May 2008
Volume 49, Issue 13
ARVO Annual Meeting Abstract  |   May 2008
Efficacy and Pharmacokinetics of Intraocular Ketorolac and Diclofenac
Author Affiliations & Notes
  • D. E. Baranano
    Ophthalmology, Wilmer Eye Institute, Baltimore, Maryland
  • S. J. Kim
    Ophthalmology, Emory University, Atlanta, Georgia
  • H. F. Edelhauser
    Ophthalmology, Emory University, Atlanta, Georgia
  • U. B. Kompella
    University of Nebraska Medical Center, Omaha, Nebraska
  • C. Durairaj
    University of Nebraska Medical Center, Omaha, Nebraska
  • J. T. Handa
    Ophthalmology, Wilmer Eye Institute, Baltimore, Maryland
  • Footnotes
    Commercial Relationships  D.E. Baranano, None; S.J. Kim, None; H.F. Edelhauser, None; U.B. Kompella, None; C. Durairaj, None; J.T. Handa, None.
  • Footnotes
    Support  This work was supported by grants from the Macula Society, an unrestircted grant from Research to Prevent Blindness, and National Eye Institute grant R-24-EY017045
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 5606. doi:
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      D. E. Baranano, S. J. Kim, H. F. Edelhauser, U. B. Kompella, C. Durairaj, J. T. Handa; Efficacy and Pharmacokinetics of Intraocular Ketorolac and Diclofenac. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5606. doi:

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : To determine the efficacy and pharmacokinetics of intravitreally delivered nonsteroidal anti-inflammatory drugs (NSAID) in a rabbit model of panuveitis.

Methods: : Lipopolysaccharide was injected into the vitreous of rabbit eyes as an experimental model of panuveitis. Treated eyes were injected with 3 mg of ketorolac or 0.3 mg of diclofenac (0.05 ml.) Twenty-four hours later, aqueous and vitreous was sampled. Total leukocyte concentration was determined by hemocytometer. Protein concentration was determined by Bradford assay. Prostaglandin concentration was determined by enzyme-linked immunoassay. For intraocular pharmaocokinetics, 0.1 ml of ketorolac (3 mg) and 0.1 ml of diclofenac (0.3 mg) were injected into eyes of rabbits. At 0.15, 1, 2, 4, 24, and 48 hours after injection, eyes were snap frozen in liquid nitrogen and the vitreous and retina/choroid were later isolated. Reverse-phase high performance liquid chromatography was used for analysis.

Results: : Eyes treated with ketorolac and diclofenac demonstrated aqueous leukocyte concentrations that were reduced 72% and 74% respectively compared to untreated controls (p<0.05.) Both aqueous and vitreous prostaglandin E2 concentrations were markedly reduced in ketorolac and diclofenac treated eyes compared to untreated eyes. Vitreous concentration of ketorolac peaked at 0.15 minutes at 234 µg/ml and peaked for diclofenac at 1 hour at 15 µg/ml. After 48 hours, ketorolac was still detectable with a concentration of 0.06 µg/ml, while diclofenac was undetectable after 24 hours. The concentration of each drug in the retina/choroid was 201 µg/g for ketorolac and 4 µg/g for diclofenac after 0.15 hours, and peaked at 280 µg/g after 2 hours and 4 µg/g after 1 hour, respectively. Both drugs were undetectable in the retina/choroid after 48 hour.

Conclusions: : Both ketorolac and diclofenac were found to have potent anti-inflammatory effects when delivered intravitreally. Pharmacokinetic analysis demonstrated good penetration into the retina/choroid and rapid clearance by 48 hours. Future studies evaluating these intraocular NSAIDs in animal models of macular edema will be useful.

Keywords: uveitis-clinical/animal model • inflammation • retina 

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