大鼠脑损伤局部谷氨酸的异常释放对乳酸含量变化的影响

目的探讨谷氨酸(Glu)在大鼠脑损伤局部的异常释放以及其对乳酸(Lac)含量变化的影响。方法采用大鼠局部脑损伤动物模型,分为对照组、损伤组、干预组。伤前15min干预组注射Riluzole(一种Glu突触前释放抑制剂),损伤组注射等容量的生理盐水,对照组仅开骨窗不损伤脑。应用微透析技术检测各组伤后不同时间透析液中Glu含量(Glu]d)及Lac含量(Lac]d)变化。结果Glu]d及Lac]d在伤后15min、30min和45min干预组明显低于损伤组(P<0.05),而明显高于对照组(P<0.05);在伤后60min,损伤组仍明显高于对照组(P<0.05)。伤后不同时间Glu]d和Lac]d变化呈显著正相关(P<0.01)。结论脑损伤后受损脑组织细胞液中Glu水平的升高是Glu神经元末梢大量释放Glu所致,并继而引起了Lac的含量升高。

Effect of Regional Abnomal Glutamate Release on Lactate Content in Rats with Traumatic Brain Injury: a Microdialysis Study

Objective To explore the regional abnormal glutamate(Glu) release and its effect on lactate (Lac) content of extracel-lular fluid (ECF) of brain tissues in rat with traumatic brain injury (TBI). Methods Twenty-one rats with local cerebral injury caused by free dropping were divided into three groups, i.e. control group, injured group and intervention group, in which the animals were treated by injection of Riluzole (a inhibitor of presypnatic release of Glu) 15 minutes before the TBI. The content of Glu and Lac in the dialysate (Glud and Lacd) were assayed. The relationship between Glud and Lacd was analyzed. Results At 15, 30 and 45 minutes after TBI, Glud and Lacd in the intervention group were significantly lower than that in the injured group (P<0.05) and significantly higher than that in the control group (P<0.05). The change in Glud was positively related with that in Lacd at different time after TBI. Conclusion A large number of Glu release from the nerve endings after TBI cause the increase in Glu of the extracellular fluid of brain tissues, which causes the increase in Lac of the extracellular fluid of brain tissues.