Controlled low-pressure perfusion at the beginning of reperfusion attenuates neurologic injury after spinal cord ischemia

Objective Paraplegia caused by spinal cord ischemia remains a serious complication after surgical repair of thoracoabdominal aortic aneurysms. This study tests the hypothesis that controlled low-pressure perfusion at the beginning of reperfusion can attenuate neurologic injury of the spinal cord after transient ischemia. Methods Spinal cord ischemia was accomplished in rabbits by occlusion of the infrarenal aorta with a balloon catheter for 25 minutes. In the normal reperfusion group, reperfusion was completely restored immediately after ischemia, whereas perfusion pressure was controlled between 45 and 55 mm Hg during the first 10 minutes followed by complete reperfusion in the low-pressure reperfusion group. Functional evaluation with the Tarlov score during a 14-day observation period, histopathologic assessment of the lumbar spinal cord, and measurements of malondialdehyde levels and amyloid precursor protein immunoreactivity were performed. Results Neurologic impairment was remarkably attenuated in the low-pressure reperfusion group (compared with the Tarlov scores of the normal reperfusion group, P < .05 at day 2; P < .01 at days 1, 7, and 14). Compared with the normal reperfusion group, malondialdehyde levels were significantly lower in the low-pressure reperfusion group ( P < .05), and the large motor neurons of the low-pressure reperfusion group were preserved to a much greater extent ( P < .05). White matter injury of the low-pressure reperfusion group was also markedly attenuated as evidenced by reduction of vacuolation area of the white matter ( P < .05) and decrease of the amyloid precursor protein immunoreactivity ( P < .05). Conclusion Reperfusion initiated with low-pressure perfusion exerts neuroprotective effects on the spinal cord against ischemia/reperfusion injury.