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The purpose of the present study is to investigate the morphologic sites of breakdown in eyes pretreated with nilvadipine (a calcium channel blocker) that has been shown to inhibit the acute rise of aqueous flare induced by prostaglandin E2 (PGE2). Nilvadipine (100 ?g/kg body weight) was injected intravenously in pigmented rabbits. Thirty minutes later, vehicle or PGE2 (10, 50 or 250 ?g/ml) was applied on the cornea by use of a glass cylinder. Forty-five minutes later, the animals received horseradish peroxidase (HRP) intravenously and the eyes were enucleated. Distribution of HRP in the anterior segments was observed by electron microscopy. Without nilvadipine pretreatment, HRP was seen in the intercellular space of nonpigmented cells of the eyes treated with 50 ?g/ml PGE2 and in the iris stroma of the eyes treated with 250 ?g/ml PGE2. With nilvadipine pretreatment, HRP was not observed in these sites. Our results indicate that nilvadipine suppresses disruption of the different sites of the blood-aqueous barrier.
C. Kadoi, Department of Ophthalmology, Toyama Medical and Pharmaceutical University, Toyama; Japan
12.8.10 Woundhealing antifibrosis (Part of: 12 Surgical treatment > 12.8 Filtering surgery)