Department of Ophthalmology, Tianjin Medical University General Hospital, Tianjin, China.
Curr Eye Res. 2012 Oct;37(10):941-8. doi: 10.3109/02713683.2012.691599. Epub 2012 Jun 5.
To create an animal (rat) model of force percussion injury (FPI) to the optic nerve for clinical and experimental research.
Seventy-one healthy female Wister rats, with no ocular disorders, were used in this study. Sixty-six rats were subjected to bilateral blunt trauma to the eyes via FPI; five rats were not subjected to trauma. According to the degree of optic nerve injury, injured eyes were divided into two groups: severe optic nerve injury group, with beat pressures of 699.14 ± 60.79 kPa and mild optic nerve injury group, with beat pressures of 243.18 ± 20.26 kPa. Eight rats were examined using flash visual-evoked potential (F-VEP) monitoring and magnetic resonance imaging (MRI) before, 1 and 3 days, and 1, 2, 4, 6, and 8 weeks after optic nerve injury. Fifty-six rats were examined by histopathology and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay for apoptosis at 1 and 3 days, and 1, 2, 4, 6, and 8 weeks after optic nerve injury. Two rats were examined by transmission electron microscopy (TEM) 4 and 8 weeks after optic nerve injury. The presence or absence of optic nerve injury was evaluated in all trauma eyes.
Latency was prolonged in the severe injury group compared with controls 1 day after optic nerve injury (p < .05). Amplitude decreased during the first 2 weeks after optic nerve injury (p < .05) and then stabilized (p > .05). Latency was prolonged in the mild optic nerve injury group compared with controls 1 day after optic nerve injury (p < .05) Amplitude decreased during the first 4 weeks (p < .05) following injury and then stabilized (p > .05). As measured by MRI, an abnormally high signal was seen 1 day after injury and remained significantly high 8 weeks after injury. A ruptured capillary was detected in the ganglion cell layer (GCL) 1 day after injury. Acellular regions in the ganglion cell layer were observed 4 weeks after optic nerve injury. TUNEL-positive cells were present in each layer of the retina 3 days after injury. The number of TUNEL-positive cells began to increase 1-2 weeks after injury, and then gradually decreased 4 weeks after injury (p < .05).
We successfully created a reproducible experimental animal (rat) model of optic nerve injury using FPI. Optic nerve injury was demonstrated by F-VEP and MRI, and confirmed histologically. Our model is a simple, reliable, reproducible, and stable tool for use in investigations on the mechanism(s) of and treatment for optic nerve injury.
建立一种针对视神经的力击伤（FPI）动物（大鼠）模型，用于临床和实验研究。
本研究纳入 71 只健康雌性 Wistar 大鼠，无眼部疾病。66 只大鼠双侧眼接受 FPI 所致钝挫伤；5 只大鼠未接受创伤。根据视神经损伤程度，受伤眼分为两组：严重视神经损伤组，打击压力为 699.14±60.79kPa；轻度视神经损伤组，打击压力为 243.18±20.26kPa。8 只大鼠在视神经损伤前、损伤后 1 天、3 天、1 周、2 周、4 周、6 周和 8 周时接受闪光视觉诱发电位（F-VEP）监测和磁共振成像（MRI）检查。56 只大鼠在视神经损伤后 1 天、3 天、1 周、2 周、4 周、6 周和 8 周时行组织病理学和末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记（TUNEL）检测凋亡。2 只大鼠在视神经损伤后 4 周和 8 周时行透射电子显微镜（TEM）检查。所有创伤眼均评估视神经损伤的存在或不存在。
严重损伤组与对照组比较，视神经损伤后 1 天潜伏期延长（p＜0.05）。损伤后前 2 周振幅降低（p＜0.05），然后稳定（p＞0.05）。轻度视神经损伤组与对照组比较，视神经损伤后 1 天潜伏期延长（p＜0.05）。损伤后 4 周振幅降低（p＜0.05），然后稳定（p＞0.05）。MRI 显示，损伤后 1 天可见异常高信号，损伤后 8 周仍明显升高。损伤后 1 天在节细胞层（GCL）检测到破裂的毛细血管。视神经损伤后 4 周观察到节细胞层的无细胞区。损伤后 3 天视网膜各层均有 TUNEL 阳性细胞。损伤后 1-2 周 TUNEL 阳性细胞数开始增加，4 周后逐渐减少（p＜0.05）。
我们成功地使用 FPI 建立了一种可重现的视神经损伤实验动物（大鼠）模型。F-VEP 和 MRI 显示视神经损伤，组织学证实。我们的模型是一种简单、可靠、可重现和稳定的工具，可用于研究视神经损伤的机制和治疗。
