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Modification of Response to Circulating Bacterial Endotoxin

Keye L. Wong, MD; Edward Lee Howes, Jr, MD

Arch Ophthalmol. 1983;101(2):275-279.

Abstract
• Circulating bacterial endotoxin in the rabbit produces a transient iridocyclitis. Alteration in the ocular vascular permeability was measured by accumulation of iodonated I 125 serum albumin. The role of local mediator release in modifying the effect of endotoxin was investigated by pretreatment with intravitreal injections of prostaglandin E₂ (alprostadil), prostaglandin E₂ (dinoprostone), prostaglandin F₂ (dinoprost), histamine dihydrochloride, histamine phosphate, bradykinin triacetate, and serotonin creatinine sulfate. Histamine, bradykinin, and serotonin by themselves did not produce an alteration in ocular vascular permeability in the manner studied, nor did their prior injection alter the ocular response to circulating endotoxin. By contrast, prostaglandin E₁, prostaglandin E₂, and prostaglandin F₂ produced an alteration in ocular vascular permeability. After resolution of this alteration, the eye became partially refractory to endotoxin-induced inflammation. Neither the production of an inhibitory substance nor cyclic adenosine monophosphate seemed to be involved in this decreased responsiveness. Possible mechanisms of this anti-inflammatory effect are discussed.

Author Affiliations
From the Department of Anatomic Pathology and Ophthalmology, San Francisco General Hospital, University of California, San Francisco.

Footnotes
Accepted for publication Feb 19, 1982.

Reprint requests to Department of Anatomic Pathology, San Francisco General Hospital, San Francisco, CA 94110 (Dr Howes).

This study was supported in part by Public Health Service grant EY-00056-11.

Virginia K. Cruse and Michael A. Hoffman provided technical assistance.

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ABSTRACT