REDUCTION OF CORNEAL EDEMA IN ENDOTOXIN-INDUCED UVEITIS AFTER APPLICATION OF L-NAME AS NITRIC-OXIDE SYNTHASE INHIBITOR IN RATS BY IONTOPHORESIS

PURPOSE. TO investigate the involvement of the cornea during endotoxin -induced uveitis (EIU) in the fat and the effect of N-gamma-nitro-L-ar ginine methyl ester (L-NAME) as nitric oxide synthase (NOS) inhibitor, administered by iontophoresis. METHODS. EIU was induced in Lewis rats that were killed at 8 and 16 hours after lipopolysaccharide (LPS) inj ection. The severity of uveitis was evaluated clinically at 16 hours, and nitrite levels were evaluated in the aqueous humor at 8 hours. Cor neal thickness was measured, 16 hours after LPS injection, on histolog ic sections using an image analyzer. Transmission electron microscopy (TEM) was used for fine analysis of the cornea. Transcorneoscleral ion tophoresis of L-NAME (100 mM) was performed either at LPS injection or at 1 and 2 hours after LPS injection. RESULTS. At 16 hours after LPS injection, mean corneal thickness was 153.7 +/- 5.58 mu m in the group of rats injected with LPS (n = 8) compared with 126.89 +/- 11.11 mu m in the saline-injected rats (n = 8) (P < 0.01). TEM showed stromal ed ema and signs of damage in the endothelial and epithelial layers. In t he group of rats treated by three successive iontophoreses of L-NAME ( n = 8), corneal thickness was 125.24 +/- 10.36 mu m compared with 146. 76 +/- 7.52 mu m in the group of rats treated with iontophoresis of sa line (n = 8), (P = 0.015). TEM observation showed a reduction of strom al edema and a normal endothelium. Nitrite levels in the aqueous humor were significantly reduced at 8 hours by L-NAME treatment (P = 0.03). No effect on corneal edema was observed after a single iontophoresis of L-NAME at LPS injection (P = 0.19). Iontophoresis of saline by itse lf induced no change in corneal thickness nor in TEM structure analysi s compared with normal rats. CONCLUSIONS. Corneal edema is observed du ring EIU. This edema is significantly reduced by three successive iont ophoreses of L-NAME, which partially inhibited the inflammation. A rol e of nitric oxide in the corneal endothelium functions may explain the antiedematous effect of L-NAME.