Blight A R
Center for Paralysis Research, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907.
J Neurol Sci. 1991 Dec;106(2):158-74. doi: 10.1016/0022-510x(91)90253-4.
A model of spinal cord trauma in guinea pigs, based on compression to a set thickness, was described previously. Compression injuries of the lower thoracic cord were produced in 11 anesthetized, adult guinea pigs, and the outcome monitored, using successive behavioral tests and morphometry of the lesion at 2-3 months. This report describes changes in the vascularity of the spinal cord, based on light microscopic analysis of 1 micron plastic transverse sections through the center of the lesion. Mean blood vessel density in these lesions was approximately twice that found in equivalent regions of normal, uninjured spinal cords, and hypervascularity of the white matter extended at least four spinal cord segments cranially and caudally from the lesion center. Capillary diameter distribution was significantly shifted to larger values and large perivascular spaces surrounded most capillaries and pre- and post-capillary vessels. Extent of hypervascularity was not correlated with the overall severity of the injury, but there was a significant positive correlation between the density of blood vessels in the outer 400 microns of the white matter and secondary loss of neurological function below the lesion, seen between one day and eight weeks after injury. This suggests that hypervascularization of the lesion is related to secondary pathological mechanisms in spinal cord injury, possibly inflammatory responses, that are relatively independent of the primary mechanical injury but more closely connected with loss and recovery of function.
先前已描述了一种基于压缩至设定厚度的豚鼠脊髓损伤模型。对11只麻醉的成年豚鼠造成下胸段脊髓压缩损伤,并通过连续的行为测试和2 - 3个月时损伤部位的形态学测量来监测结果。本报告基于对穿过损伤中心的1微米塑料横切片的光学显微镜分析,描述了脊髓血管的变化。这些损伤部位的平均血管密度约为正常未损伤脊髓相应区域的两倍,白质的血管增多向损伤中心头侧和尾侧至少延伸四个脊髓节段。毛细血管直径分布显著向较大值偏移,大多数毛细血管以及毛细血管前和后血管周围有大的血管周围间隙。血管增多的程度与损伤的总体严重程度无关,但在损伤后一天至八周之间,白质外层400微米处的血管密度与损伤以下神经功能的继发性丧失之间存在显著正相关。这表明损伤部位的血管增生与脊髓损伤的继发性病理机制有关,可能是炎症反应,相对独立于原发性机械损伤,但与功能丧失和恢复更密切相关。