TY - JOUR
T1 - Spinal cord ischemia and reperfusion metabolism
T2 - The effect of hypothermia
AU - From the Department of Surgery, Vascular Surgery Section, and the Department of Medicine, Wsahington University School of Medicine, St. Louis.
AU - Allen, Brent T.
AU - Davis, Christopher G.
AU - Osborne, Dale
AU - Karl, Irene
PY - 1994
Y1 - 1994
N2 - 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.)
AB - 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.)
UR - http://www.scopus.com/inward/record.url?scp=0028295048&partnerID=8YFLogxK
U2 - 10.1016/S0741-5214(94)70108-3
DO - 10.1016/S0741-5214(94)70108-3
M3 - Article
C2 - 7906741
AN - SCOPUS:0028295048
SN - 0741-5214
VL - 19
SP - 332
EP - 340
JO - Journal of Vascular Surgery
JF - Journal of Vascular Surgery
IS - 2
ER -