• 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 F2α (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 F2α 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.
Wong KL, Howes EL. Intraocular Injection of Prostaglandins: Modification of Response to Circulating Bacterial Endotoxin. Arch Ophthalmol. 1983;101(2):275–279. doi:10.1001/archopht.1983.01040010277019
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