Evolution of spinal cord injury in a porcine model of prolonged aortic occlusion
Evolution of spinal cord injury in a porcine model of prolonged aortic occlusion
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DOI：
10.1016/j.jss.2005.10.007
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发表时间：
2006-06-15
影响因子：
2.2
通讯作者：
Kappas, Angelos M.
中科院分区：
文献类型：
--
作者：
Papakostas, John C.;Matsagas, Miltiadis I.;Kappas, Angelos M.
背景。脊髓损伤和随后的截瘫仍然是胸腹主动脉手术不可预测和毁灭性的并发症。本研究的目的是探讨长时间胸腹主动脉阻塞引起的脊髓损伤。材料和方法。我们使用了一个高度可重复的猪胸腹主动脉阻塞45分钟模型，该模型由两个球囊阻塞导管完成。实验结束后由独立观察员根据Tarlov量表进行神经学评估。分别于10、48和120 h采集下胸腰椎脊髓（每个时间点n = 6只），用苏木精和伊红（H&E）染色和TUNEL法进行组织学检查。分析大鼠Tarlov评分、神经元数量及炎症程度。H&E染色显示，运动神经元数量在再灌注0 ~ 10 h和48 ~ 120 h两个阶段均有减少，脊髓切片出现炎症反应，并在48 h达到高峰，凋亡神经元TUNEL反应在任何时间点均呈阴性。在猪模型中，我们证明，胸腹主动脉阻断45分钟后，运动神经元死亡似乎分两个阶段发生（即时和延迟）。炎症是一过性延长脊髓缺血的后续事件，可能是延迟神经元死亡的主要原因。TUNEL染色在再灌注的任何时间点均未发现神经元凋亡的迹象。(c) 2006爱思唯尔公司版权所有。
Background. Spinal cord injury and subsequent paraplegia remains an unpredictable and devastating complication of thoracoabdominal aortic surgery. The aim of this study was to investigate spinal cord injury due to prolonged thoracoabdominal aortic occlusion.Materials and methods. We used a highly reproducible porcine model of 45-min thoracoabdominal aortic occlusion, which was accomplished by two balloon occlusion catheters. Neurological evaluation after the end of experiment was performed by an independent observer according to the Tarlov scale. The lower thoracic and lumbar spinal cords were harvested at 10, 48, and 120 h (n = 6 animals per time point) and examined histologically with hematoxylin and eosin (H&E) stain and TUNEL method. Tarlov scores, number of neurons, and the grade of inflammation were analyzed.Results. H&E staining revealed reduction in the number of motor neurons which occurred in two phases (between 0 and 10 h and between 48 and 120 h of reperfusion), as well as development of inflammation in spinal cord sections during the reperfusion period, reaching a peak at 48 h. TUNEL reaction was negative for apoptotic neurons at any time point.Conclusions. In this porcine model, we demonstrated that, after 45 min of thoracoabdominal aortic occlusion, motor neuron death seems to occur in two phases (immediate and delayed). Inflammation was a subsequent event of transient prolonged spinal cord ischemia and possibly a major contributor of delayed neuronal death. Using TUNEL straining we found no evidence of neuronal apoptosis at any time point of reperfusion. (c) 2006 Elsevier Inc. All rights reserved.