Dijkhuizen R M, de Graaf R A, Tulleken K A, Nicolay K
Department of Neurosurgery, University Hospital Utrecht, The Netherlands.
J Cereb Blood Flow Metab. 1999 Mar;19(3):341-9. doi: 10.1097/00004647-199903000-00012.
The reduction of the apparent diffusion coefficient (ADC) of brain tissue water in acute cerebral ischemia, as measured by diffusion-weighted magnetic resonance imaging, is generally associated with the development of cytotoxic edema. However, the underlying mechanism is still unknown. Our aim was to elucidate diffusion changes in the intracellular environment in cytotoxic edematous tissue. The ADC of intracellular metabolites was measured by use of diffusion-weighted 1H-magnetic resonance spectroscopy after (1) unilateral N-methyl-D-aspartate (NMDA) injection and (2) cardiac arrest-induced global ischemia in neonatal rat brain. The distinct water ADC drop early after global ischemia was accompanied by a significant reduction of the ADC of all measured metabolites (P < 0.01, n = 8). In the first hours after excitotoxic injury, the ADC of water and the metabolites taurine and N-acetylaspartate dropped significantly (P < 0.05, n = 8). At 24 and 72 hours after NMDA injection brain metabolite levels were diminished and metabolite ADC approached contralateral values. Administration of the NMDA-antagonist MK-801 1.5 hours after NMDA injection completely normalized the water ADC but not the metabolite ADC after 1 to 2 hours (n = 8). No damage was detected 72 hours later and, water and metabolite ADC had normal values (n = 8). The contribution of brain temperature changes (calculated from the chemical shift between the water and N-acetylaspartate signals) and tissue deoxygenation to ischemia-induced intracellular ADC changes was minor. These data lend support to previous suggestions that the ischemia-induced brain water ADC drop may partly be caused by reduced diffusional displacement of intracellular water, possibly involving early alterations in intracellular tortuosity, cytoplasmic streaming, or intracellular molecular interactions.
通过扩散加权磁共振成像测量，急性脑缺血时脑组织水的表观扩散系数（ADC）降低，这通常与细胞毒性水肿的发展有关。然而，其潜在机制仍不清楚。我们的目的是阐明细胞毒性水肿组织细胞内环境中的扩散变化。在新生大鼠脑内进行（1）单侧N-甲基-D-天冬氨酸（NMDA）注射和（2）心脏骤停诱导的全脑缺血后，使用扩散加权1H磁共振波谱测量细胞内代谢物的ADC。全脑缺血后早期明显的水ADC下降伴随着所有测量代谢物的ADC显著降低（P < 0.01，n = 8）。在兴奋性毒性损伤后的最初几个小时内，水、牛磺酸和N-乙酰天门冬氨酸的ADC显著下降（P < 0.05，n = 8）。NMDA注射后24和72小时，脑代谢物水平降低，代谢物ADC接近对侧值。NMDA注射后1.5小时给予NMDA拮抗剂MK-801，1至2小时后水ADC完全恢复正常，但代谢物ADC未恢复正常（n = 8）。72小时后未检测到损伤，水和代谢物ADC具有正常数值（n = 8）。脑温度变化（根据水和N-乙酰天门冬氨酸信号之间的化学位移计算）和组织脱氧对缺血诱导的细胞内ADC变化的影响较小。这些数据支持了先前的观点，即缺血诱导的脑水ADC下降可能部分是由于细胞内水扩散位移减少所致，可能涉及细胞内曲折度、细胞质流动或细胞内分子相互作用的早期改变。
