Hertelendy Péter, Menyhárt Ákos, Makra Péter, Süle Zoltán, Kiss Tamás, Tóth Gergely, Ivánkovits-Kiss Orsolya, Bari Ferenc, Farkas Eszter
1 Department of Medical Physics and Informatics, Faculty of Medicine & Faculty of Science and Informatics, University of Szeged, Szeged, Hungary.
2 Department of Anatomy, Histology and Embryology, Faculty of Medicine, University of Szeged, Szeged, Hungary.
J Cereb Blood Flow Metab. 2017 May;37(5):1763-1775. doi: 10.1177/0271678X16643735. Epub 2016 Jan 1.
Spreading depolarizations of long cumulative duration have been implicated in lesion development and progression in patients with stroke and traumatic brain injury. Spreading depolarizations evolve less likely in the aged brain, but it remains to be determined at what age the susceptibility to spreading depolarizations starts to decline, especially in ischemia. Spreading depolarizations were triggered by epidural electric stimulation prior and after ischemia induction in the cortex of 7-30 weeks old anesthetized rats ( n = 38). Cerebral ischemia was achieved by occlusion of both common carotid arteries. Spreading depolarization occurrence was confirmed by the acquisition of DC potential and electrocorticogram. Cerebral blood flow variations were recorded by laser-Doppler flowmetry. Dendritic spine density in the cortex was determined in Golgi-COX stained sections. Spreading depolarization initiation required increasingly greater electric charge with older age, a potential outcome of consolidation of cortical connections, indicated by altered dendritic spine distribution. The threshold of spreading depolarization elicitation increased with ischemia in all age groups, which may be caused by tissue acidosis and increased K conductance, among other factors. In conclusion, the brain appears to be the most susceptible to spreading depolarizations at adolescent age; therefore, spreading depolarizations may occur in young patients of ischemic or traumatic brain injury at the highest probability.
长时间累积持续时间的扩散性去极化与中风和创伤性脑损伤患者的病变发展和进展有关。在老年大脑中，扩散性去极化发生的可能性较小，但在什么年龄对扩散性去极化的易感性开始下降仍有待确定，尤其是在缺血情况下。在7 - 30周龄麻醉大鼠（n = 38）的皮层中，在缺血诱导之前和之后通过硬膜外电刺激触发扩散性去极化。通过双侧颈总动脉闭塞实现脑缺血。通过采集直流电位和脑电图确认扩散性去极化的发生。用激光多普勒血流仪记录脑血流变化。在高尔基-柯克斯染色切片中测定皮层中的树突棘密度。随着年龄增长，扩散性去极化的起始需要越来越大的电荷量，这是皮层连接巩固的潜在结果，表现为树突棘分布改变。在所有年龄组中，扩散性去极化引发的阈值随缺血而增加，这可能是由组织酸中毒和钾电导增加等因素引起的。总之，大脑在青少年时期似乎对扩散性去极化最敏感；因此，缺血性或创伤性脑损伤的年轻患者发生扩散性去极化的可能性最高。
