Paraplegia caused by ischemia-reperfusion injury of the spinal cord remains a devastating and unpredictable complication of thoracoabdominal aortic aneurysm repair [1,2]. Cross-clamping of the aorta during the repair reduces the arterial pressure distal to the clamping site, which causes spinal cord ischemia with resultant paraplegia, renal dysfunction, and colonic ischemia [3]. In addition, aortic occlusion increases arterial pressure proximal to the clamp. This hypertension results in increased cardiac afterload and elevated cerebrospinal fluid (CSF) pressure. The latter may worsen spinal cord ischemia by decreasing the perfusion pressure. Many interventions have been proposed to prevent the consequences of aortic occlusion, including distal aortic perfusion [4], CSF drainage [5], hypothermia [6], production of heat shock proteins by preconditioning procedures [7,8], and pharmacological agents such as oxygen-free radical scavengers [9], iron chelators [10], N-methyl-D-asparate (NMDA) receptor antagonists [11,12], opiate antagonists [13], and vasodilators [14]. A number of studies have reported beneficial effects of these interventions, but most of them remain controversial. One of the reasons for the controversy is that the mechanism(s) of spinal cord ischemia-induced paraplegia is not fully understood. As mentioned above, aortic occlusion causes not only a pressure drop in the feeding artery of the spinal cord but also causes an increase in CSF pressure. In order to clarify the mechanism and reduce the incidence of paraplegia, a simple model of spinal ischemia that reduces blood flow to the spinal cord without increasing CSF pressure nor decreasing distal arterial pressure should be used to analyze the effect of treatment.