Prostaglandins and ocular inflammation

Evidence for prostaglandins as mediators of some inflammatory responses is briefly, but critically discussed. The hypothesis that prostaglandins are mediators of ocular inflammation is presented and discussed according to the tenets of Miller & Melmon (1970). Prostaglandins are released after mechanical stimulation, paracentesis, laser irradiation, (non)-immunogenic uveitis in experimental animals, and in patients with acute anterior uveitis. Prostaglandins were neither found after antidromic stimulation of the trigeminal nerve, oculomotor nerve stimulation, intracameral formaldehyde, topical nitrogen mustard, nor in patients with open angle glaucoma.Administering of prostaglandins produces transient ocular hypertension, increased vascular permeability and miosis. Ocular hypotension has been shown to follow the hypertensive response. Hypertension is considered to be due to a breakdown of the blood-aqueous barrier of the ciliary processes and iris. Prostaglandins of the E series are the most potent, and species differences occur. Prostaglandin E₁ potentiates the histamine-induced increase in vascular permeability of the conjunctiva, but not the uvea. Polyphloretin phosphate aspecifically blocks the ocular actions of prostaglandins. Non-steroidal anti-inflammatory drugs inhibit prostaglandin synthetase and the ocular effects of arachidonic acid, its substrate. Prostaglandins are poorly catabolised by the eye, but are removed from ocular fluids by a transport mechanism in the anterior uvea. This becomes inoperative in (non)-immunogenic uveitis in rabbits allowing prostaglandins to accumulate. Anti-inflammatory steroids decrease the availability of arachidonic acid for prostaglandin synthetase. Intermediates formed in the biosynthesis of prostaglandins may well be more important in inflammation than the prostaglandins themselves.Part of this review was presented at the 171st Congress of the Dutch Ophthalmological Society.