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目的探讨高眼压后活性氧自由基对视网膜组织的损伤情况及外源性超氧化物歧化酶（ｓｕｐｅｒｏｘｉｄｅｄｉｓｍｕｔａｓｅ，ＳＯＤ）对高眼压致视网膜损伤的保护作用。方法观察６．６７ｋＰａ（１ｋＰａ＝７．５ｍｍＨｇ）、维持１．５ｈ的高眼压解除２４ｈ内兔视网膜组织中脂质过氧化产物丙二醛（ｍａｌｏｎｄｉａｌｄｅｈｙｄｅ，ＭＤＡ）含量、ＳＯＤ活性、谷胱甘肽过氧化物酶（ｇｌｕｔａｔｈｉｏｎｅｐｅｒｏｘｉｄａｓｅ，ＧＳＨ－Ｐｘ）活性和还原型谷胱甘肽（ＧＳＨ）含量的变化情况及球后注射Ｃｕ－Ｚｎ－ＳＯＤ对高眼压解除后１２ｈ时兔视网膜组织中ＭＤＡ含量和ＳＯＤ活性的影响。结果ＭＤＡ在高眼压解除后０～１２ｈ逐渐增加，１２～２４ｈ维持较高水平。ＳＯＤ活性和ＧＳＨ－Ｐｘ活性在高眼压解除即刻均低于正常水平，以后有不同程度增高，其中ＳＯＤ活性在高眼压解除４ｈ后又开始下降。ＧＳＨ在高眼压解除后２４ｈ内无明显变化。球后注射Ｃｕ－Ｚｎ－ＳＯＤ能减少兔视网膜组织中ＭＤＡ生成，增加ＳＯＤ活性。结论活性氧自由基参与了高眼压致视网膜损伤，球后注射大剂量ＳＯＤ对提高视网膜抗氧化损伤能力有积极意义。
Objective To investigate the damage of reactive oxygen species (ROS) to retinal tissue and the protective effect of exogenous superoxide dismutase (SOD) on retinal damage induced by intraocular hypertension. Methods The contents of malondialdehyde (MDA) and superoxide dismutase (SOD) in the peritoneal membrane of the rabbit retina were measured after intraocular pressure (IhPa) of 1.5h at 6.67kPa (1kPa = 7.5mmHg) The changes of glutathioneperoxidase (GSH-Px) activity and glutathione (GSH) content and the content of MDA in rabbit retinal tissue at 12h after intraocular pressure injection of Cu-Zn-SOD SOD activity. Results MDA increased gradually from 0 to 12 hours after the release of intraocular pressure and maintained at a high level from 12 to 24 hours. SOD activity and GSH-Px activity in the immediate release of intraocular pressure were lower than normal immediately after the increase in varying degrees, including SOD activity in the 4h after the release of intraocular pressure began to decline. GSH in the intraocular pressure within 24h after lifting no significant change. Post-ball injection of Cu-Zn-SOD can reduce the retinal tissue MDA production and increase SOD activity. Conclusion Reactive oxygen species are involved in retinal damage induced by intraocular hypertension. High dose of SOD after injecting the ball possesses positive significance for improving the anti-oxidative damage ability of retina.