【摘要】 目的:早产儿视网膜病变(Retinopathy of prematurity,ROP)是一种严重影响早产儿生存质量的疾病,目前对ROP的防治研究着重于抑制视网膜新生血管的形成,本实验通过建立高氧诱导的早产儿视网膜病变的动物模型,探讨长效糖皮质激素类药物曲安奈德在抑制视网膜新生血管方面的作用。方法:选择鼠龄为7 d的C57 BL/6 J幼鼠60只,分为大、小剂量治疗组和正常及高氧对照组。大、小剂量治疗组一眼玻璃体腔内分别注射曲安奈德5μl及2.5μl,对侧眼注射相同体积的平衡盐溶液(BSS)作为对照。血管灌注法视网膜铺片,观察视网膜血管情况;视网膜组织切片HE染色观察并计数突破视网膜内界膜的血管内皮细胞核数目。结果:高氧环境对照组与正常环境对照组相比,视网膜有大量新生血管形成,说明高氧诱导的早产儿视网膜病变动物模型制作成功;药物治疗组与高氧对照组相比视网膜血管分布规则、密度减少,且突破视网膜内界膜的血管内皮细胞核数目明显减少(P<0.001)。大、小剂量治疗组相比差异不明显(P>0.05),视网膜组织切片未见视网膜毒性及炎症反应。结论:曲安奈德有抑制视网膜新生血管形成的作用。更多还原

【Abstract】 Objective:Retinopathy of prematurity(ROP)is a severe disease affecting the quality of life of premature infants.The studies of prevention and treatment of ROP focus on the inhibition in retinal neurovascularization.This study established the animal model of ROP induced by hyperxia and discussed in effect of triamcinolone acetonide(TA)on retinal neurovascularization in ROP.Methods:60C57 BL/6 J young rabbits aged in 7 days were selected and divided into four groups:treatment group in massive dose or minute dose of TA,normal group and control group with hyperxia.one eye in treatment group received intravitreous TA in dose of 5 ul or 2.5 ul,and conralateral eyes received the same volume of BSS as controls.The retinal vassels was observed by ink perfusion,and the numbers of vascular endothelial necleus breakthrough layer of retina were counted in retinal chip with HE staining.Results:Compared with control group in normal condition,retina with massive neurovascularization showed successful animal model of ROP.In treatment group,the retinal vessels arranged regularly with lower density and less vascular endothelial necleus breakthrough layer of retina than that in control group with hyperxia(P<0.001).The difference between treatment groups in massive dose and minute group was not significant(P>0.05).There was no retinal toxic and inflammational reaction in retinal slip.Conclusion:TA play an role in inhibiting retinal neurovascularization.更多还原