To evaluate the effect of single or repeated topical applications of prostaglandin E2 (PGE2) to the cornea on the blood-aqueous barrier, we have measured the extent of flare in the anterior chamber of rabbit eyes at various time intervals. PGE2 was applied to the cornea for 4 min with the use of a glass cylinder in pigmented rabbits. Aqueous flare was measured by a laser flare cell meter. The flare intensity following the second application of 25 or 50 μg/ml of PGE2 was smaller than that following the first application. When 50 μg/ml of PGE2 was applied every day for 6 days, the flare intensity decreased significantly day by day. After consecutive applications of 10 μg/ml of PGE2 at hourly intervals, flare intensity increased up to 3 h, remained elevated from 3 to 5 h, and decreased thereafter. Repeated applications of 10 μg/ml of PGE2, every hour for 14 h every Monday, significantly decreased flare intensity week by week. Weekly applications of 50 μg/ml of PGE2 did not change flare intensity. This study indicates that the extent of the breakdown of the blood-aqueous barrier in the rabbit eye, as measured by the development of flare in the anterior chamber, is reduced with repeated PGE2 application.
An oncocytoma of the upper eyelid that occurred in an 82-year-old male was studied immunohistologically according to the avidin-biotin-peroxidase complex method (secretory component, carbohydrate antigen 19–9, carcinoembryonic antigen, anticytokeratin AE1/AE3, S–100 protein, myoglobin, actin, vimentin). The staining properties of columnar-type oncocytes were the same as those of epithelial cells of excretory ducts µ of Moll’s gland, but those of polygonal-type oncocytes were similar to those of myoepithelial cells of Moll’s gland. Our results suggested that excretory duct epithelial cells of Moll’s gland are the origin of oncocytoma of the eyelid.
The purpose of this study was to examine the anti-inflammatory effect of the calcium channel blocker nicardipine. Intraocular inflammation was induced by argon laser photocoagulation of the iris of pigmented rabbits and was assessed by measuring aqueous flare and intraocular pressure. This resulted in a marked increase in the aqueous flare that peaked at approximately one hour following coagulation and returning to the original values after six hours. Intraocular pressure increased within 15 minutes following laser treatment and returned to baseline levels at 60 minutes. Pre-treatment of the rabbits with an intravenous injection of 2 mg/kg of nicardipine completely abolished both the increase in aqueous flare and intraocular pressure induced by laser photocoagulation as compared to the control experiment. Earlier work from the author's group has shown that nicardipine can also block aqueous flare and intraocular pressure increases induced by topical administration of prostaglandin E2. From these combined experiments they would like to draw the conclusion that the inflammatory reaction induced by photocoagulation of the iris is partly mediated by prostaglandins and that blockade of calcium channels by nicardipine can inhibit the effects induced by prostaglandin E2.
Oncocytoma rarely arises from the eyelid and only 2 cases have been reported previously. We present a case of oncocytoma in the upper eyelid around the lacrimal punctum. Anatomical location and histological findings suggested that oncocytes of this tumor originated from the epithelium of Moll’s gland or the lacrimal canaliculus.
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