Jiang Xiaojing, Shi Enyi, Li Liwen, Nakajima Yoshiki, Sato Shigehito
Department of Anesthesiology, Hamamatsu University School of Medicine, Hamamtsu, Japan.
Life Sci. 2008 Mar 12;82(11-12):608-14. doi: 10.1016/j.lfs.2007.12.026. Epub 2008 Jan 18.
Postconditioning can induce cardioprotection against ischemia. However, the data on postconditioning of the spinal cord is very limited. We investigated here whether co-application of ischemic preconditioning (IPC) and postconditioning can provide additive neuroprotection against prolonged spinal cord ischemia. Spinal cord ischemia was produced in rabbits by infrarenal aortic occlusion with a balloon catheter for 30 min. The four treatment groups were control (n=10): no intervention; IPC (n=10): a 5-minute aortic occlusion was performed 20 min before the prolonged ischemia; Postcon (n=10): postconditioning comprised of four cycles of 1-minute occlusion/1-minute reperfusion was applied one minute after the start of reperfusion. IPC+postcon (n=11): both IPC and postconditioning were applied. Functional evaluation with Tarlov score was performed during a 14-day observation period. Neurologic impairment was noticeably attenuated in the IPC+postcon group (compared with the control group, P<0.01, at day 1, day 2, day 7 and day 14, respectively), but not in either the IPC or Postcon group. Plasma malondialdehyde levels after reperfusion were significantly decreased to a similar extent in the IPC, Postcon and IPC+Postcon groups (compared with the control group (P<0.01). In the IPC+Postcon group, many more large motor neurons were preserved than in the control group (P<0.05) and white matter injury was also markedly attenuated as evidenced by reduction of the vacuolation area of the white matter (P<0.01) and decreased amyloid precursor protein immunoreactivity (P<0.01). From this, we conclude that the combination of IPC and postconditioning induces additive neuroprotective effects for spinal cord against ischemia and reperfusion injuries.
缺血后处理可诱导心脏产生抗缺血保护作用。然而，关于脊髓缺血后处理的数据非常有限。我们在此研究了缺血预处理（IPC）与缺血后处理联合应用是否能对延长的脊髓缺血提供额外的神经保护作用。通过用球囊导管阻断肾下主动脉30分钟在兔身上制造脊髓缺血模型。四个治疗组分别为：对照组（n = 10）：不进行干预；IPC组（n = 10）：在长时间缺血前20分钟进行5分钟的主动脉阻断；后处理组（Postcon，n = 10）：在再灌注开始1分钟后进行由四个1分钟阻断/1分钟再灌注周期组成的后处理；IPC + 后处理组（n = 11）：同时应用IPC和后处理。在14天的观察期内用Tarlov评分进行功能评估。IPC + 后处理组的神经功能损害明显减轻（与对照组相比，分别在第1天、第2天、第7天和第14天，P < 0.01），但IPC组或后处理组均未出现这种情况。再灌注后，IPC组、后处理组和IPC + 后处理组的血浆丙二醛水平均显著下降至相似程度（与对照组相比，P < 0.01）。在IPC + 后处理组中，保留的大型运动神经元比对照组更多（P < 0.05），并且白质损伤也明显减轻，这表现为白质空泡化面积减小（P < 0.01）和淀粉样前体蛋白免疫反应性降低（P < 0.01）。由此，我们得出结论，IPC与后处理联合应用可对脊髓缺血再灌注损伤产生额外的神经保护作用。
