Ff. Beharcohen et al., REDUCTION OF CORNEAL EDEMA IN ENDOTOXIN-INDUCED UVEITIS AFTER APPLICATION OF L-NAME AS NITRIC-OXIDE SYNTHASE INHIBITOR IN RATS BY IONTOPHORESIS, Investigative ophthalmology & visual science, 39(6), 1998, pp. 897-904
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.