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

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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.