Effects of Argon Laser Iridotomy on the Corneal Endothelium of Pigmented Rabbit Eyes
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Purpose: In Asian countries, laser iridotomy for the treatment of angle-closure glaucoma is a common cause ofbullous keratopathy, which may be associated with a shallow anterior chamber and dark iris pigmentation inAsians. Several cases of corneal decompensation after argon laser iridotomy have been reported. In the presentstudy, we evaluated the harmful effects of argon laser iridotomy on the corneal endothelium. Methods: Argon laser iridotomy was performed on the right eyes of pigmented rabbits. Changes in cornealthickness and endothelial cell density after laser iridotomy were evaluated. Terminal deoxynucleotidyl transferasedUTP nick end labeling (TUNEL) was performed for assessment of corneal endothelial cell apoptosis. Combined staining with alizarin red and trypan blue, as well as a live/dead cell assay, were performed for evaluationof damage to the corneal endothelium induced by laser iridotomy. Results: Corneal thickness did not change immediately after laser iridotomy; however, a significant increasewas observed 24 hours after iridotomy (p = 0.001). The endothelial cell density of laser-treated eyes four daysafter laser iridotomy was significantly decreased compared with control eyes (p < 0.001). TUNEL stainingshowed many TUNEL-positive cells in the corneal endothelium and corneal stroma. No endothelial trypanblue-stained cell nuclei were observed after laser iridotomy; however, several large endothelial cells with damagedmembrane integrity were observed. The live/dead cell assay clearly showed a large number of deadcells stained red in several areas throughout the entire corneal button 24 hours after iridotomy. Conclusions: Argon laser iridotomy induces corneal endothelial cell apoptosis in pigmented rabbit eyes, resultingin decreased endothelial cell density.
Abstract
Purpose: In Asian countries, laser iridotomy for the treatment of angle-closure glaucoma is a common cause ofbullous keratopathy, which may be associated with a shallow anterior chamber and dark iris pigmentation inAsians. Several cases of corneal decompensation after argon laser iridotomy have been reported. In the presentstudy, we evaluated the harmful effects of argon laser iridotomy on the corneal endothelium. Methods: Argon laser iridotomy was performed on the right eyes of pigmented rabbits. Changes in cornealthickness and endothelial cell density after laser iridotomy were evaluated. Terminal deoxynucleotidyl transferasedUTP nick end labeling (TUNEL) was performed for assessment of corneal endothelial cell apoptosis. Combined staining with alizarin red and trypan blue, as well as a live/dead cell assay, were performed for evaluationof damage to the corneal endothelium induced by laser iridotomy. Results: Corneal thickness did not change immediately after laser iridotomy; however, a significant increasewas observed 24 hours after iridotomy (p = 0.001). The endothelial cell density of laser-treated eyes four daysafter laser iridotomy was significantly decreased compared with control eyes (p < 0.001). TUNEL stainingshowed many TUNEL-positive cells in the corneal endothelium and corneal stroma. No endothelial trypanblue-stained cell nuclei were observed after laser iridotomy; however, several large endothelial cells with damagedmembrane integrity were observed. The live/dead cell assay clearly showed a large number of deadcells stained red in several areas throughout the entire corneal button 24 hours after iridotomy. Conclusions: Argon laser iridotomy induces corneal endothelial cell apoptosis in pigmented rabbit eyes, resultingin decreased endothelial cell density.
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