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A. Kehler, K.H. Jensen, C. Aalkjaer, T. Bek; The Dilatation of Retinal Vessels Induced by Carbonic Anhydrase Inhibitors in vitro Is Independent on the Presence of Surrounding Perivascular Retinal Tissue . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4479.
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Inhibition of carbonic anhydrase (CAI) is an important intervention mode for reducing the intraocular pressure. However, it has been suggested that the beneficial mechanism of action of this drug in glaucoma is to improve perfusion of the optic nerve secondary to vasodilatation. However, the basic mechanisms underlying vasodilatation in the optic nerve are unknown. The action of the drug may be on both the vessel walls or be mediated by surrounding factors.
The contractility of porcine retinal arterioles to the thromboxane analogue U46619 was studied, and the influence of increasing concentrations (between 10–6 M and 10–2 M) of the carbonic anhydrase inhibitors Acetazolamide, Dorzolamide, Ethyl–bromopyruvate, Methyl–bromopyruvate, and none (controls) on the vascular tone was examined. Concentration–response relations were obtained with and without the retinal tissue preserved around the arteriole, and at least six experiments were performed with each compound.
All the tested carbonic anhydrase inhibitors elicited a significant vasodilatation at a concentration of 10–2 M (p<0.05, n=51), but not at lower concentrations. The presence of perivascular retinal tissue did not affect the response significantly (p>0.05).
The dilatation of retinal vessels induced by carbonic anhydrase inhibitors in vitro is initiated at concentrations that are several orders of magnitude higher than the clinically relevant concentration. The vasodilatation observed in vitro is independent on the presence of perivascular retinal tissue.
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