Real-time direct measurement of spinal cord blood flow at the site of compression - Relationship between blood flow recovery and motor deficiency in spinal cord injury
Real-time direct measurement of spinal cord blood flow at the site of compression - Relationship between blood flow recovery and motor deficiency in spinal cord injury
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DOI：
10.1097/brs.0b013e3181316310
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发表时间：
2007-08-15
期刊：
影响因子：
3
通讯作者：
Yamamoto, Haruyasu
中科院分区：
文献类型：
--
作者：
Hamamoto, Yuichiro;Ogata, Tadanori;Yamamoto, Haruyasu
研究设计.一项使用新开发的装置在压迫部位实时测量大鼠脊髓血流量的体内研究。目标.目的：评价胸段脊髓受压后血流的变化，并阐明脊髓受压后血流恢复与运动功能障碍之间的关系。背景数据总结。到目前为止，还没有在压迫部位进行脊髓血流量的实时测量。此外，还没有明确确定脊髓损伤后血流恢复是否与运动功能有关。方法.我们的血流测量系统是一个非接触式激光多普勒系统和脊髓压迫装置的组合。在第11椎骨处暴露大鼠胸脊髓，并在压迫之前、期间和之后连续测量压迫部位处的脊髓血流量。通过Basso，Beattie和Bresnahan评分量表和自愿站立的频率评价动物后肢的功能。在受压的脊髓组织中观察到血-脊髓屏障通透性、小胶质细胞增生和凋亡细胞死亡等组织学变化。结果脊髓血流量随着压迫力的增加而减少。在施加5 g重量后，血流量下降至<预压缩水平的40%。使用20 g砝码达到完全缺血。减压后，20分钟完全缺血组的血流量水平明显高于40分钟完全缺血组。完全缺血40 min组后肢运动功能明显低于假手术组（无压迫），而缺血20 min组与假手术组无明显差异。在20分钟缺血组中，与完全恢复血流的大鼠相比，脊髓血流恢复不完全的大鼠表现出明显的运动功能丧失。在40分钟完全缺血组中检测到血-脊髓屏障完整性的广泛破坏以及随后的小胶质细胞增殖和凋亡细胞死亡。结论缺血/压迫的持续时间和脊髓的血流恢复是脊髓损伤后运动功能恢复的重要因素。
Study Design. An in vivo study to measure rat spinal cord blood flow in real-time at the site of compression using a newly developed device. Objectives. To evaluate the change in thoracic spinal cord blood flow by compression force and to clarify the association between blood flow recovery and motor deficiency after a spinal cord compression injury. Summary of Background Data. Until now, no real-time measurement of spinal cord blood flow at the site of compression has been conducted. In addition, it has not been clearly determined whether blood flow recovery is related to motor function after a spinal cord injury. Methods. Our blood flow measurement system was a combination of a noncontact type laser Doppler system and a spinal cord compression device. The rat thoracic spinal cord was exposed at the 11th vertebra and spinal cord blood flow at the site of compression was continuously measured before, during, and after the compression. The functioning of the animal's hind-limbs was evaluated by the Basso, Beattie and Bresnahan scoring scale and the frequency of voluntary standing. Histologic changes such as permeability of blood-spinal cord barrier, microglia proliferation, and apoptotic cell death were examined in compressed spinal cord tissue. Results. The spinal blood flow decreased on each increase in the compression force. After applying a 5-g weight, the blood flow decreased to < 40% of the precompression level. Complete ischemia was reached using a 20-g weight. After decompression, the blood flow level in the 20-minute complete ischemia group was significantly higher than that in the 40-minute complete ischemia group. The hind-limb motor function in the 40-minute complete ischemia group was significantly less than that in the sham group ( without compression), while no significant difference was observed between the 20-minute ischemia group and the sham group. In the 20-minute ischemia group, the rats whose spinal cord blood flow recovery was incomplete showed significant motor function loss compared with rats that completely recovered blood flow. Extensive breakdown of blood-spinal cord barrier integrity and the following microglia proliferation and apoptotic cell death were detected in the 40-minute complete ischemia group. Conclusion. Duration of ischemia/compression and blood flow recovery of the spinal cord are important factors in the recovery of motor function after a spinal cord injury.