Allen B T, Davis C G, Osborne D, Karl I
Department of Surgery, Vascular Surgery Section, and the Department of Medicine, Washington University School of Medicine, St. Louis, MO.
J Vasc Surg. 1994 Feb;19(2):332-9; discussion 339-40. doi: 10.1016/s0741-5214(94)70108-3.
The metabolic and neurologic functional effects of regional hypothermia induced by cold (4 degrees C) heparinized saline perfusion on spinal cord ischemia were evaluated in 35 rabbits.
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.
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 degrees +/- 0.43 degrees C to 22.8 degrees +/- 0.00 degrees 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.
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.
在35只兔中评估通过冷(4℃)肝素化盐水灌注诱导的局部低温对脊髓缺血的代谢和神经功能影响。
在麻醉动物中通过肾下主动脉阻断诱导脊髓缺血20分钟。通过经肾下主动脉导管灌注供应脊髓的腰动脉来实现局部脊髓低温。在缺血期结束时或常温再灌注及神经观察24小时后,立即用液氮将腰段脊髓原位“速冻”并取材。脊髓代谢研究包括测定能荷以及三磷酸腺苷、葡萄糖、乳酸、谷氨酸和天冬氨酸的细胞内浓度。
除一只接受低温治疗的动物外,所有动物术后神经功能均正常,而常温缺血导致所有动物瘫痪(p = 0.002)。与全身温度从38.8℃降至36.1℃(p = 0.0001)相比,缺血和低温灌注20分钟期间脊髓温度从37.5℃±0.43℃降至22.8℃±0.00℃(p = 0.0001)。低温减少了缺血期间能荷、三磷酸腺苷浓度和葡萄糖浓度的下降,但对显著升高的乳酸水平无影响。常温组和低温组动物再灌注后高能磷酸盐均得以恢复,且与术后截瘫无关。常温缺血期间细胞内谷氨酸和天冬氨酸浓度未变,但所有瘫痪动物再灌注后均降低。在神经检查结果正常或轻度异常的动物中,低温灌注期间细胞内谷氨酸和天冬氨酸浓度升高,再灌注后仍保持升高。
我们得出结论,冷肝素化盐水灌注诱导的脊髓低温是一种简单的技术,可预防20分钟缺血后的截瘫,并保留重要代谢物的细胞内浓度。