Research for ischemic tolerance in the spinal cord induced by the electrical convulsion therapy.

本研究旨在探讨脊髓电刺激是否也能诱导对暂时性主动脉闭塞引起的缺血性脊髓损伤的缺血耐受。硬膜外银电极预刺激（5mA，10s）。通过将2F Fogarty导管插入胸降主动脉并随后膨胀并结合全身性低血压（40mmHg）诱导脊髓缺血（SCI）。实验动物分为四组：快速预处理组（Rapid Preconditioning）：在硬膜外电刺激假预处理30min后，将硬膜外电极植入大鼠主动脉阻断9min RC组（n=8）或硬膜外电刺激组（n = 8）RE组（n=8）在异氟醚麻醉下，植入硬膜外电极的延迟预处理大鼠在硬膜外电刺激假预处理后24h，阻断主动脉9min DC组（n=8）和DE组（n=8）。另外，在硬膜外电刺激或假刺激后24小时，大鼠暴露于6至111分钟的SCI。P50组代表SCI持续时间与50%的截瘫概率相关，我们的研究结果表明，在缺血前24小时而不是30分钟进行电刺激预处理，可以保护脊髓免受主动脉阻断造成的缺血性损伤，与对照组相比，这种刺激使P50延长约15.0%。由于DE组和DC组在主动脉阻断期间用激光流量计测量的脊髓血流量没有差异，因此DE组的神经保护作用不是由于脊髓侧支流量增加而引起的。

This study examines whether electrical stimuli on the spinal cord is also capable of inducing ischemic tolerance to ischemic spinal cord injury induced by transient aortic occlusion. The pretreatment of epidural electrical-stimulation(5mA,10s) was administered via the epidural silver electrodes. Spinal cord ischemia (SCI) was induced by the placement and subsequent inflation of a 2F Fogarty catheter which was inserted the descending thoracic aorta and combined with systemic hypotension(40mmHg). Animals were divided into four groups employed as follows ; Rapid Preconditioning-rats implanted with the epidural electrodes were exposed 9min of aortic occlusion 30min after the sham pretreatment of epidural electrical-stimulation (group RC:n=8) or the pretreatment of epidural electrical-stimulation (group RE:n=8) under isoflurane anesthesia, Delayed Preconditioning-rats implanted with the epidural electrodes were exposed 9min of aortic occlusion,24 hours after the sham pretreatment of epidural electrical-stimulation (group DC:n=8) or the pretreatment of epidural electrical-stimulation(group DE:n=8) under isoflurane anesthesia. In addition, rats were exposed with 6 up to l11min of SCI at 24 hours after epidural electrical-stimulation or sham stimulation. The group P50 represents the duration of SCI associated with 50% probability of resultant paraplegia.Our results showed that pretreatment of electrical stimulation at 24h, but not 30min before ischemia, protect the spinal cord against ischemic insults by aortic occlusion and that this stimulation prolong P50 by a approximately 15.0% compared with the control group. Since there is no difference in the spinal cord blood flow, measured by laser flow meter, during aortic occlusion between the group DE and DC, the neuroprotective effect in the group DE is not caused by the increase of collateral flow in spinal cord.