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T. Miyake, A. Nishiwaki, Y. Ogura, S. Ugawa, S. Shimada; Amiloride Potently Reduces Retinal Ischemia–Reperfusion Injury in the Rat . Invest. Ophthalmol. Vis. Sci. 2006;47(13):886.
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A diuretic drug amiloride is an inhibitor of epithelial Na+ channels (ENaCs) and acid–sensing ion channels (ASICs). Previously, some members belonging to the ENaC and ASIC families were detected in mammalian retina. In experimental animal models, amiloride potently blocks brain damages induced by ischemia through the blockade of ASICs, especially of Ca2+–permeable ASIC1a channels. We investigated whether amiloride can protect rat retina subjected to ischemia–reperfusion insults.
Transient retinal ischemia for 60 min was induced in male Long–Evans rats (n=16) by the temporary ligation of the optic nerve. Just before the induction of ischemia, experimental eyes were subjected to intravitreal injection of amiloride (final conc. of amiloride was 100µM). At 7 days after reperfusion, full–field electroretinograms (ERG) were recorded. Histologic studies were carried out to evaluate retinal damages.
In the ERG evaluation, the retinal ischemia caused a reduction of A– and B–wave amplitudes (A–wave 172.3±76.2µV, B–wave 435.0±199.5µV). The amiloride treatment significantly prevented the change in the A– and B–wave (A–wave 324.1±123.2µV, B–wave 851.4±331.8µV). In the histological evaluation, the ischemia–reperfusion injury caused a significant reduction of inner retinal thickness. Retinal damages were substantially prevented in the amiloride–treated group.
The present study demonstrated that amiloride showed a potent neuroprotective effect against retinal ischemia in the rat. We speculated that the neuroprotective mechanisms of amiloride might reduce toxic Ca2+ influx into the retinal cells with the inhibition of ASICs in the ischemic retina.
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