PURPOSE: We used N-methyl-N-nitrosourea (MNU) to induce chorioretinopathy as a model of retinitis pigmentosa, and compared the histological localization of indocyanine green (ICG) with ICG angiographic features. METHODS: Brown-Norway pigmented rats received a single intraperitoneal injection of MNU (75 mg/kg body weight). At 3 and 21 days after treatment, we compared ICG angiographic findings with histological localization of ICG in the retina and choroid. Histological localization of ICG was observed with an infrared light microscope. RESULTS: 3 days after treatment, destruction of the photoreceptor cells and photoreceptor segments had developed, and the retinal pigment epithelial cells (RPEs) were also damaged. In ICG angiography, diffuse hyperfluorescence was evident. In histological localization of ICG, RPEs were stained by ICG, and ICG was seen in the sensory retina through the damaged RPEs. At 21 days after treatment, the inner nuclear layer directly contact with the choroid. The photoreceptor cells, RPEs and choriocapillaris had disappeared. In ICG angiography, hypofluorescence was seen in the chorioretinal atrophic area. In histological localization of ICG, there was no ICG in the atrophic area, but ICG leaked from the remaining choriocapillaris into the neighboring sensory retina. CONCLUSION: These results support the precise interpretation of ICG angiographic findings in clinical use.
PURPOSE: We used N-methyl-N-nitrosourea (MNU) to induce chorioretinopathy as a model of retinitis pigmentosa, and compared the histological localization of indocyanine green (ICG) with ICG angiographic features. METHODS: Brown-Norway pigmented rats received a single intraperitoneal injection of MNU (75 mg/kg body weight). At 3 and 21 days after treatment, we compared ICG angiographic findings with histological localization of ICG in the retina and choroid. Histological localization of ICG was observed with an infrared light microscope. RESULTS: 3 days after treatment, destruction of the photoreceptor cells and photoreceptor segments had developed, and the retinal pigment epithelial cells (RPEs) were also damaged. In ICG angiography, diffuse hyperfluorescence was evident. In histological localization of ICG, RPEs were stained by ICG, and ICG was seen in the sensory retina through the damaged RPEs. At 21 days after treatment, the inner nuclear layer directly contact with the choroid. The photoreceptor cells, RPEs and choriocapillaris had disappeared. In ICG angiography, hypofluorescence was seen in the chorioretinal atrophic area. In histological localization of ICG, there was no ICG in the atrophic area, but ICG leaked from the remaining choriocapillaris into the neighboring sensory retina. CONCLUSION: These results support the precise interpretation of ICG angiographic findings in clinical use.