Abstract
PURPOSE. Prostaglandin F 2a (PGF 2a) and several other prostaglandins cause surface hyperemia of the eye when applied topically. The purpose of the present study was to investigate the role of sensory nerves in prostaglandin-induced ocular hyperemia. METHODS. The ophthalmic branch of the trigeminal nerve was unilaterally electrocoagulated in rabbits using a stereotaxic technique. Two weeks later the animals received bilaterally one drop of PGF 2a -isopropyl ester (PGF 2a -IE) at a dose of 1 µg/ eye. The blood flow to the different parts of the eye was measured with the radioactively labeled microsphere technique before, 30 and 60 min after treatment with PGF 2a -IE. RESULTS. In the control eyes with intact sensory innervation, PGF 2a -IE caused a marked increase in blood flow to the surface structures of the eye (conjunctiva, anterior sclera, eyelids and nictitating membrane) and the iris, and a moderate increase in the blood flow to the ciliary processes, but no increase in the choroidal blood flow. In the denervated eyes the increase in blood flow to the surface structures was almost completely abolished, and there was also a tendency toward less increase in blood flow in the anterior uvea. CONCLUSIONS. These results indicate that PGF 2a -induced ocular surface hyperemia, at least at the early stage, is mediated to a large extent by sensory nerves.
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