Ultrastructural Changes of Corneal Edema in Endotoxin-induced Uveitis Model

ABSTRACT

It has been well known that Nitrogen Oxide (NO)plays an important role in endotoxin-induced uveitis (EIU)model,but there has been few researches on development of corneal toxicity in this model. This study was planned to elucidate ultrastructural changes of corneal opacities and edema in EIU model. Lewis rats were separated into 3 groupsA,B and ontrol. Lipopolysaccharide(LPS)was administered subcutaneously into footpads in group A and B for induction of uveitis, while balanced salt solution was injected into those in control rats. NG-nitro-L-arginine methyl ester (L-NAME), known as inhibitor of NO synthase, was applied topically into eyes in group B before and after injection of LPS, respectively. 24 hours after injection of LPS, all of these eyes were observed with light microscope and electron microscope to assess severity of uveitis and corneal status. More severe corneal edema and opacity,along with more intense uveitis were noted in group A than in group B. Corneal thickness was 93.21 +/-8 .9 4 micrometerin control group,161.97+/-11.93micrometerin A group,and 121.67+/-11.35micrometerin B group.The rats treated with L-NAME showed less corneal edema,which was statistically significant(p<0.05). Ultrastructural alterations observed were as folloews vacuolated necrosis in epithelium;increased perikeratocyte space, derangement of collagen fibrils due to stromal edema;and condensed chromatin,mitochondrial swelling, increased intercellular space in endothelium. Atypical pyknotic pattern of cellular necrosis due to intranuclear and perinuclear vacuoles was charactreristic. However, ultrastructures were relatively well preserved in group B except for intracytoplasmic vacuoles.These results suggest that L-NAME inhibits corneal toxicity caused by endotoxin. In conclusion,this study support the hypothesis that NO plays an important role in corneal toxicity.