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目的建立大鼠慢性高眼压模型,对其眼压、视网膜节细胞(RGCs)和视神经轴突损伤进行研究。方法对40只大鼠行慢性高眼压模型手术,分为4组:术后即刻、5 d、2周和4周,每组10只,分别测定眼压。采用全视网膜-RGCs Cresyl Violet染色,术后2周和4周对大鼠视网膜进行RGCs计数,并对视神经进行对位苯二胺(PPD)染色。对照组20只大鼠,分为2组,每组10只。结果31只大鼠眼压升高,眼压升高率为77.5%,且4周内眼压维持稳定。眼压升高2周时中心和周边RGCs分别减少11.0%和11.3%,眼压升高4周时中心和周边视网膜分别丢失RGCs达17%和24.6%,与正常对照组比较差异均有统计学意义(P<0.05);而眼压未升高的RGCs未见明显丢失,与正常对照组相比差异无统计学意义(P>0.05)。高眼压组大鼠视神经轴突在颞上方有大约5.3%损伤,球后1 mm的视神经在光镜下可以看到视神经轴突水肿和髓鞘碎屑。结论慢性高眼压动物模型是一种可以重复且有效的青光眼模型,它模拟了人类慢性眼压升高所导致的RGCs丢失和视神经的损伤。
Objective To establish a rat model of chronic ocular hypertension and study its intraocular pressure, retinal ganglion cells (RGCs) and optic nerve axon injury. Methods Forty rats underwent chronic ocular hypertension. The rats were divided into 4 groups: immediately after operation, 5 days, 2 weeks and 4 weeks, with 10 rats in each group. Intraocular pressure was measured respectively. Retinal RGCs were stained with Cresyl Violet. RGCs were counted in the retina at 2 and 4 weeks after operation, and para-phenylenediamine (PPD) staining was performed on the optic nerve. Twenty rats in the control group were divided into two groups of 10 rats each. Results The intraocular pressure (IOP) of 31 rats increased and the intraocular pressure (IOP) increased by 77.5%. Intraocular pressure remained stable within 4 weeks. At 2 weeks after IOP elevation, the central and peripheral RGCs decreased by 11.0% and 11.3%, respectively. The intraocular pressure and the surrounding retina lost RGCs by 17% and 24.6% respectively at 4 weeks after IOP elevation. Compared with the normal control group, there were statistically significant differences (P <0.05). However, there was no obvious loss of RGCs with no increase in intraocular pressure (P> 0.05). The oculomotor axon in the IOP group had an injury of about 5.3% on the temporal superior side. The optic nerve of 1 mm posterior to the ball could see optic nerve axon edema and myelin debris under light microscope. Conclusion The chronic ocular hypertension animal model is a repeatable and effective model of glaucoma. It simulates the loss of RGCs and the damage of the optic nerve caused by chronic elevated intraocular pressure in humans.