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J Thorac Cardiovasc Surg 2003;125:1030-1036
© 2003 The American Association for Thoracic Surgery
Cardiopulmonary Support and Physiology |
From the Departments of Cardiothoracic Surgerya and Pathology,b University Hospital of Ioannina, School of Medicine, Ioannina, Greece, and St Luke's/Roosevelt Hospital Center at Columbia University,c New York, NY.
Supported by a grant from St Jude Medical/Greece and Michaeledion Foundation of the University of Ioannina Heart Center.
Read at the Eighty-second Annual Meeting of The American Association for Thoracic Surgery, Washington, DC, May 5-8, 2002.
Received for publication May 12, 2002. Revisions requested July 17, 2002; revisions received July 22, 2002. Accepted for publication Aug 14, 2002. Address for reprints: Constantine E. Anagnostopoulos, MD, St Luke's/Roosevelt Hospital Center at Columbia University, 45 East 89th St, New York, NY 10128 (E-mail: cea8{at}columbia.edu).
Objective: Postoperative neurologic deficits after thoracic aortic reconstruction vary widely. Our previous study showed that delayed ischemic preconditioning could prevent spinal cord injury caused by occlusion of the descending thoracic aorta in pigs. We investigated early ischemic preconditioning in the same model.
Methods: Twenty-eight pigs were divided into 4 groups: group 1 (n = 6) underwent a sham operation, group 2 (n = 6) underwent aortic occlusion for 20 minutes, group 3 (n = 8) underwent aortic occlusion for 35 minutes, and group 4 (n = 8) underwent aortic occlusion for 20 minutes and underwent aortic occlusion 80 minutes later without hypotension for 35 minutes. Aortic occlusion was accomplished by using 2 balloon occlusion catheters placed fluoroscopically at T6 to T8 above the diaphragm and at the aortic bifurcation. Neurologic evaluation was performed by an independent observer according to the Tarlov scale (0-4). The lower thoracic and lumbar spinal cords were harvested at 120 hours and examined histologically with hematoxylin-and-eosin stain. Histologic results (number of neurons and grade of inflammation) were scored (0-4) and were similarly analyzed. Statistical analysis was by means of the Kruskal-Wallis test.
Results: Group 4 had a better neurologic outcome at 24, 48, and 120 hours in comparison with group 3 (P < .001). The histologic changes were proportional to the neurologic test scores, with the more severe and extensive gray matter damage in animals of group 3 (number of neurons, P < .001; grade of inflammation, P < .001).
Conclusion: Early ischemic preconditioning without hypotension protects against spinal cord injury after aortic occlusion, as confirmed by using the Tarlov score and histopathology.
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