首页> 外文OA文献 >Magnetic resonance analysis of the effects of acute ammonia intoxication on rat brain. Role of NMDA receptors
【2h】

Magnetic resonance analysis of the effects of acute ammonia intoxication on rat brain. Role of NMDA receptors

机译:急性氨中毒对大鼠脑的影响的磁共振分析。 NMDA受体的作用

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Acute ammonia intoxication leads to rapid death, which is prevented by blocking N-methyl-d-aspartate (NMDA) receptors. The subsequent mechanisms leading to death remain unclear. Brain edema seems an important step. The aim of this work was to study the effects of acute ammonia intoxication on different cerebral parameters in vivo using magnetic resonance and to assess which effects are mediated by NMDA receptors activation. To assess edema induction, we injected rats with ammonium acetate and measured apparent diffusion coefficient (ADC) in 16 brain areas. We also analyzed the effects on T1, T2, and T2* maps and whether these effects are prevented by blocking NMDA receptors. The effects of acute ammonia intoxication are different in different brain areas. T1 relaxation time is reduced in eight areas. T2 relaxation time is reduced only in ventral thalamus and globus pallidus. ADC values increased in hippocampus, caudate-putamen, substantia nigra and cerebellar cortex, reflecting vasogenic edema. ADC decreased in hypothalamus, reflecting cytotoxic edema. Myo-inositol increased in cerebellum and substantia nigra, reflecting vasogenic edema. N-acetyl-aspartate decreased in cerebellum, reflecting neuronal damage. Changes in N-acetyl-aspartate, T1 and T2 are prevented by blocking NMDA receptors with MK-801 while changes in ADC or myo-inositol (induction of edema) are not. © 2007 The Authors.
机译:急性氨中毒会导致快速死亡,这可以通过阻止N-甲基-d-天冬氨酸(NMDA)受体来预防。导致死亡的后续机制仍不清楚。脑水肿似乎是重要的一步。这项工作的目的是利用磁共振研究急性氨中毒对体内不同大脑参数的影响,并评估NMDA受体激活介导的影响。为了评估水肿诱导作用,我们向大鼠注射了乙酸铵,并在16个脑区测量了表观扩散系数(ADC)。我们还分析了对T1,T2和T2 *图的影响,以及是否通过阻断NMDA受体阻止了这些影响。急性氨中毒的作用在不同的大脑区域是不同的。 T1松弛时间减少了八个区域。 T2弛豫时间仅在腹侧丘脑和苍白球减少。海马,尾状-丘脑,黑质和小脑皮质的ADC值增加,反映了血管性水肿。下丘脑ADC降低,反映出细胞毒性水肿。小脑和黑质中的肌醇增加,反映了血管性水肿。小脑中的N-乙酰天门冬氨酸减少,反映了神经元损伤。 N-乙酰天门冬氨酸,T1和T2的变化可通过用MK-801阻断NMDA受体来防止,而ADC或肌醇的变化(水肿的诱导)则不会。 ©2007作者。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号