Effects of moderate hypothermia on extracellular lactic acid and amino acids after severe compression injury of rat spinal cord
Effects of moderate hypothermia on extracellular lactic acid and amino acids after severe compression injury of rat spinal cord
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DOI：
10.1089/neu.1997.14.63
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发表时间：
1997-01-01
影响因子：
4.2
通讯作者：
Olsson, Y
中科院分区：
文献类型：
--
作者：
Farooque, M;Hillered, L;Olsson, Y
我们在大鼠身上评估了亚低温(30-31摄氏度)对严重脊髓压迫后细胞外氨基酸水平的影响，特别是对兴奋性氨基酸(EaAS)谷氨酸和天冬氨酸、乳酸和丙酮酸的影响。Th-7和Th-8椎板切除。在SERE加压前1.5h和加压5min后分别进行微透析1.5h和4h。每隔10分钟收集一次透析液样本，并用高效液相色谱法进行分析。在常温(37.5摄氏度)的动物中，谷氨酸的含量增加了几倍，在创伤后的前10分钟达到峰值。低体温动物在创伤后也表现出类似的升高，直到伤后20分钟才有统计学意义。与常温动物相比，低温动物伤后20~70min谷氨酸水平显著升高。天冬氨酸氨基转移酶在受伤后也有明显增加。两组的峰值浓度相似，而体温过低的动物恢复较慢。常温和低温动物的精氨酸、牛磺酸、丙氨酸、谷氨酰胺、组氨酸、甘氨酸、苏氨酸、酪氨酸和天冬氨酸无显著差异。低温对乳酸或乳酸/丙酮酸无明显影响。然而，在体温过低的动物中，乳酸的平均水平趋于较低，恢复较快。本研究的结果表明，在我们的模型中，亚低温不能减少EaS在细胞外的积聚，也不能显著改善能量代谢。相反，我们的发现提出了适度低温延长谷氨酸受体过度激活持续时间的可能性。由于低温有效地抑制了中枢神经系统和脊髓缺血模型中谷氨酸的释放，我们的结果提示，在缺血和创伤中，EaAs的细胞外蓄积机制不同。
We evaluated in rats, the effect of moderate hypothermia (30-31 degrees C) on extracellular levels of amino acids, with special emphasis on the excitatory amino acids (EAAs) glutamate and aspartate, lactate and pyruvate, after severe spinal cord compression. A laminectomy of Th-7 and Th-8 was made. A probe was inserted in a dorsal horn and microdialysis was performed for 1.5 h before and 4 h after applying se vere compression for 5 min. Dialysate samples were collected at intervals of 10 min and analyzed by high-performance liquid chromatography. In normothermic (37.5 degrees C) animals there was a several-fold rise of glutamate that peaked in the first 10 min fraction after trauma. Hypothermic animals showed a similar increase after trauma, which was statistically significant until 20 min after injury. The level of glutamate was significantly higher in hypothermic animals from 20 to 70 min after injury, compared with normothermic animals. Aspartate also showed a marked increase following injury. The peak concentration was similar for both groups, whereas recovery was delayed in hypothermic animals. There was no significant difference between the normothermic and hypothermic animals for arginine, taurine, alanine, glutamine, histadine, glycine, threonine, tyrosine, and asparagine. No significant effect of hypothermia on lactate or lactate/pyruvate was noted. However, the mean level of lactate tended to be lower and recovery was quicker in hypothermic animals. The results of the present study suggest that moderate hypothermia does not attenuate extracellular accumulation of EAAs or markedly improve energy metabolism in our model. Instead, our findings raise the possibility that moderate hypothermia prolongs the duration of glutamate receptor overactivation. Since hypothermia effectively attenuates glutamate release in CNS and spinal cord ischemia models our results suggest different mechanisms of extracellular accumulation of EAAs in ischemia and trauma.