摘要
目的 研究二次脑损伤 (SBI)大鼠脑皮层代谢性谷氨酸受体 1α(m Glu R1α)的变化及意义 .方法 SD大鼠 90只 ,随机分为假手术对照、单纯脑损伤、脑损伤合并 SBI3组 .在 Marmarou大鼠加速性弥漫性脑损伤模型基础上 ,以抽血造成低血压为 SBI指标 .在伤后不同时间进行免疫组化和病理学研究 .结果 与假手术对照相比 ,单纯脑损伤组脑皮层m Glu R1α阳性神经元在伤后 1h表达明显增加 ,为 13.9±3.2 (P<0 .0 5 ) ,2 4h达到 15 .3± 3.7的峰值 (P<0 .0 1) ;脑损伤合并 SBI组 m Glu R1α阳性神经元表达在伤后 0 .5 h即明显增加 :13.5± 3.8(P<0 .0 5 ) ,伤后 6 h达高峰 :15 .6± 3.7(P<0 .0 1) .结论 在弥漫性脑损伤发生、发展过程中 ,m Glu R1α改变可能是导致脑损害加重的因素之一 ,合并 SBI组脑皮层m Glu R1α阳性神经元表达的增强和高峰的提前提示m Glu R1α参与缺血过程 .
AIM To study the changes of metabotropic glutamate receptor 1α in a rodent model of diffuse brain injurywith secondary insults. METHODS Based on Marmarou's rodent model of diffuse brain injury, hypotension was made by blood as secondary brain insults (SBI). Ninety male SD rats were randomized into three groups: sham, head injury alone and head injury with SBI. The mGluR1α immunohistochemistry and pathology of cerebral cortex were studied at different time after brain injury. RESULTS Compared with that of sham group, the number of mGluR1α positive neuron increased as 13.9±3.2 ( P <0.05)1 h after injury, and the most robust increase of 15.3±3.7 ( P <0.01) occurred at 24 h after injury in the injured cerebral cortex in head injury alone group. However, in head injury with SBI group there was a significant increase of the number of mGluR1α positive neuron at 0.5 h after injury 13.5±3.8 ( P <0.01) and the most robust increase occurred at 6 hours after injury 15.6±3.0 ( P <0.01). CONCLUSION In the development of diffuse brain injury the role of mGluR1α may be a key factor in the aggravation of brain damage. mGluR1α is also involved in brain hypoxia leading to brain damage as shown in head injury with SBI.
出处
《第四军医大学学报》
2000年第10期1273-1276,共4页
Journal of the Fourth Military Medical University
基金
全军"九五"医学科研规划基金!(98M10 1)
高等学校骨干教师资助计划项目
