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Treatment with a platelet-activating factor receptor antagonist, SRI 63-441, inhibited interleukin 1-induced increases in vascular permeability and leukocyte infiltration in the rabbit eye following the intravitreal injection of human interleukin 1-alpha. Treatment with the prostaglandin-synthetase inhibitor, flurbiprofen, or the corticosteroid, prednisolone, resulted in comparable attenuation of the increase in vascular permeability. In contrast to the effect of flurbiprofen, SRI 63-441 did not reduce interleukin 1-induced increases in prostaglandin E2 levels. Combined treatment with the platelet-activating factor antagonist and inhibitors of prostaglandin synthesis nearly prevented interleukin 1-induced increases in vascular permeability or cellular infiltration. These findings suggest a role for platelet-activating factor in interleukin 1-induced inflammation. Platelet-activating factor and prostaglandins may act synergistically as mediators of interleukin 1-induced vascular permeability.
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