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Effect of oxygen inhalation on the retinae of newborn rats and its mechanism
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- Author:
- No author available
- Journal Title:
- CHINESE JOURNAL OF OCULAR FUNDUS DISEASES
- Issue:
- 5
- DOI:
- 10.3760/j.issn:1005-1015.2003.05.011
- Key Word:
- 视网膜病,早产儿;超氧化物歧化酶;丙二醛;疾病模型,动物
Abstract： 目的探讨吸氧对新生鼠视网膜的影响及其机制. 方法高氧环境下用新生鼠视网膜的变化模拟早产儿视网膜病变(retinopathy of prematurity, ROP).将118只新生鼠放入含氧80%的吸氧箱中连续饲养7 d,再置于空气中饲养7 d,以一直在空气中饲养的同龄鼠为对照组.分别检测1、2、4、7、8、9、11、14 d龄鼠的动脉血氧分压及视网膜超氧化物歧化酶(superoxide dismutase, SOD)、丙二醛(malondialdehyde, MDA)的含量;血管灌注及密度计数检测7、14 d龄鼠视网膜血管主干直径及周边血管覆盖率;HE染色检测8、9、11、14 d龄鼠视网膜新生血管. 结果实验组1、2、4、7 d龄鼠血氧分压明显高于对照组(P＜0.01), 8、9、11、14 d龄鼠血氧分压低于对照组,但差异无显著性的意义(P＞0.05),实验组1、2、4、7、8 d龄鼠视网膜的SOD含量低于对照组(P＜0.01,P＜0.05), 而1、2、4、7、8 d龄鼠MDA高于对照组(P＜0.01,P＜0.05);实验组7 d龄鼠视网膜血管主干直径是对照组鼠的75%,周边血管覆盖率是对照组的22%,14 d龄鼠视网膜血管主干直径是对照组的61%,周边血管覆盖率为对照组的73%.实验组中,16.7%的鼠视网膜发现新生血管,而对照组未发现. 结论高氧环境下的自由基损伤及停止吸氧后的缺氧状态可能是ROP发生的一个重要原因.
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