The School of Medical Sciences, Level 4, Medical School South, The University of Adelaide , Adelaide, South Australia, Australia .
J Neurotrauma. 2013 Nov 1;30(21):1812-23. doi: 10.1089/neu.2013.2993. Epub 2013 Sep 28.
Although clinical spinal cord injury (SCI) occurs within a closed environment, most experimental models of SCI create an open injury. Such an open environment precludes the measurement of intrathecal pressure (ITP), whose increase after SCI has been linked to the development of greater tissue damage and functional deficits. Raised ITP may be potentiated by edema, which we have recently shown to be associated with substance P (SP) induced neurogenic inflammation in both traumatic brain injury and stroke. The present study investigates whether SP plays a similar role as a mediator of neurogenic inflammation after SCI. A closed balloon compression injury was induced at T10 in New Zealand white rabbits. Animals were thereafter assessed for blood spinal cord barrier (BSCB) permeability, edema, ITP, histological outcome, and functional outcome from 5 h to 2 weeks post-SCI. The balloon compression model produced significant increases in BSCB permeability, edema, and ITP along with significant functional deficits that persisted for 2 weeks. Histological assessment demonstrated decreased SP immunoreactivity in the injured spinal cord while NK1 receptor immunoreactivity initially increased before returning to sham levels. In addition, aquaporin 4 immunoreactivity increased early post-SCI, implicating this water channel in the development of edema after SCI. The changes described in the present study support a role for SP as a mediator of neurogenic inflammation after SCI.
尽管临床脊髓损伤 (SCI) 发生在封闭的环境中，但大多数 SCI 的实验模型都会造成开放性损伤。这种开放性环境使得无法测量鞘内压 (ITP)，而 SCI 后 ITP 的升高与组织损伤和功能缺陷的发展有关。水肿会加剧 ITP，我们最近发现，在创伤性脑损伤和中风中，SP 诱导的神经源性炎症与水肿有关。本研究探讨 SP 是否在 SCI 后作为神经源性炎症的介质发挥类似作用。在新西兰白兔的 T10 处诱导封闭的球囊压迫损伤。此后，从 SCI 后 5 小时到 2 周，对动物的血脊髓屏障 (BSCB) 通透性、水肿、ITP、组织学结果和功能结果进行评估。球囊压迫模型导致 BSCB 通透性、水肿和 ITP 显著增加，同时存在持续 2 周的显著功能缺陷。组织学评估显示，损伤脊髓中的 SP 免疫反应性降低，而 NK1 受体免疫反应性最初增加，然后恢复到假手术水平。此外，水通道蛋白 4 的免疫反应性在 SCI 后早期增加，表明该水通道在 SCI 后水肿的发展中起作用。本研究中描述的变化支持 SP 在 SCI 后作为神经源性炎症的介质的作用。
