MORPHOMETRIC ANALYSIS OF EXPERIMENTAL SPINAL-CORD INJURY IN THE CAT - THE RELATION OF INJURY INTENSITY TO SURVIVAL OF MYELINATED AXONS
MORPHOMETRIC ANALYSIS OF EXPERIMENTAL SPINAL-CORD INJURY IN THE CAT - THE RELATION OF INJURY INTENSITY TO SURVIVAL OF MYELINATED AXONS
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DOI：
10.1016/0306-4522(86)90025-4
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发表时间：
1986-09-01
期刊：
影响因子：
3.3
通讯作者：
DECRESCITO, V
中科院分区：
文献类型：
--
作者：
BLIGHT, AR;DECRESCITO, V
本文采用1 μ m轴突取样法研究了猫胸脊髓实验性挫裂伤中轴突破坏和脱髓鞘的模式。M厚塑料切片用光学显微镜。损伤是由失重装置造成的，撞击下的椎体（T9）由横突下的支撑物稳定。研究了体重和身高两种组合的影响：10或13克落在直径为5毫米的撞击区域20厘米处。损伤后饲养3-5个月，灌注固定后进行组织学分析。研究发现，存活的有髓轴突数量随使用的重量和脊髓的大小而变化。撞击强度的测量来源于撞击时重量的计算动量除以脊髓的横截面积（从固定后病变的吻侧和尾侧测量的尺寸插值）。在冲击强度为> ~ 0.02 kg-m/cm2时，损伤部位中心轴突几乎没有存活，并且颅底边缘几乎完全破坏。在0.08和0.2 kg-m/s/cm2之间，存活轴突的数量在10万到2000之间变化，近似于负指数函数（r = -0.88）。存活在外100亩的轴突数量。在相同的损伤强度范围内，脊髓的M值在接近正常和小于正常的1%之间几乎呈线性变化（r = -0.82）。存活轴突的数量随着深度的增加而减少，也近似于负指数函数，在大约500 μ m时密度减少10倍。在损伤强度范围内，这种关系的平均斜率与深度保持相似，尽管斜率与给定强度下不同个体轴突存活率的变化呈负相关。有人认为轴突的损失可能主要是由撞击时的机械拉伸决定的。其离心模式可以用脊髓中央内容物的纵向位移来解释，反映了脑膜管内实质流动的粘弹性“边界层”特性。这是通过参考明胶模型在压缩下的行为来说明的。大口径轴突的优先丧失和特征性向异常薄髓鞘的转变（由创伤后脱髓鞘引起）在程度上与损伤强度和总体轴突存活无关。这些影响被认为是独立过程的结果，由创伤性损伤触发，显然在时间上延迟，但最终叠加在最初的机械破坏上。
The pattern of axonal destruction and demyelination that occurs in experimental contusion injury of cat thoracic spinal cord was studied by line sampling of axons in 1 .mu.m thick plastic sections with the light microscope. Injuries were produced by a weight-drop apparatus, with the vertebral body (T9) below the impact stabilized by supports under the transverse processes. The effects of two combinations of weight and height were examined: 10 or 13 g dropped 20 cm into an impact area of 5 mm diameter. Animals were kept for 3-5 months after injury, then fixed by perfusion for histological analysis. The number of surviving myelinated axons was found to vary both with the weight used and with the size of the spinal cord. A measure of impact intensity was derived from the calculated momentum of the weight at impact divided by the cross sectional area of the cord (interpolated from dimensions measured rostral and caudal of the lesion following fixation). At impact intensities > 0.02 kg-m/cm2 there was practically no survival of axons at the center of the injury site, combined with almost complete breakdown of the pial margin. Between 0.08 and 0.2 kg-m/s/cm2 the number of surviving axons varied between 100,000 and 2000, approximating a negative exponential function (r = -0.88). The number of axons surviving in the outer 100 .mu.M of the cord varied practically linearly (r = -0.82) between near normal and < 1% of normal over the same range of injury intensity. The number of surviving axons decreased with depth from the pia, also approximating a negative exponential function, with a 10-fold decrease in density over approximately 500 .mu.m. The average slope of this relation with depth remained similar over the range of injury intensity examined, though the slope appeared inversely related to variation in axonal survival for different individuals at a given intensity. It is argued that the loss of axons is probably determined primarily by mechanical stretch at the time of impact. Its centrifugal pattern may be explained by longitudinal displacement of the central contents of the cord, reflecting the viscoelastic "boundary layer" properties of parenchymal flow within the meningeal tube. This is illustrated with reference to the behavior of a gelatin model under compression. The preferential loss of large caliber axons and the characteristic shift to abnormally thin myelin sheaths (resulting from post-traumatic demyelination) both varied in extent independently of injury intensity and overall axonal survival. These effects are concluded to be the result of independent processes, triggered by traumatic injury, apparently delayed in time, but ultimately superimposed on the initial mechanical disruption.