| Objective: To observe whether limb ischemic preconditioning(IP) can exert protective effect on reperfusion injury of spinal cord following acute and chronic ischemia in experimental animal model, meanwhile, to assess the efficacy of limb IP by determination of imaging, spinal cord blood flow(SCBF), biochemistry, electrophysiology and histopathology , and to explore the protective mechanism primarily.Methods: 1. The first part : (DAcute ischemia-reperfusion model of lumbar cord was established by occluding the descending aorta below the renal artery with an aneurysm clip in rabbits. Rabbits were divided into three groups: sham-operated control group(S), ischemia-reperfusion group(IR), limb ischemic preconditioning group(LIP). The IR group and LIP group had infrarenal aorta temporarily occluded for 40 min, while the S group had laparotomy without aortic occlusion. The method of LIP: four cycles of 5 min occlusion on one hindlimb using tourniquet and 10 min reperfusion. (2)Compared investigation of the differences ofhindlimb function, cortical somatosensory evoked potential (CSEP) and histopathology in the three groups. 2.The second part: (1)Experimental model was established by anterior approach implanting one titanium screw through C5 to compress the cervical spinal cord gradually, under the monitoring of CSEP. Rabbits with compressive myelopathy were randomly divided into two groups: control group and experiment group. Before decompression, the rabbits in experiment group were performed the same ischemic preconditioning as the first part. (2) Compared investigation of the differences of hindlimb function, spinal cord blood flow(SCBF), cortical somatosensory evoked potential (CSEP) , magnetic resonance imaging(MRI), Malondialdehyde(MDA) and histopathology in the two groups at the different time points were studied.Results:1.The first part: (DThe hindlimb function was normal in S group. Hindlimb function scores in the LIP group were significantly higher than that of the IR group (P<0.05) . (2) One week after reperfusion, histopathology showed that, neurons edema, neurons partly loss and white matter demyelination. Histopathological changes were little in the LIP group. No change was observed in the S group. (3)After artery clamped, CSEP disappeared completely in IR group at the time 13.6±2.2 min, while the LIP group was disappeared at the time 27.2± 1.7 min. CSEP reoccured was in 7.1±5.0 min after reperfusion in IR group, while the LIP group was in 2.1± 1.8 min. The results suggested that CSEP was very sensitive to ischemia. 2. The second part: (1)After decompression, hindlimb function scores in the experiment group were significantly higher than that of the control group. Parts of the rabbits incontrol group were suffered from delayed motor dysfunction. (2)MRI Tl weight can clearly displayed the morphological changes of the spinal cord caused by decompression, and indirectly reflected the pathological changes. However, MRI had hysteresis corresponding to the pathological changes. (3) Smooth transition of SCBF was observed in experiment group. SCBF sustained over the baseline. While SCBF significantly decreased 2 hours after reperfusion in control group, i.e., delated postischemic spinal cord hypoperfusion. (4) MDA content of spinal cord in experiment group was significantly lower than that of spinal cord in control group, especially during the first 24 hours of reperfusion. (5) hi control group, histopathological observation showed that, neurons presented ischemic alterations; glial cell proliferation; neurs phagocytosis. Edema and demyelination were found in white matter. While the experiment group showed little change. (6) Heat shock protein 70(HSP70) staining showed that, HSP70 was positive in experiment group 24 hours after reperfusion, and up to 7 days. While the control group showed negative all the time. (7) After decompression, although amplitude of wave of CSEP had difference, with time flowed, amplitude of wave presented no difference. The result indicate...
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