Objective: To determine whether ultrasound oscillations in the anterior chamber cause corneal endothelial injury by free radicals.
Methods: A phacoemulsification probe was introduced into the anterior chamber of rabbits' eyes through a limbal incision, and ultrasound oscillation was performed without emulsifying the lens. Rabbits were assigned to 4 treatment groups: (1) no treatment (controls); (2) only irrigation with a salt solution; (3) ultrasound only; and (4) ultrasound oscillations with a salt solution of 0.001M ascorbic acid. The corneas were immunohistochemically examined for oxidative stress using 8-hydroxy-2-deoxyguanosine (8-OHdG), apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) staining, and ultrastructural changes by electron microscopy. The lipid peroxide levels in the aqueous humor were also measured.
Results: In the ultrasound-only group, 8-OHdG-positive cells and TUNEL-positive cells were detected at 24 hours; necrotic cells were detected at 12 to 24 hours. Also, lipid peroxide levels were significantly increased at later times in the ultrasound group. Such changes were not observed in other groups.
Conclusion: Free radicals induced by ultrasound oscillation can cause corneal endothelial damages. Clinical Relevance Clinicians should be aware that free radicals associated with ultrasound oscillation can injure the corneal endothelial cells.