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H. Yamada, Y. Chen, K. Kashiwagi, Y. Suzuki, M. Araie; Lomerizine, a Ca2+ Channel Blocker, Reduces Hypoxic Damage in Purified Retinal Ganglion Cells . Invest. Ophthalmol. Vis. Sci. 2003;44(13):3595.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Lomerizine, a Ca2+ channel blocker, is an antimigraine drug. It is not associated with any significant abnormalities in blood pressure or pulse rate, and selectively increases cerebral blood flow. We evaluated the neuroprotective effect of lomerizine on the hypoxia-induced retinal ganglion cell death using purified rat retinal ganglion cell cultures. Methods: Purified retinal ganglion cell (RGC) cultures were obtained from retina of 5- to 7-day-old rats accoding to two step immno-panning procedure. RGCs were cultured under hypoxic condition(5% O2, 5%CO2, 37°C) for 12 hours. Lomerizine (0.01-1µM) and nimodipine(0.01-1µM) were added to the medium. The viability of the cultures was assessed by counting the number of the viable cells. Results: The viability of RGC cultures after 12 hours of hypoxia was 44.0%+/-4.5% without drug treatment. The viability increased in a dose dependent fashion with exposure to lomerizine (0.01µM:45.0%+/-3.8%; NS, 0.1µM:50.6%+/-4.1%; p<0.1, 0.01µM:60.2%+/-5.9%; p<0.05, n=7) and nimodipine(0.01µM:49.3+/-1.5%; p<0.1, 0.1µM:53.0+/-2.4%; p<0.05, 0.01µM:55.4%+/-3.9%; p<0.05, n=7). Conclusions: Lomerizine protects RGC against hypoxia at least partly through a mechanism unrelated to its vasodilator effect. Lomerizine reduces RGC hypoxic damage, presumably through a Ca2+ channel blocking effect by an action that may involve a direct protection of RGC.
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