Stoffel Michael, Plesnila Nikolaus, Eriskat Jörg, Fürst Monika, Baethmann Alexander
Department of Neurosurgery, Rheinische Friedrich-Wilhelms-Universität, Bonn, Germany.
J Neurotrauma. 2002 Apr;19(4):467-77. doi: 10.1089/08977150252932415.
A cortical tissue necrosis from focal trauma expands between 30% and 300% from its initial size within 24 h, depending on the species studied. To shed light on the pathophysiological processes in the penumbra 1 zone after a focal cortical lesion, the release of excitatory amino acids into the traumatic penumbra zone 1 was measured throughout the entire period of necrosis expansion. A microdialysis probe was inserted at an oblique angle into the cortex of Sprague-Dawley rats 2 mm below the brain surface. One day later, a highly standardized cortical freezing lesion was induced at the brain cortex above the microdialysis probe. Dialysate was continuously collected prior to, during, and up to 24 h after trauma and analyzed for primary amino acids. In each animal, it was confirmed histologically that the tip of the microdialysis probe was localized in the gray matter in close proximity to the primary lesion. Following induction of the trauma, a statistically significant sharp increase of the dialysate level of aspartate, glutamate, glycine, and serine was observed. Thereafter, the dialysate levels of these amino acids returned to baseline levels without any further increase throughout the remaining observation period. This process ranged in time from a few minutes to a few hours. The level of alanine in the dialysate was essentially not altered throughout the experiment. Although the early post-traumatic increase of the excitatory neurotransmitters aspartate and glutamate may well contribute to the secondary lesion growth of a cortical necrosis after trauma, glutamate receptor targeted therapeutic intervention may be in view of these findings of limited use when initiated post trauma.
根据所研究的物种不同，局灶性创伤引起的皮质组织坏死在24小时内会从其初始大小扩大30%至300%。为了阐明局灶性皮质损伤后半暗带1区的病理生理过程，在坏死扩大的整个期间测量了兴奋性氨基酸向创伤半暗带1区的释放情况。将微透析探针以倾斜角度插入Sprague-Dawley大鼠脑表面以下2mm处的皮质中。一天后，在微透析探针上方的脑皮质处诱导出高度标准化的皮质冷冻损伤。在创伤前、创伤期间以及创伤后24小时持续收集透析液，并分析其中的主要氨基酸。在每只动物中，通过组织学确认微透析探针尖端位于紧邻原发性病变的灰质中。创伤诱导后，观察到透析液中天冬氨酸、谷氨酸、甘氨酸和丝氨酸水平在统计学上显著急剧升高。此后，在剩余的观察期内，这些氨基酸的透析液水平恢复到基线水平，没有进一步升高。这个过程持续时间从几分钟到几小时不等。整个实验过程中，透析液中丙氨酸水平基本未改变。尽管创伤后早期兴奋性神经递质天冬氨酸和谷氨酸的增加很可能促成创伤后皮质坏死的继发性病变生长，但鉴于这些发现，创伤后启动的针对谷氨酸受体的治疗干预可能作用有限。
