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Protective effect of betaxolol on optic nerves after experimental retinal ischemiareperfusion injury

ObjectiveTo investigate the protective effect and mechanism of betaxolol on optic nerves after experimental retinal ischemia-reperfused injury.MethodsRetinal ischemia was induced in SD rats by increasing intraocular pressure through intracameral infusion. Sixty-eight rats were randomly divided into 3 groups: normal control (eight rats), 0.25% betaxolol treatment (thirty rats) and saline control group (thirty rats). The latter two groups were subdivided into group 1 day, 3 and 7 days after reperfusion, respectively, with 10 rats in each group. Betaxolol and normal saline was applied to the right eyes of the rats in the treatment group and to the ones in normal saline control group, respectively. The amplitude of bwave of electron retinograph (ERG) was observed and the histological and ultrastructural changes were detected by light and electron microscopy. The expression of neural nitrogen oxide synthase (nNOS) was detected by immunohistochemistry. The content of malonyldialdehyde (MDA) and the superoxide dismutase (SOD) activity were measured by spectrophotometer.ResultsBegan from the first day after reperfusion, in saline control group, the amplitudes of ERG bwave reduced continuously, the histopathological damages of retina were aggravating, the expression of nNOS increased, MDA level increased and SOD level decreased persistently, which significantly differed from the normal control group （P＜0.01）; in contrast to the saline control group, the amplitudes of bwave of ERG in betaxolol treatment group after reperfusion got right obviously（P＜0.01）, with alleviated histopathological damages, decreased nNOS positive neurons（P＜0.01）, decreased MDA content（P＜0.01）, and increased SOD activity （P＜0.01）, in which no statistical significance of nNOS positive neurons was found between the treatment group and normal control group （P＞0.01）. ConclusionBetaxolol, by reducing intracellular overfreight ofCa2+, inhibiting production of NO and elevating the ability of anti-oxidation in rat retina, can protect retinal neurons from ischemiareperfused injury.(Chin J Ocul Fundus Dis, 2005,21:249-252)