Metabolite concentrations and relaxation in perinatal cerebral hypoxic-ischemic injury
Metabolite concentrations and relaxation in perinatal cerebral hypoxic-ischemic injury
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DOI：
10.1007/bf02532414
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发表时间：
1996-09-01
影响因子：
4.4
通讯作者：
Cady, EB
中科院分区：
文献类型：
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作者：
Cady, EB
局部脑代谢物浓度，主要是含胆碱化合物（Cho）、总肌酸（Cr）、N-乙酰天冬氨酸（Naa）和乳酸（Lac），可通过体内质子磁共振波谱进行定量。为了估计代谢物浓度，通常需要测量横向弛豫时间（T-2）。代谢产物T（2）s依赖于细胞溶质粘度：当[腺苷三磷酸]福尔斯下降导致Na+/K+泵衰竭时，细胞溶质水增加，T（2）s延长。在人类婴儿的中央灰质中，Naa可能几乎完全是神经元的：Naa T-2可能指示神经元水肿和能量产生。在这份初步报告中，对怀疑围产期缺氧缺血性脑损伤的人类婴儿的中央灰质中的代谢物浓度和T（2）s进行了测量。在发生严重脑损伤或死亡的婴儿中，[Cho]和[Naa]较低（后者表明神经元丢失），[Lac]和所有代谢产物T（2）均增加：Naa T-2增加可能反映了一部分剩余神经元能量产生失败后的神经元水肿。
Regional cerebral metabolite concentrations, principally of choline-containing compounds (Cho), total creatine (Cr), N-acetylaspartate (Naa), and lactate (Lac), can be quantified by in vivo proton magnetic resonance spectroscopy. In order to estimate a metabolite concentration, it is often necessary to measure the transverse relaxation time (T-2). Metabolite T(2)s depend on cytosolic viscosity: as [adenosine triphosphate] falls leading to Na+/K+ pump failure, cytosolic water increases and T(2)s lengthen. In central grey-matter in human infants, Naa may be almost exclusively neuronal: Naa T-2 may index neuronal edema and energy generation. In this preliminary report, metabolite concentrations and T(2)s have been measured in central grey matter in human infants suspected of perinatal hypoxic-ischemic cerebral injury. In infants who developed serious cerebral injury or died, [Cho] and [Naa] were low (the latter suggesting neuronal loss), [Lac] and all metabolite T(2)s were increased: the Naa T-2 increase possibly reflected neuronal edema following failure of energy generation in a fraction of remaining neurons.