February 1990
Volume 31, Issue 2
Free
Articles  |   February 1990
Time course of rabbit ocular inflammatory response and mediator release after intravitreal endotoxin.
Author Affiliations
  • S Csukas
    Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Research Institute, University of Louisville School of Medicine 40292.
  • C A Paterson
    Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Research Institute, University of Louisville School of Medicine 40292.
  • K Brown
    Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Research Institute, University of Louisville School of Medicine 40292.
  • P Bhattacherjee
    Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Research Institute, University of Louisville School of Medicine 40292.
Investigative Ophthalmology & Visual Science February 1990, Vol.31, 382-387. doi:
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      S Csukas, C A Paterson, K Brown, P Bhattacherjee; Time course of rabbit ocular inflammatory response and mediator release after intravitreal endotoxin.. Invest. Ophthalmol. Vis. Sci. 1990;31(2):382-387.

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Abstract

An inflammatory response was elicited in the rabbit eye by intravitreal injection of endotoxin. The appearance in aqueous humor of selected metabolites of arachidonic acid metabolism at various times was correlated with the influx of protein and myeloperoxidase activity in the iris-ciliary body. After intravitreal injection of endotoxin, aqueous humor protein levels increased substantially within 2 hr. This aqueous humor protein increase occurred before a significant appearance of prostaglandin E2 (PGE2) in the aqueous humor. Myeloperoxidase activity in the iris-ciliary body, a measure of polymorphonuclear leukocyte (PMN) infiltration, showed little elevation until 6 hr after endotoxin injection and then increased rapidly through 24 hr. The appearance of the leukotriene B4 (LTB4) followed a similar time course: levels in the aqueous humor were partially elevated until 6 hr after endotoxin injection, when levels begin to rise rapidly. These findings are interpreted to demonstrate the dependence of PMN infiltration on the release and accumulation of LTB4; the initial breakdown of the blood-aqueous barrier and influx of protein appears to be independent of significant release of PGE2.

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