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Abstract #10493 Published in IGR 6-1

Effectiveness of levobetaxolol and timolol at blunting retinal ischaemia is related to their calcium and sodium blocking activities: relevance to glaucoma

Osborne NN; Wood JPM; Chidlow G; Casson R; DeSantis L; Schmidt KG
Brain Research Bulletin 2004; 62: 525-528


Glaucoma is a chronic optic neuropathy in which retinal ganglion cells die over a number of years. The initiation of the disease and its progression may involve an ischemic-like insult to the ganglion cell axons caused by an alteration in the quality of blood flow. Thus, to effectively treat glaucoma it may be necessary to counteract the ischemic-like insult to the region of the optic nerve head. Studies on the isolated optic nerve suggest that substances that reduce the influx of sodium would be particularly effective neuroprotectants. Significantly, of the presently used antiglaucoma substances, only β-blockers can reduce sodium influx into cells. Moreover, they also reduce the influx of calcium and this would be expected to benefit the survival of insulted neurones. Betaxolol is the most effective antiglaucoma drug at reducing sodium/calcium influx. The electroretinographic data indicated that topical application of levobetaxolol to rats attenuated the effects of ischemia/reperfusion injury. Timolol was also effective but to a lesser extent. Based on these data, it is concluded that β-blockers may be able to blunt ganglion cell death in glaucoma, and that levobetaxolol may be a more effective neuroprotectant than timolol because of its greater capacity to block sodium and calcium influx.

Dr. N.N. Osborne, Nuffield Laboratory of Ophthalmology, Oxford University, Walton Street, Oxford OX2 6AW, UK


Classification:

11.3.4 Betablocker (Part of: 11 Medical treatment > 11.3 Adrenergic drugs)



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