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多模态 MRI 评估小鼠脑出血后灰质和白质损伤及血脑屏障破坏

Multimodality MRI assessment of grey and white matter injury and blood-brain barrier disruption after intracerebral haemorrhage in mice.

机构信息

Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and The Ministry of Education of China, Institute of Neuroscience, Department of Neurology, the Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

Department of Anesthesiology/Critical Care Medicine, The Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.

出版信息

Sci Rep. 2017 Jan 13;7:40358. doi: 10.1038/srep40358.

Abstract

In this study, we examined injury progression after intracerebral haemorrhage (ICH) induced by collagenase in mice using a preclinical 11.7 Tesla MRI system. On T2-weighted MRI, lesion and striatal volumes were increased on day 3 and then decreased from days 7 to 28. On day 3, with an increase in striatal water content, vasogenic oedema in the perihaematomal region presented as increased T2 and increased apparent diffusion coefficient (ADC) signal. With a synchronous change in T2 and ADC signals, microglial activation peaked on day 3 in the same region and decreased over time. Iron deposition appeared on day 3 around the haematoma border but did not change synchronously with ADC signals. Vascular permeability measured by Evans blue extravasation on days 1, 3, and 7 correlated with the T1-gadolinium results, both of which peaked on day 3. On diffusion tensor imaging, white matter injury was prominent in the corpus callosum and internal capsule on day 3 and then partially recovered over time. Our results indicate that the evolution of grey/white matter injury and blood-brain barrier disruption after ICH can be assessed with multimodal MRI, and that perihaematomal vasogenic oedema might be attributable to microglial activation, iron deposition, and blood-brain barrier breakdown.

摘要

在这项研究中,我们使用临床前 11.7T MRI 系统检查了胶原酶诱导的小鼠脑出血 (ICH) 后的损伤进展。在 T2 加权 MRI 上,病变和纹状体体积在第 3 天增加,然后从第 7 天到第 28 天减少。第 3 天,随着纹状体水含量的增加,血肿周围出现血管源性水肿,表现为 T2 增加和表观扩散系数 (ADC) 信号增加。T2 和 ADC 信号同步变化,同一区域的小胶质细胞激活在第 3 天达到峰值,并随时间减少。铁沉积在血肿边界周围的第 3 天出现,但与 ADC 信号不同步变化。第 1、3 和 7 天 Evans 蓝外渗测量的血管通透性与 T1-钆结果相关,两者均在第 3 天达到峰值。在弥散张量成像上,第 3 天胼胝体和内囊的白质损伤明显,随后随时间部分恢复。我们的结果表明,ICH 后灰质/白质损伤和血脑屏障破坏的演变可以通过多模态 MRI 进行评估,血肿周围的血管源性水肿可能归因于小胶质细胞激活、铁沉积和血脑屏障破坏。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eb8/5234017/aedc2a8cad22/srep40358-f1.jpg

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