dinoprost and Corneal-Edema

Topics: Administration, Topical; Adult; Ciliary Body; Corneal Edema; Dinoprost; Female; Glaucoma; Humans; Intraocular Pressure; Laser Therapy; Latanoprost; Ocular Hypertension; Prostaglandins F, Synthetic; Retinitis Pigmentosa

The involvement of prostaglandins (PGs) in the development of anterior segment ischaemia after occlusion of the bilateral long posterior ciliary arteries was investigated in rabbit eyes. In this experimental ischaemia, the tissue weight and protein content in the peripheral cornea and the protein content in the aqueous humour increased on the first postoperative day. Topically applied cyclooxygenase inhibitor diclofenac (0.1%) reduced corneal inflammation and further suppressed the elevation in the tissue weight and protein content in the peripheral cornea on day 1 after ischaemia, but did not affect the changes in the aqueous humour. Subconjunctivally administered PGE1 and PGE2 induced corneal oedema and increased corneal protein content in diclofenac-treated and ischaemia-induced eyes, but PGD2, PGF2alpha, and the stable PGI2 analogue cicaprost did not evoke any change. In fact, PGE2 content was markedly increased in the aqueous humour on day 1 after ischaemia, and diclofenac suppressed the increase. In addition, CPT-cAMP increased the corneal tissue weight and protein content in organ culture. These observations suggest that PGE2 may play an important role in developing corneal oedema at the initial stage of ischaemic damage, possibly through the cAMP-mediated pathway.

Topics: Alprostadil; Animals; Anterior Eye Segment; Aqueous Humor; Cornea; Corneal Diseases; Corneal Edema; Cyclic AMP; Cyclooxygenase Inhibitors; Diclofenac; Dinoprost; Dinoprostone; Ischemia; Male; Organ Culture Techniques; Prostaglandins; Proteins; Rabbits