Protective effect of betaxolol on optic nerves after experimental retinal ischemia-reperfusion injury
- VernacularTitle:倍他洛尔对实验性视网膜缺血再灌注损伤后视神经的保护作用
- Author:
Hua RONG
;
Ming AI
;
Yiqiao XING
- Publication Type:Journal Article
- Keywords:
Betaxolol/therapeutic use;
Retina/drug effects
- From:
Chinese Journal of Ocular Fundus Diseases
2000;0(04):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect and mechanism of betaxolol on optic nerves after experimental retinal ischemia-reperfused injury. Methods Retinal 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. Results [WTBZ]Began 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 (P0.01). Conclusion Betaxolol, by reducing intracellular overfreight of Ca~(2+),inhibiting production of NO and elevating the ability of anti-oxidation in rat retina, can protect retinal neurons from ischemia-reperfused injury.