Ultrastructural Changes of Corneal Edema in Endotoxin-induced Uveitis Model

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 groups:A,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.

A Histopathologic Study of the Iris in a Patient with Exfoliation Syndrome

The pathogenesis of the exfoliation syndrome is still unknown. To clarify the etiology of the exfoliation syndrome, we examined the iris taken from a patient with exfoliative glaucoma during cataract surgery using light microscope, polarization microscopy and electron microscopy. The amorphous substance around the iris pigment epithelium and stroma were stained purplish red in PAS staining and showed purplish red metachromasia in toluidine blue staining. In electromicroscopic examination, we observed that many fibrillar materials were deposited at basement membrane and partially detached basement membrane around the pigment epithelium of the iris. Therefore we concluded that the exfoliative materials in this syndrome is a sort of glycoprotein and originated from the abnormal synthesis and metabolism of the basement membrane in the eye.

Hematic cyst formation after repair of blow-out fracture

Alloplastic implants are known to be inert for many years, though complications are infrequently reported many years after their insertion. We report the case of a patient who had undergone a blow-out fracture repair five years before the discovery of a hematic cyst. He had been free of symptoms for the first five years after his orbital floor repair but then developed pain on eyeball movement and persistent vertical diplopia, which finally led to surgical intervention. At surgery, a hematic cyst was found to have formed around the implanted silastic plate. When alloplastic material is used in orbital fracture repair, we should be alert for late complications which may occur many years after surgery.