Department of Cell Biology and Anatomy, New York Medical College, Valhalla; and.
J Neurosurg Spine. 2014 Feb;20(2):164-71. doi: 10.3171/2013.10.SPINE13113. Epub 2013 Dec 6.
Traumatic injury to the spinal cord results in considerable delayed tissue loss. The authors investigated the extent to which ischemia occurs following contusion-induced spinal cord injury and whether ischemia exacerbates tissue damage that leads to the loss of locomotor function. They also determined if ischemia is reversed with β2-adrenoceptor agonist treatment, which has been established to be neuroprotective following contusion injury.
The extent and role of circulation loss in spinal cord injury was determined in an established experimental model of contusion injury. The spinal cord dura mater of Wistar rats was exposed by performing a laminectomy at T-8 to T-11. Laser Doppler perfusion imaging was then used to measure microcirculation in the exposed spinal cord. After imaging, a moderately severe contusion injury was produced using a weight-drop device unto the exposed dura at T-10. Perfusion imaging was again performed, scans were quantitated, and integrated intensities were compared.
Postinjury imaging revealed an 18%-27% reduction in perfusion in regions rostral and caudal to the injury site, and a 68% reduction was observed at the contusion epicenter. These perfusion losses persisted for at least 48 hours. At 24 hours after injury, some rats were intraperitoneally injected with 2 mg/kg of the β2-adrenoceptor agonist clenbuterol, which has been shown to promote the partial recovery of locomotor function and spare spinal cord tissue when administered within 2 days after contusion injury. Clenbuterol injection caused a gradual increase in perfusion, which was detectable at 30 minutes postinjection and continued over time, resulting in an 127% overall increase in perfusion at the epicenter 24 hours after treatment.
These results suggest that the occurrence of chronic perfusion loss after contusion contributes to delayed damage and tissue loss. In contrast, β2-adrenoceptor agonist treatment may exert neuroprotection by restoring perfusion, thereby preventing ischemic neurodegeneration. The ability of laser Doppler imaging to measure the loss of perfusion and its restoration upon treatment suggests that it may have clinical utility in the assessment and treatment of spinal cord injury.
脊髓创伤会导致大量延迟性组织损失。作者研究了挫伤性脊髓损伤后发生缺血的程度,以及缺血是否会加剧导致运动功能丧失的组织损伤。他们还确定了β2-肾上腺素能受体激动剂治疗是否可以逆转缺血,该治疗在挫伤损伤后已被证实具有神经保护作用。
在挫伤损伤的既定实验模型中,确定了脊髓损伤中循环损失的程度和作用。通过在 T-8 到 T-11 进行椎板切除术来暴露 Wistar 大鼠的脊髓硬脑膜。然后使用激光多普勒灌注成像来测量暴露的脊髓中的微循环。成像后,使用重物掉落装置在 T-10 处的暴露硬脑膜上产生中度严重的挫伤损伤。再次进行灌注成像,对扫描进行定量,并比较积分强度。
损伤后的成像显示,在损伤部位的近端和远端区域,灌注减少了 18%-27%,在挫伤中心区域观察到 68%的减少。这些灌注损失至少持续了 48 小时。在损伤后 24 小时,一些大鼠通过腹腔注射 2 毫克/千克的β2-肾上腺素能受体激动剂克仑特罗,当在挫伤损伤后 2 天内给予时,它已被证明可以促进运动功能的部分恢复,并保留脊髓组织。克仑特罗注射引起灌注逐渐增加,可在注射后 30 分钟检测到,并随时间持续增加,导致治疗后 24 小时中心区域的总灌注增加 127%。
这些结果表明,挫伤后慢性灌注损失的发生导致了延迟性损伤和组织损失。相比之下,β2-肾上腺素能受体激动剂治疗可能通过恢复灌注来发挥神经保护作用,从而防止缺血性神经退行性变。激光多普勒成像测量灌注损失及其治疗后恢复的能力表明,它可能在脊髓损伤的评估和治疗中具有临床应用价值。