From the Department of Anesthesiology (SR), Department of Ophthalmology and Visual Sciences, University of Illinois (SR), Anesthesia and Critical Care, University of Chicago, Chicago, Illinois (JD), Department of Ophthalmology and Neurology (NJN) and Department of Neurological Surgery, Emory University School of Medicine, Atlanta, Georgia, USA (NJN).
Eur J Anaesthesiol. 2018 Nov;35(11):840-847. doi: 10.1097/EJA.0000000000000829.
Mechanisms of peri-operative ischaemic optic neuropathy remain poorly understood. Both specific pre-operative and intra-operative factors have been examined by retrospective studies, but no animal model currently exists.
To develop a rodent model of peri-operative ischaemic optic neuropathy. In rats, we performed head-down tilt and/or haemodilution, theorising that the combination damages the optic nerve.
Animal study.
Laboratory.
A total of 36 rats, in four groups, completed the functional examination of retina and optic nerve after the interventions.
Anaesthetised groups (n>8) were supine (SUP) for 5 h, head-down tilted 70° for 5 h, head-down tilted/haemodiluted for 5 h or SUP/haemodiluted for 5 h. We measured blood pressure, heart rate, intra-ocular pressure and maintained constant temperature.
Retinal function (electroretinography), scotopic threshold response (STR) (for retinal ganglion cells) and visual evoked potentials (VEP) (for transmission through the optic nerve). We imaged the optic nerve in vivo and evaluated retinal histology, apoptotic cells and glial activation in the optic nerve. Retinal and optic nerve function were followed to 14 and 28 days after experiments.
At 28 days in head down tilted/haemodiluted rats, negative STR decreased (about 50% amplitude reduction, P = 0.006), VEP wave N2-P3 decreased (70% amplitude reduction, P = 0.01) and P2 latency increased (35%, P = 0.003), optic discs were swollen and glial activation was present in the optic nerve. SUP/haemodiluted rats had decreases in negative STR and increased VEP latency, but no glial activation.
An injury partly resembling human ischaemic optic neuropathy can be produced in rats by combining haemodilution and head-down tilt. Significant functional changes were also present with haemodilution alone. Future studies with this partial optic nerve injury may enable understanding of mechanisms of peri-operative ischaemic optic neuropathy and could help discover preventive or treatment strategies.
围手术期缺血性视神经病变的发病机制仍不清楚。回顾性研究已经检查了特定的术前和术中因素，但目前尚无动物模型。
建立围手术期缺血性视神经病变的啮齿动物模型。在大鼠中，我们进行了头低位倾斜和/或血液稀释，理论上这种组合会损害视神经。
动物研究。
实验室。
共有 36 只大鼠，分为四组，在干预后完成视网膜和视神经的功能检查。
麻醉组（n>8）仰卧 5 小时，头低位倾斜 70°5 小时，头低位倾斜/血液稀释 5 小时或仰卧/血液稀释 5 小时。我们测量血压、心率、眼内压并保持体温恒定。
视网膜功能（视网膜电图）、暗适应阈值反应（STR）（用于视网膜神经节细胞）和视觉诱发电位（VEP）（用于视神经传输）。我们对活体视神经进行成像，并评估视网膜组织学、视神经中的凋亡细胞和胶质细胞激活。在实验后 14 天和 28 天观察视网膜和视神经功能。
在头低位倾斜/血液稀释大鼠中，28 天时 STR 负值降低（约 50%的振幅降低，P=0.006），VEP 波 N2-P3 降低（70%的振幅降低，P=0.01），P2 潜伏期延长（35%，P=0.003），视盘肿胀，视神经胶质激活。仰卧/血液稀释大鼠的 STR 负值降低，VEP 潜伏期延长，但无胶质激活。
通过组合血液稀释和头低位倾斜，可在大鼠中产生类似于人类缺血性视神经病变的损伤。单纯血液稀释也会引起明显的功能改变。未来对这种部分视神经损伤的研究可能有助于理解围手术期缺血性视神经病变的发病机制，并有助于发现预防或治疗策略。
