March 1988
Volume 29, Issue 3
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Articles  |   March 1988
Quantitation of acute experimental ocular inflammation with 111indium-leukocytes.
Author Affiliations
  • E L Howes, Jr
    Department of Pathology, San Francisco General Hospital, CA 94110.
  • P W Cole
    Department of Pathology, San Francisco General Hospital, CA 94110.
  • V K Cruse
    Department of Pathology, San Francisco General Hospital, CA 94110.
  • M Pollycove
    Department of Pathology, San Francisco General Hospital, CA 94110.
Investigative Ophthalmology & Visual Science March 1988, Vol.29, 429-436. doi:
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      E L Howes, P W Cole, V K Cruse, M Pollycove; Quantitation of acute experimental ocular inflammation with 111indium-leukocytes.. Invest. Ophthalmol. Vis. Sci. 1988;29(3):429-436.

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Abstract

The cellular component of an acute ocular inflammation in rabbits was measured with autologous leukocytes exogenously labeled with 111Indium tropolonate. Inflammation was induced by intravitreal bacterial lipopolysaccharide (LPS). After 16 hr blood was removed, leukocytes separated, labeled with 111Indium tropolonate and reinjected. Three cell fractions were examined: a leukocyte rich fraction which had been prepared with Dextran; and polymorphonuclear and mononuclear leukocyte fractions which had been prepared using a discontinuous Percoll gradient. Two hours after labeled leukocytes were injected, measurements of 111Indium were made in blood, plasma, the whole eye and in ocular compartments. From these data the numbers of each leukocyte population present were estimated and compared directly to histopathologic changes. Both polymorphonuclear and mononuclear leukocytes entered ocular tissues during the 2 hr period beginning 20 hr after LPS injection. Altered ocular vascular permeability was successfully measured with 125Iodine-albumin in some of these same rabbits. Both the number and type of inflammatory cell entering ocular tissues during a set period of time of the inflammatory response could thus be measured. This technique provides an opportunity to define the relationship of leukocyte infiltration and altered ocular vascular permeability in ocular tissues during the inflammatory response.

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