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A Water-Soluble Carbon Monoxide-Releasing Molecule (CORM-3) Lowers Intraocular Pressure in Rabbits
  1. Edoardo Stagni (edo.stagni{at}tin.it),
  2. Maria Giovanna Privitera (giovanna.privitera{at}tin.it),
  3. Claudio Bucolo (bucocla{at}unict.it),
  4. Gian Marco Leggio (gianmarcoleggio{at}libero.it),
  5. Roberto Motterlini (roberto.motterlini{at}imperial.ac.uk),
  6. Filippo Drago (fdrago{at}tin.it)
  1. Dept. Experimental and Clinical Pharmacology, University of Catania, Italy
  2. Dept. Experimental and Clinical Pharmacology, University of Catania, Italy
  3. Dept. Experimental and Clinical Pharmacology, University of Catania, Italy
  4. Dept. Experimental and Clinical Pharmacology, University of Catania, Italy
  5. Dept. of Surgical Research, Vascular Biology Unit, Northwick Park Inst. for Medical Research, Harrow, United Kingdom
  6. Dept. Experimental and Clinical Pharmacology, University of Catania, Italy

    Abstract

    Background: Carbon monoxide-releasing molecules (CO-RMs) are a novel group of substances that are capable of modulating physiological functions via the liberation of CO.

    Aims: This study was undertaken to investigate the effects of CORM-3, a water-soluble CO-releasing agent, on two rabbit models of ocular hypertension.

    Methods: Ocular hypertension was induced by injecting a-chymotrypsin in the rabbit eye. The dose-response effect of CORM-3 on IOP was assessed by topical administration of the drug (0.001, 0.01, 0.1 and 1%). Ocular hypertension was also obtained by weekly subconjunctival injection of betamethasone, and animals were treated topically with CORM-3. A group of animals in both models was treated with the inactive form of the drug (iCORM-3).

    Results: CORM-3 induced a dose-dependent reduction of IOP in rabbits treated with a-chymotrypsin. A similar reduction in IOP was observed in rabbits with betamethasone-induced ocular hypertension treated with the drug. Treatment with the iCORM-3 had no effect on IOP in both models.

    Conclusions: Treatment with CORM-3 is associated with a reduction of IOP in two different rabbit models of ocular hypertension. These results support our previous findings on the effect of heme oxygenase-derived CO on IOP and suggest a direct involvement of CO system in the regulation of ocular pressure probably through the modulation of aqueous humor dynamics.

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