Blight A R
Center for Paralysis Research, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907.
J Neurol Sci. 1991 Jun;103(2):156-71. doi: 10.1016/0022-510x(91)90159-5.
A model of spinal cord trauma in guinea pigs is described, based on the concept of compression to a set thickness, as an alternative to compression or contusion with a set force or displacement. The model is technically simple and reliable and circumvents some of the biomechanical problems of contusion techniques. It was designed initially to produce moderate injuries, allowing significant recovery of function. A pair of forceps was modified to form an instrument to compress the spinal cord laterally, over a 5-mm length, to a thickness of 1.2 mm. Such compression injuries of the lower thoracic cord were produced in 12 anesthetized, adult guinea pigs, and the outcome monitored, using successive behavioral tests and morphometry of the lesion at 2-3 months. Chronic histopathology was examined quantitatively with line-sampling of axons in 1-micron plastic sections through the lesion center, stained with toluidine blue. The type and distribution of damage to axons was similar to that seen following weight-drop contusion trauma in cats. Spinal cord function was examined by means of hindlimb reflex testing and motor behavior, vestibulospinal reflex testing, and mapping the receptive field of the cutaneus trunci muscle (CTM) reflex. These injuries characteristically resulted in a delayed onset of functional deficits at 1-2 days after injury, followed by partial recovery over the course of several weeks. Overall, functional outcome correlated significantly with the number of surviving axons in the lesion. The phenomenon of "secondary" pathology was striking at the behavioral level, whereas evidence of delayed injury has been indirect in most animal models. The onset of this secondary process occurred with a longer delay than has been assumed or implied by most suggested mechanisms of secondary pathology. The time course of secondary loss and recovery may be related to that of the inflammatory response at the injury site, particularly the phagocytic activity of macrophages.
本文描述了一种豚鼠脊髓损伤模型，该模型基于将脊髓压缩至设定厚度的概念，作为设定力或位移的压缩或挫伤的替代方法。该模型技术简单且可靠，避免了挫伤技术的一些生物力学问题。它最初设计用于产生中度损伤，使功能有显著恢复。将一把镊子进行改造，制成一种可在5毫米长度上横向压缩脊髓至1.2毫米厚度的器械。在12只麻醉的成年豚鼠身上造成下胸段脊髓的这种压缩性损伤，并通过连续的行为测试和损伤2 - 3个月时的形态学测量来监测结果。通过对穿过损伤中心的1微米塑料切片中的轴突进行线取样，并使用甲苯胺蓝染色，对慢性组织病理学进行定量检查。轴突损伤的类型和分布与猫体重下降挫伤性创伤后所见相似。通过后肢反射测试、运动行为、前庭脊髓反射测试以及绘制躯干皮肤肌（CTM）反射的感受野来检查脊髓功能。这些损伤的特征是在损伤后1 - 2天出现功能缺陷的延迟发作，随后在数周内部分恢复。总体而言，功能结果与损伤部位存活轴突的数量显著相关。“继发性”病理现象在行为水平上很明显，而在大多数动物模型中延迟损伤的证据一直是间接的。这种继发性过程的发作延迟时间比大多数继发性病理机制所假设或暗示的要长。继发性损失和恢复的时间进程可能与损伤部位的炎症反应，特别是巨噬细胞的吞噬活性的时间进程有关。
