实验性脑损伤后延髓脊髓区兴奋性氨基酸的变化及意义

目的 :探讨实验性大鼠脑损伤继发延髓脊髓区损伤的可能机制 ,以及延髓组织中兴奋性氨基酸的变化及在创伤后高血压中的作用。方法 :应用流体冲击装置致大鼠脑损伤模型 ,用氨基酸自动分析仪检测延髓颈脊髓组织中天冬氨酸、谷氨酸的含量变化 ,采用氢清除法定量监测脊髓灰质血流量的相应改变。结果 :大鼠脑损伤后即刻平均动脉压显著升高 ,与伤前比较差异非常显著 (P<0 .0 1) ,此后血压基本保持平稳。脑损伤后 0 .5小时延髓脊髓区谷氨酸和天冬氨酸显著增加 ,与伤前比较差异均显著 (P均 <0 .0 1) ;脑损伤 1小时以后 ,该区组织中谷氨酸和天冬氨酸的含量与伤前无显著差异 (P均 >0 .0 5 )。伤后 0 .5小时高位颈脊髓灰质血流量显著降低 ,与伤前比较差异非常显著 (P<0 .0 1) ,之后血流量恢复到伤前水平。结论 :实验性脑损伤后延髓脊髓区组织中兴奋性氨基酸谷氨酸和天冬氨酸的增加 ,一方面刺激延髓血管运动中枢神经元兴奋 ,诱发脊髓中间外侧柱交感神经元兴奋引起高血压反应 ;另一方面促进了高位颈髓灰质血流量的减少 ,加重了延髓颈髓区继发性损害 ,不利于脑功能的恢复。

Changes of excitatory amino acids in medulla-spinal site following experimental brain injury in rats

Objective:To explore the potential mechanism of secondary medullaspinal injury,and to investigate excitatory amino acids in the medullaspinal site on hypertension following experimental brain injury in rats.Methods:Experimental rats injured by fluid percussion device was used as brain injury model,the content of aspartate and glutamate in medullaspinal tissues were determined with amino acid analyzer,blood flow in gray matter of the cervical cord was quatified by hydrogen clear method.Results:Mean artery blood pressure markedly elevated immediately after brain impact in rats in comparison with preinjury( P <0 01),hereafter the blood pressure maintained relatively stable.At 0 5 hour postinjury the content of glutamate and aspartate in medullaspinal site were significantly increased in contrast with preinjury (both P <0 01), decreased to preinjury level at 1 hour postinjury (both P >0 05).The gray blood flow in the high cervical segment was significantly decreased in contrast to preinjury( P <0 01),returned to the preinjury level afterwards. Conclusions: Following experimental brain injury,the increases in excitatory amino acids glutamate and aspartate in medullaspinal site may excite for neurons in the vasomotor center to activate sympathetic preganglionic neurons,which induces reactive hypertension,on the other hand contribute to the decrease in the gray blood flow in the high cervical segment.These may aggravate the secondary injury in the medullaspinal area which become an obstacle to brain function to recover.