BACKGROUND: The morphologic changes of the retina, choroid, and respective vasculatures in an experimental model of diffuse photothrombosis and photodynamic injury were studied. METHODS: After intravenous injection of rose bengal (40 mg/kg), eyes of 21 albino rats were exposed to a light intensity of 15-17,000 ft-cd for 2 to 15 minutes. Survival times ranged from 15 minutes to 6 days. The specimens were studied by light and electron microscopy. RESULTS: Photothrombosis of retinal and choroidal vessels was variable in extension and duration. Vascular lesions included vacuolation and sloughing off of endothelium, and necrosis and apoptosis of pericytes and smooth muscle cells. Retinal and choroidal injuries exhibited considerable regional and structural differences, such as predominance in the outer versus inner retina, or focal versus diffuse injury. CONCLUSION: Damage produced by this model was irregular in extent and character, due to several hard-to-control parameters. It was presumably due not only to ischemia but also to free radical chain reactions initiated by photodynamic action. This model may not be suitable for rapid quantitative assessment of ischemic retinal injury, but it provides opportunities for the investigation of pathophysiologic mechanisms.
BACKGROUND: The morphologic changes of the retina, choroid, and respective vasculatures in an experimental model of diffuse photothrombosis and photodynamic injury were studied. METHODS: After intravenous injection of rose bengal (40 mg/kg), eyes of 21 albino rats were exposed to a light intensity of 15-17,000 ft-cd for 2 to 15 minutes. Survival times ranged from 15 minutes to 6 days. The specimens were studied by light and electron microscopy. RESULTS:Photothrombosis of retinal and choroidal vessels was variable in extension and duration. Vascular lesions included vacuolation and sloughing off of endothelium, and necrosis and apoptosis of pericytes and smooth muscle cells. Retinal and choroidal injuries exhibited considerable regional and structural differences, such as predominance in the outer versus inner retina, or focal versus diffuse injury. CONCLUSION: Damage produced by this model was irregular in extent and character, due to several hard-to-control parameters. It was presumably due not only to ischemia but also to free radical chain reactions initiated by photodynamic action. This model may not be suitable for rapid quantitative assessment of ischemic retinal injury, but it provides opportunities for the investigation of pathophysiologic mechanisms.