Stein S C, Cracco R Q, Farmer P, Kiest C A
Neurosurgery. 1979 Mar;4(3):239-43. doi: 10.1227/00006123-197903000-00008.
Several investigators have implicated norepinephrine and other toxic substances released in the region of a spinal cord injury in the genesis of the progressive pathological and clinical changes that follow spinal trauma. To test this hypothesis, we subjected cats to T-10 to T-12 laminectomy and monitored epidural spinal evoked potentials from sciatic nerve stimulation. The spinal subarachnoid space was perfused with normal saline, with norepinephrine solution, or with heparinized autologous blood or the pial surface of the spinal cord was exposed to macerated gray matter taken from the upper cervical cord. During 1- to 2-hour exposure periods, we noted no significant changes in the base line spinal evoked potentials. In another series of cats, we have shown that norepinephrine perfused over the spinal cord in this manner diffuses rapidly into the subpial white matter. Therefore, its failure to affect spinal evoked potentials does not represent a failure to penetrate the spinal cord. Putative toxins must originate either in extravasated blood or damaged neural tissue in the region of the spinal cord injury. The failure of ascending spinal tracts to react to blood or cord tissue in our experiment suggests that toxins are not involved in the spinal cord dysfunction that occurs soon after injury.
几位研究者认为，脊髓损伤区域释放的去甲肾上腺素和其他有毒物质与脊髓创伤后发生的渐进性病理和临床变化的发生有关。为了验证这一假设，我们对猫进行了T-10至T-12椎板切除术，并监测坐骨神经刺激引起的硬膜外脊髓诱发电位。脊髓蛛网膜下腔用生理盐水、去甲肾上腺素溶液、肝素化自体血灌注，或者将脊髓软膜表面暴露于取自上颈髓的浸软灰质。在1至2小时的暴露期间，我们注意到基线脊髓诱发电位没有显著变化。在另一组猫中，我们已经表明，以这种方式灌注在脊髓上的去甲肾上腺素会迅速扩散到软膜下白质中。因此，它未能影响脊髓诱发电位并不代表未能穿透脊髓。假定的毒素一定起源于脊髓损伤区域外渗的血液或受损的神经组织。在我们的实验中，脊髓上行束对血液或脊髓组织没有反应，这表明毒素与损伤后不久发生的脊髓功能障碍无关。
