PURPOSE: To examine the effects of saline-induced bleb detachments in rabbit retina. METHODS: Retinal bleb detachments were produced by the injection of 50 microl of balanced salt solution (BSS) into the subretinal space of one eye of each of six rabbits using a glass pipette with a flat tip, 50 microm in diameter. The retina was examined by biomicroscopy, scanning laser ophthalmoscopy (SLO), auto-fluorescence and simultaneous fluorescein and indocyanine green (ICG) angiography. Histological examination was carried out at 1, 2, 3 and 4 months after surgery. RESULTS: All rabbits showed leakage of fluorescein for at least a day after detachment, but within 1 month the leakage ceased. ICG staining developed gradually at the level of the RPE or Bruch's membrane near sites of previous staining. Lipofuscin fluorescence also developed gradually around areas of staining. Histology revealed the source of the excessive lipofuscin to be in the RPE layer, especially in cells migrating away from Bruch's membrane. CONCLUSIONS: Short-term bleb detachments cause a transient breakdown in the blood-retinal barrier, long-term ICG staining at or deep to the RPE layer, hyperlipofuscinosis and migration of the RPE. The abnormal lipofuscin accumulation is apparent on fluorescence ophthalmoscopy and can be confused with markers such as green fluorescent protein.
PURPOSE: To examine the effects of saline-induced bleb detachments in rabbit retina. METHODS:Retinal bleb detachments were produced by the injection of 50 microl of balanced salt solution (BSS) into the subretinal space of one eye of each of six rabbits using a glass pipette with a flat tip, 50 microm in diameter. The retina was examined by biomicroscopy, scanning laser ophthalmoscopy (SLO), auto-fluorescence and simultaneous fluorescein and indocyanine green (ICG) angiography. Histological examination was carried out at 1, 2, 3 and 4 months after surgery. RESULTS: All rabbits showed leakage of fluorescein for at least a day after detachment, but within 1 month the leakage ceased. ICG staining developed gradually at the level of the RPE or Bruch's membrane near sites of previous staining. Lipofuscin fluorescence also developed gradually around areas of staining. Histology revealed the source of the excessive lipofuscin to be in the RPE layer, especially in cells migrating away from Bruch's membrane. CONCLUSIONS: Short-term bleb detachments cause a transient breakdown in the blood-retinal barrier, long-term ICG staining at or deep to the RPE layer, hyperlipofuscinosis and migration of the RPE. The abnormal lipofuscin accumulation is apparent on fluorescence ophthalmoscopy and can be confused with markers such as green fluorescent protein.