorrhage and progressed to a full-thickness macular hole. Indocyanine green angiography revealed no perfusion of the choriocapillaris beneath the lesion centers. Fluorescein angiography demonstrated mild enlargement of the foveal avascular zone due to loss of perifoveal capillaries. Histopathologic evaluation showed replacement of the choriocapillaris with fibroblasts and connective tissue. CONCLUSIONS: Nd:YAG laser-induced macular holes result in long-term impairment of choroidal perfusion at the base of the hole due to choroidal scarring and obliteration of the choriocapillaris. Evaluation of choroidal perfusion may be useful in assessment of laser-injured patients. Impairment in choroidal perfusion may have functional implications for surviving photoreceptors.