November 1992
Volume 33, Issue 12
Free
Articles  |   November 1992
Treatment of alkali-injured rabbit corneas with a synthetic inhibitor of matrix metalloproteinases.
Author Affiliations
  • G S Schultz
    Department of Obstetrics and Gynecology, University of Florida, Gainesville 32610.
  • S Strelow
    Department of Obstetrics and Gynecology, University of Florida, Gainesville 32610.
  • G A Stern
    Department of Obstetrics and Gynecology, University of Florida, Gainesville 32610.
  • N Chegini
    Department of Obstetrics and Gynecology, University of Florida, Gainesville 32610.
  • M B Grant
    Department of Obstetrics and Gynecology, University of Florida, Gainesville 32610.
  • R E Galardy
    Department of Obstetrics and Gynecology, University of Florida, Gainesville 32610.
  • D Grobelny
    Department of Obstetrics and Gynecology, University of Florida, Gainesville 32610.
  • J J Rowsey
    Department of Obstetrics and Gynecology, University of Florida, Gainesville 32610.
  • K Stonecipher
    Department of Obstetrics and Gynecology, University of Florida, Gainesville 32610.
  • V Parmley
    Department of Obstetrics and Gynecology, University of Florida, Gainesville 32610.
Investigative Ophthalmology & Visual Science November 1992, Vol.33, 3325-3331. doi:
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    • Get Citation

      G S Schultz, S Strelow, G A Stern, N Chegini, M B Grant, R E Galardy, D Grobelny, J J Rowsey, K Stonecipher, V Parmley; Treatment of alkali-injured rabbit corneas with a synthetic inhibitor of matrix metalloproteinases.. Invest. Ophthalmol. Vis. Sci. 1992;33(12):3325-3331.

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Abstract

Healing of corneal alkali injuries remains a severe clinical challenge. The authors evaluated the effect of a new synthetic inhibitor of matrix metalloproteinases (GM6001 or N-[2(R)-2-(hydroxamido carbonylmethyl)-4-methylpentanoyl]-L-tryptophane methylamide) on preventing ulceration of rabbit corneas after alkali injury. Topical treatment of corneas with severe alkali injuries with 400 micrograms/ml or 40 micrograms/ml GM6001 alone prevented ulceration for 28 days, although 8 of 10 corneas treated with vehicle perforated. Corneas treated with 4 micrograms/ml GM6001 had midstromal depth ulcers. Corneas treated with 400 micrograms/ml of GM6001 contained very few inflammatory cells and had significantly reduced vessel ingrowth compared with vehicle-treated corneas. Epithelial regeneration after moderate alkali injuries also was investigated. Persistent epithelial defects developed 4 days after moderate alkali injury in rabbit corneas treated with vehicle and progressively increased to an average of 20% of the original 6 mm diameter wound by 27 days after moderate alkali injury. By contrast, epithelial regeneration was complete and persisted for 21 days for corneas treated with a formulation containing GM6001 (400 micrograms/ml), epidermal growth factor (10 micrograms/ml), fibronectin (500 micrograms/ml), and aprotinin (400 micrograms/ml). Sporadic punctate staining developed in 20% of the corneas treated with the combination of agents between days 21-28 after moderate alkali injury. These results demonstrate that topical application of GM6001 prevented corneal ulceration after severe alkali injury and that a combination containing GM6001, epidermal growth factor, fibronectin, and aprotinin promoted stable regeneration of corneal epithelium after moderate alkali injury.

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