Ishikawa T, Marsala M
Department of Anesthesiology-Resuscitology, Yamaguchi University School of Medicine, Japan.
No To Shinkei. 1996 Mar;48(3):259-63.
Acute spinal cord trauma may initiate a cascade of hemodynamic and biochemical events characterized by direct mechanical destruction of neurons, hemorrhages and significant increases in active substances (glutamate, prostaglandins (PGs), ets.). However, there are no data which define the effect of acute spinal cord trauma on biochemical changes in the spinal cord. The aim of the present study was to examine time-dependent biochemical changes in the spinal cord by intrathecal microdialysis in the acute stage of spinal cord turama.
Male Sprague-Dawley rats (300-325g) were implanted with a dialysis catheter and PE-10 catheter in the intrathecal space of the lumbar spinal cord. Three days later the animals were anesthetized with halothane and 10-min dialysis samples were collected. Compression spinal cord injury was produced by inflating an extradural 2F-Fogarty balloon catheter (L4-L5) for 60 sec. After compression, samples were collected while the animals remained anesthetized for 30 min, and additional samples were collected until 4hr post-injury. At the end of the dialysis period neurological function was briefly evaluated. Microdialysate samples were analyzed for glutamate, aspartate, and taurine by HPLC-UV and for PGE2 by RIA.
Compression of the spinal cord caused significant increases in the levels of all amino acids. The greatest in creases were in glutamate and aspartate at 10 min, followed by a decrease over the rest of the 4-hr period. Similarly, PGE2 showed an immediate increase after compression, with normalization between 1-2 hr, but this was followed by a secondary increase at 2-4 hr. Neurologically, all animals displayed complete paralysis with loss of sensory function that remained unchanged for the 4-hr period.
The present study clearly demonstrated the time course of spinal amino acids and PGE2 release by using a chronically implanted dialysis catheter after spinal cord compression and also showed a correlation with neurological deterioration. These biochemical changes in the extracellular space may display various, multiphasic patterns reflecting progressively developing edema and corresponding ischemia.
急性脊髓损伤可能引发一系列血流动力学和生化事件，其特征为神经元的直接机械性破坏、出血以及活性物质（谷氨酸、前列腺素（PGs）等）显著增加。然而，尚无数据明确急性脊髓损伤对脊髓生化变化的影响。本研究的目的是通过鞘内微透析检查脊髓损伤急性期脊髓内随时间变化的生化改变。
将雄性Sprague-Dawley大鼠（300 - 325克）在腰段脊髓鞘内植入透析导管和PE - 10导管。三天后，用氟烷麻醉动物，并收集10分钟的透析样本。通过向硬膜外2F - Fogarty球囊导管（L4 - L5）充气60秒造成压迫性脊髓损伤。压迫后，在动物麻醉状态下持续30分钟收集样本，并在损伤后4小时内额外收集样本。透析期结束时简要评估神经功能。通过高效液相色谱 - 紫外法分析微透析液样本中的谷氨酸、天冬氨酸和牛磺酸，通过放射免疫分析法分析前列腺素E2。
脊髓压迫导致所有氨基酸水平显著升高。谷氨酸和天冬氨酸在10分钟时升高最为明显，随后在4小时剩余时间内下降。同样，前列腺素E2在压迫后立即升高，在1 - 2小时恢复正常，但随后在2 - 4小时再次升高。神经学上，所有动物均表现为完全瘫痪且感觉功能丧失，在4小时内保持不变。
本研究通过在脊髓压迫后使用长期植入的透析导管，清楚地展示了脊髓氨基酸和前列腺素E2释放的时间过程，并且还显示出与神经功能恶化的相关性。细胞外空间的这些生化变化可能呈现出各种多相模式，反映出逐渐发展的水肿和相应的局部缺血。
