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一过性主动脉阻断所致的脊髓缺血损伤的缺血耐受。经硬膜外银电极行硬膜外电刺激(5 mA，10s)前处理。脊髓缺血(SCI)是通过置入2F Fogarty导管并充气后插入降主动脉并合并全身降压(40 Mm Hg)所致。将动物分为4组：植入硬膜外电极的快速预适应组在异氟醚麻醉下，分别于假手术前硬膜外电刺激(RC：N=8)或硬膜外电刺激前30min(RE：N=8)后暴露于主动脉阻断9min；延迟预适应-大鼠在异氟醚麻醉下暴露于主动脉阻断后9min(DC：n=8)或硬膜外电刺激前(DE：N=8)。另外，大鼠在硬膜外电刺激或假刺激后24小时暴露于脊髓损伤6~11min。P50组代表脊髓损伤持续时间与50%发生截瘫的可能性相关。我们的结果显示，在缺血前24小时而不是30分钟进行电刺激，可保护脊髓免受主动脉阻断造成的缺血损伤，与对照组相比，这种刺激使P50延长约15.0%。由于DE组和DC组在阻断主动脉时激光血流仪测得的脊髓血流量无明显差异，因此DE组的神经保护作用不是由于脊髓侧支循环增加所致。

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.