Brain ischemia leads to insufficient oxygen supply or hypoxia and thus to ischemic stroke or chronic hypoperfusion, which results in neuronal death and white matter damage is irreversible or partially recoverable under the interruption of blood flow more than a few minutes. The present study investigated the abnormal characteristics of white matter integrity after the chronic cerebral ischemia in a mouse model of bilateral carotid artery stenosis and the acute cerebral ischemia in a mouse model of middle cerebral artery occlusion via longitudinal diffusion tensor imaging, which revealed that the mean diffusivity of corpus callosum (cc) was decreased as early as the 1 st day after chronic cerebral ischemia, and then the damage gradually aggravated and lasted to the 28th day. Moreover, the brain regions, including cingulum (cg), dorsal hippocampal commissure (dhc), forceps major of the corpus callosum (fmj), alveus of the hippocampus (alv) and medial lemniscus (ml), were damaged in duration of 7∼28 days after chronic cerebral ischemia. Oppositely, white matter signals in the contralateral hemisphere appeared compensatory increase in the internal capsule (ic) at the 1 st day after acute cerebral ischemia, simultaneously the ipsilateral hemisphere signals were decreased in alv, cerebral peduncle (cp), external capsule (ec), ml, fimbria of the hippocampus (fi), ic, forceps minor of the corpus callosum (fmi) and dhc. While these regional white matter signals were decreased in the bilateral hemisphere at the 7th day after acute cerebral ischemia. In addition, the motor function was impaired after acute cerebral ischemia, and cognitive function were impaired after chronic and acute cerebral ischemia. Furthermore, voxel-wise analysis revealed the obvious differences of white matter integrity in these two models of ischemia. The chronic cerebral ischemia showed better white matter integrity in the ipsilateral hemisphere of acute cerebral ischemic model at the 1 st day after surgery, but worse in the contralateral hemisphere. Subsequently, these differences were reduced significantly and just only the ipsilateral cp and bilateral ml signals were higher in chronic cerebral ischemia. Taken together, the present study demonstrates that the chronic and acute cerebral ischemia cause progressive damages of white matter that are irreversible in a relatively long time, of which the contralateral white matter present transient compensation in acute cerebral ischemia but not in chronic cerebral ischemia. These might be helpful to better diagnosis of clinical different cerebral ischemia.

中文翻译：

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慢性脑缺血和急性脑缺血中弥散张量成像上白质完整性的纵向追踪。

脑缺血会导致氧气供应不足或缺氧，从而导致缺血性中风或慢性低灌注，这会导致神经元死亡，并且在超过几分钟的血流中断下，白质损伤是不可逆的或部分可恢复的。本研究通过纵向弥散张量成像研究了双侧颈动脉狭窄小鼠模型在慢性脑缺血后白质完整性的异常特征和中脑动脉阻塞模型在急性脑缺血中的白质完整性异常。慢性脑缺血后第1天，call体的扩散率降低，然后损伤逐渐加重并持续到第28天。而且，大脑区域，包括扣带（cg），慢性脑缺血后7到28天，海马背侧连合（dhc），corp体大钳（fmj），海马肺泡（alv）和内榄肌（ml）受损。相反，急性脑缺血后第1天，对侧半球中的白质信号在代囊内（ic）出现代偿性增加，同时同侧半球的alv，脑柄（cp），外囊（ec）均减少，ml，海马毛细血管（fi），ic，call体小镊子（fmi）和dhc。急性脑缺血后第7天，双侧半球这些区域性白质信号减少。此外，急性脑缺血后运动功能受损，慢性和急性脑缺血后，其认知功能受损。此外，体素分析揭示了这两种局部缺血模型中白质完整性的明显差异。慢性脑缺血在手术后第一天在急性脑缺血模型的同侧半球中显示出较好的白质完整性，但在对侧半球中显示出更佳的白质完整性。随后，这些差异显着降低，在慢性脑缺血中仅同侧cp和双侧ml信号升高。综上所述，本研究表明，慢性和急性脑缺血可导致白质进行性损害，这种损害在相当长的时间内是不可逆的，其中对侧白质在急性脑缺血中表现出短暂的补偿，而在慢性脑缺血中则没有。这些可能有助于更好地诊断临床上不同的脑缺血。