谷氨酸受体拮抗剂在严重烧伤大鼠脑组织中的作用

目的 探讨烧伤后谷氨酸对脑组织的影响及谷氨酸受体拮抗剂的作用。方法 采用30％TBSAⅢ度烧伤大鼠模型，伤后2、6、12和24h测定了脑水含量、脑组织K^ 、Na^ 、Ca^2 、Mg^2 和-氧化氮(NO)代谢产物NO2^-／NO3^-浓度，在光镜和电镜下进行形态学和组织化学研究。结果 烧伤后脑水含量升高，脑组织Na^ 、Ca2^ 、NO2^-／NO3^-浓度高于对照组；脑内ATP酶减少；电镜观察毛细血管内皮细胞、神经细胞及胞浆部分线粒体肿胀，毛细血管壁出现胞饮泡。给予谷氨酸受体拮抗剂D-2-氨基-7-磷庚酸脂(D—AP7)，可使脑水含量、脑组织Na^ 、Ca^2 、NO2^-／NO3^-浓度降低，毛细血管壁胞饮泡减少，神经细胞肿胀减轻。结论 烧伤后脑微血管通透性增加、组织细胞有缺血性改变和水肿发生。烧伤后脑组织形态及代谢变化与谷氨酸过量释放有关。兴奋毒性作用通过其受体介导，谷氨酸受体拮抗剂D—AP7可减轻烧伤后脑损伤。

The effects of the receptor antagonist of glutamic acid on th e brain tissue of severely scalded rats.

OBJECTIVE: To explore the influence of glutamic acid on burned rat brain tissue and the effects of the receptor antagonist of glutamic acid. METHODS: Rats inflicted with 30% TBSA III degree scalding injury were taken as the model. The water content, K(+), Na(+), Ca(2+), Mg(2+), nitric oxide metabolites (NO(2)(-)/NO(3)(minus sign))concentrations of scalded rat brain were determined at 2, 6, 12 and 24 postburn hours (PBH). Morphological and histochemical studies of the brain tissue were carried out with LM and EM. RESULTS: The water content, Na(+), Ca(2+)and NO(2)(minus sign)/NO(3)(minus sign) concentrations of the brain tissue after scalding injury were higher than those in control group. But intracerebral ATP enzyme decreased postburn. It was found by EM examination that there existed swelling of capillary endothelium, nerve cells and some intracytoplasmic mitochondria. There appeared pinosome on capillary wall. After the administration of receptor antagonist of glutamic acid, D-2-amino-group-7-phosphoenanthate (D-AP7), the brain water content, Na(+), Ca(2+)and NO(2)(-)/NO(3)(-) concentrations in brain tissue, and the capillary wall pinosome decreased, and the swelling of nerve cells ameliorated. CONCLUSION: There might be postburn increased cerebral microvascular permeability, ischemic injury of cerebral tissue cells and the development of brain edema. The postburn alterations in the morphology and metabolism of brain tissue were correlated with the over secretion of glutamic acid. And the excitatory toxic effects of glutamic acid were mediated by its receptor. The receptor antagonist of glutamic acid D-AP7 might ameliorate postburn cerebral injury.