Spinal cord ischemia and reperfusion metabolism: The effect of hypothermia |
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| Institution: | 1. Department of Orthopedics, Cedars-Sinai, Los Angeles, CA, USA;2. Orthopedic Stem Cell Research Laboratory, Cedars-Sinai Medical Center, 8700 Beverly Blvd., Davis Building 6006, Los Angeles, CA 90048, USA;3. Cedars-Sinai Orthopedic Biomechanics Laboratory, Los Angeles, CA, USA;4. Board of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA;5. Department of Surgery, Cedars-Sinai, Los Angeles, CA, USA;6. Department of Biomedical Sciences, Cedars-Sinai, Los Angeles, CA, USA;1. College of Animal Science and Veterinary Medicine, Jilin University, Changchun, China;2. The First Hospital of Jilin University, Changchun, China;1. School of Chemistry and Chemical Engineering, Jiangsu University, Zhenjiang, Jiangsu 212013, PR China;2. Department of Orthopaedics, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, Jiangsu 215006, PR China;3. Orthopaedic Institute, Medical College, Soochow University, Suzhou 215007, PR China;4. Institute for Advanced Materials, School of Materials Science and Engineering, Jiangsu University, Zhenjiang, Jiangsu 212013, PR China |
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| Abstract: | Purpose: The metabolic and neurologic functional effects of regional hypothermia induced by cold (4° C) heparinized saline perfusion on spinal cord ischemia were evaluated in 35 rabbits.Methods: Spinal cord ischemia was induced for 20 minutes by infrarenal aortic occlusion in anesthetized animals. Regional spinal cord hypothermia was obtained by perfusing the lumbar arteries supplying the spinal cord through an infrarenal aortic catheter. The lumbar spinal cord was "snap frozen" in situ with liquid nitrogen and harvested immediately at the conclusion of the ischemic period or after 24 hours of normothermic reperfusion and neurologic observation. Spinal cord metabolic studies included determination of the energy charge and the intracellular concentrations of adenosine triphosphate, glucose, lactate, glutamate, and aspartate.Results: Postoperative neurologic function was normal in all but one animal treated with hypothermia, while normothermic ischemia resulted in paralysis in all animals ( p = 0.002). Spinal cord temperature during 20 minutes of ischemia and hypothermic perfusion decreased from 37.5° ± 0.43° C to 22.8° ± 0.00° C ( p = 0.0001) compared to a fall in systemic temperature from 38.8 to 36.1 ( p = 0.0001). Hypothermia reduced the decline in energy charge, adenosine triphosphate concentration and glucose concentration during ischemia but had no effect on markedly elevated levels of lactate acid. High-energy phosphates were restored after reperfusion in both normothermic and hypothermic animals and were not predictive of postoperative paraplegia. Intracellular glutamate and aspartate concentrations were unchanged during normothermic ischemia but decreased after reperfusion in all paralyzed animals. Intracellular glutamate and aspartate concentrations increased during hypothermic perfusion and remained elevated after reperfusion in animals with a normal or mildly abnormal neurologic examination result.Conclusions: We conclude that spinal cord hypothermia induced by cold heparinized saline perfusion is a simple technique that prevents paraplegia after 20 minutes of ischemia and preserves intracellular concentrations of important metabolites. (J VASC SURG 1994;19:332-40.) |
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