Department of Mechanical Engineering, University of Utah, Salt Lake City, Utah, United States.
Department of Bioengineering, University of Utah, Salt Lake City, Utah, United States.
Invest Ophthalmol Vis Sci. 2018 Jan 1;59(1):349-361. doi: 10.1167/iovs.17-21530.
We identify long-term ocular sequelae subsequent to experimental blast exposure.
Male Long-Evans rats were exposed to 230 kPa side-on primary blast overpressure using a compressed air driven shock tube. Visual system function and structure were assessed for 8 weeks after exposure using optokinetic nystagmus and optical coherence tomography. Vitreous protein expression and histology (TUNEL, H&E) were performed at 1 day and 1, 4, and 8 weeks. IOP was recorded bilaterally during blast in a subset of animals.
Blast pressure profiles resembled the Friedlander waveform indicative of an open field blast. Peak IOP in directly-exposed eyes (240 kPa) was similar to peak blast overpressure, but IOP in indirectly-exposed eyes was 30% lower. Contrast sensitivity of blast-exposed animals decreased significantly by 20% 1 day after blast and did not recover by 8 weeks. Significant swelling and structural damage to the corneal epithelial and stromal layers were observed 2 weeks after blast exposure. Swollen corneas increased 254 ± 143 μm from baseline by 6 weeks, and scarring developed by 8 weeks. Histology revealed additional lens pathology 1 week after blast, suggestive of cataract development. Endothelial cell density increased significantly in blast-exposed animals between 1 and 4 weeks. Neurofilament heavy chain significantly increased after blast and returned to near baseline values by 8 weeks. Inflammatory cytokine changes corroborated ocular pathology findings.
These data demonstrate immediate visual dysfunction and biochemical responses, but delayed structural pathology, in response to single primary blast exposure. The delayed pathology time course may provide a window to implement treatment strategies for improved visual outcome.
我们确定了实验性爆炸暴露后的长期眼部后遗症。
雄性长耳大仓鼠通过压缩空气驱动的激波管暴露于 230 kPa 侧面原发性爆炸超压。暴露后 8 周,使用视动性眼球震颤和光学相干断层扫描评估视觉系统功能和结构。在 1 天、1、4 和 8 周时进行玻璃体液蛋白表达和组织学(TUNEL、H&E)检测。在一部分动物中,在爆炸期间记录了双侧眼压。
爆炸压力曲线类似于弗里德兰德(Friedlander)波形,表明是开放场爆炸。直接暴露眼的眼压峰值(240 kPa)与峰值爆炸超压相似,但间接暴露眼的眼压峰值低 30%。爆炸暴露动物的对比敏感度在爆炸后 1 天显著下降了 20%,8 周后仍未恢复。在爆炸暴露后 2 周观察到角膜上皮和基质层明显肿胀和结构损伤。肿胀的角膜在 6 周内从基线增加了 254±143 μm,8 周后出现瘢痕。组织学检查显示爆炸后 1 周还存在其他晶状体病变,提示白内障发展。爆炸暴露动物的内皮细胞密度在 1 至 4 周之间显著增加。神经丝重链在爆炸后显著增加,并在 8 周后恢复到接近基线值。炎症细胞因子变化与眼部病理学发现相符。
这些数据表明单次原发性爆炸暴露会立即引起视觉功能障碍和生化反应,但会延迟结构病理学变化。延迟的病理学时间过程可能为实施改善视觉结果的治疗策略提供一个窗口。