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低血压性二次脑损伤大鼠脑皮质第Ⅱ组代谢型谷氨酸受体改变及意义

Changes and effects of group Ⅱ metabotropic glutamate receptors in the cerebral cortex of rats after diffuse brain injuries coupled with hypopiesia secondary brain insults
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摘要 目的 :研究弥漫性脑损伤 (DBI)及其合并低血压性二次脑损伤 (SBI)后脑皮质第 组代谢型谷氨酸受体 (m Glu Rs)各亚型变化及意义。方法 :SD大鼠 14 0只 ,随机分为正常对照、假手术、单纯 DBI及 DBI合并SBI组。在 Marm arou DBI模型基础上 ,制成低血压性 SBI模型。伤后 1、3、6、12、2 4、4 8和 72 h进行脑皮质m Glu R2 ,3m RNA原位杂交 ,计数阳性神经元数。结果 :与正常对照组相比 ,假手术组及单纯低血压组m Glu R2 ,3m RNA表达无明显改变 (P均 >0 .0 5 ) ;单纯 DBI组 m Glu R2 ,3在损伤 12 h后开始减少 ,4 8h降至最低 (P均 <0 .0 5 ) ;DBI合并 SBI组 m Glu R2 ,3m RNA表达伤后 6 h即开始减少 ,2 4 h降至最低 (P均 <0 .0 5 )。结论 :在 DBI及其合并 SBI过程中 ,m Glu R2 ,3m RNA表达降低 ,m Glu R2 ,3参与了 DBI和 SBI的病理生理过程 ,可能与脑保护有关。 Objective: To study the changes and effects of groupⅡmetabotropic glutamate receptors(mGluR) after diffuse brain injuries(DBI) coupled with hypopiesia secondary brain insults(SBI). Methods: Male SD rats were randomized into four groups: normal control, sham-operated, DBI alone and DBI coupled with SBI group. The SBI model was made on the basis of Marmarou's model. The mRNAs of the mGluRs were detected at 1, 3, 6, 12, 24, 48 and 72 hours after injuries by in-situ hybridization, and the positive neurons were counted. Results: Statistical analysis showed no significance between normal control group and sham-operated group, DBI group in mGluR 2, 3 mRNA (all P>0.05). The number of mGluR 2, 3 positive neurons decreased at 12 hours after injury and the peak occurred at 48 hours after injury in the injured cerebral cortex in DBI alone group(both P<0.05). However, in DBI with SBI group, there was a significant decrease of the number of mGluR2, 3 positive neurons at 6 hours after injury and the peak happened at 24 hours after injury (both P<0.05). Conclusion: mGluR2, 3, factors with the function of protecting brain, might play an important role in the pathophysiology of DBI and SBI.
出处 《中国危重病急救医学》 CAS CSCD 2003年第10期609-611,共3页 Chinese Critical Care Medicine
基金 国家自然科学基金资助项目 ( 3 0 2 70 5 3 4)
关键词 脑损伤 二次脑损伤 代谢型谷氨酸受体 病理生理 brain injury secondary brain insult metabotropic glutamate receptor pathophysiology
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