April 1995
Volume 36, Issue 5
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Articles  |   April 1995
A closed eye contact lens model of corneal inflammation. Part 1: Increased synthesis of cytochrome P450 arachidonic acid metabolites.
Author Affiliations
  • M S Conners
    Department of Pharmacology, New York Medical College Valhalla, 10595, USA.
  • R A Stoltz
    Department of Pharmacology, New York Medical College Valhalla, 10595, USA.
  • S C Webb
    Department of Pharmacology, New York Medical College Valhalla, 10595, USA.
  • J Rosenberg
    Department of Pharmacology, New York Medical College Valhalla, 10595, USA.
  • M W Dunn
    Department of Pharmacology, New York Medical College Valhalla, 10595, USA.
  • N G Abraham
    Department of Pharmacology, New York Medical College Valhalla, 10595, USA.
  • M Laniado-Schwartzman
    Department of Pharmacology, New York Medical College Valhalla, 10595, USA.
Investigative Ophthalmology & Visual Science April 1995, Vol.36, 828-840. doi:
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    • Get Citation

      M S Conners, R A Stoltz, S C Webb, J Rosenberg, M W Dunn, N G Abraham, M Laniado-Schwartzman; A closed eye contact lens model of corneal inflammation. Part 1: Increased synthesis of cytochrome P450 arachidonic acid metabolites.. Invest. Ophthalmol. Vis. Sci. 1995;36(5):828-840.

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Abstract

PURPOSE: To characterize a model of contact lens-induced corneal inflammation in the closed eye, with respect to inflammatory parameters and the metabolism of arachidonic acid by homogenates of the corneal epithelium. METHODS: Rabbit eyes were fitted with extended wear etafilcon A (58% water) hydrogel contact lenses in stacked fashion (two lenses per eye), followed by a silk suture tarsorrhaphy of approximately 90%. The anterior surface was analyzed over a 9-day period for inflammatory events through slit lamp biomicroscopy, subjective inflammatory scoring, corneal pachymetry, and corneal epithelial [1-(14)C]-arachidonic acid metabolism. RESULTS: Hydrogel contact lens wear in the closed eye resulted in a progressive anterior surface inflammatory response correlated over time (r = 0.999). Central corneal thickness progressively increased and was also correlated to the inflammatory score (r = 0.995). [1-(14)C]-arachidonic acid metabolism by homogenates of the corneal epithelium resulted in the time-dependent formation of two major products, 12-hydroxyeicosatetraenoic acid (12-HETE) and 12-hydroxyeicosatrienoic acid (12-HETrE). Correlations were established between the synthesis of 12-HETE and 12-HETrE, the subjective inflammatory score (r = 0.963) and the progressive increase in corneal thickness (r = 0.971), over 9 days. CONCLUSIONS: With this model of contact lens wear, eicosanoid synthesizing capacity of the corneal epithelium showed a time-dependent increase in the production of 12-HETE and 12-HETrE strongly correlating to the in situ inflammatory response. The relationship between 12-HETE and 12-HETrE synthesis and the degree of anterior surface inflammation implicate these eicosanoids, among others, as mediators of the inflammatory response to hydrogel contact lens wear in the closed eye.

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