Abstract：
Element dysregulation is a pathophysiologic hallmark of ischemic stroke. Prior characterization of post-stroke element dysregulation in the photothrombotic model demonstrated significant element changes for ions that are essential for the function of the neurovascular unit. To characterize the dynamic changes during the early hyperacute phase (<6 h), we employed a temporary large-vessel occlusion stroke model. The middle cerebral artery was temporarily occluded for 30 min in male C57BL/6 mice, and coronal brain sections were prepared for histology and X-ray fluorescence microscopy from 5 to 120 min post-reperfusion. Ion dysregulation was already apparent by 5 min post-reperfusion, evidenced by reduced total potassium in the lesion. Later time points showed further dysregulation of phosphorus, calcium, copper, and zinc. By 60 min post-reperfusion, the central portion of the lesion showed pronounced element dysregulation and could be differentiated from a surrounding region of moderate dysregulation. Despite reperfusion, the lesion continued to expand dynamically with increasing severity of element dysregulation throughout the time course. Given that the earliest time point investigated already demonstrated signs of ion disruption, we anticipate such changes may be detectable even earlier. The profound ion dysregulation at the tissue level after reperfusion may contribute to hindering treatments aimed at functional recovery of the neurovascular unit.
摘要：
元素失调是缺血性中风的病理生理标志。光血栓形成模型中中风后元素失调的先前表征表明，离子的显着元素变化对神经血管单元的功能至关重要。为了表征早期超急性期(<6小时)的动态变化，我们采用了临时大血管闭塞卒中模型.在雄性C57BL/6小鼠中，大脑中动脉暂时闭塞30分钟，再灌注后5至120分钟，准备冠状脑切片进行组织学和X射线荧光显微镜检查。再灌注后5分钟，离子失调已经很明显，病变中的总钾减少。后来的时间点显示磷的进一步失调，钙，铜，和锌。再灌注后60分钟，病变的中央部分显示出明显的元素失调，并且可以与中度失调的周围区域区分开。尽管再灌注,在整个时间过程中，随着元素失调的严重程度不断增加，病变继续动态扩展。鉴于研究的最早时间点已经显示出离子破坏的迹象，我们预计这种变化可能会更早地被检测到。再灌注后组织水平的严重离子失调可能会阻碍旨在恢复神经血管单元功能的治疗。
