Suppr超能文献

应用锰增强和钆增强 MRI 及光光谱学技术对猪心冷冻损伤诱导的梗死进行特征描述。

Characterization of cryoinjury-induced infarction with manganese-and gadolinium-enhanced MRI and optical spectroscopy in pig hearts.

机构信息

Department of Biochemistry and Medical Genetics, Faculty of Medicine, University of Manitoba, Winnipeg, MB, Canada.

出版信息

Magn Reson Imaging. 2010 Jun;28(5):753-66. doi: 10.1016/j.mri.2010.02.001. Epub 2010 Apr 15.

Abstract

PURPOSE

To investigate progression of cryoinjury in pigs using contrast-enhanced magnetic resonance imaging (MRI) as well as optical spectroscopy and imaging.

METHODS

Cryoinjury was produced in 16 pigs in vivo and investigated using Gd-and Mn-enhanced MRI, optical imaging/spectroscopy and histology in acute and chronic setting up to 4 weeks after the injury.

RESULTS

(1) Acute cryoinjury resulted in formation of a lesion with a severely reduced rate of sub-epicardial indocyanine green (intravascular optical flow tracer) passage. In vivo late Gd-enhanced MRI showed a approximately 10 mm deep hypointense area that was surrounded by a hyperintense rim while ex vivo Mn-enhanced MRI (MEMRI) detected a homogenous hypointense zone. Histological and spectroscopic examination revealed embolic erythrocytes blockages within the cryolesion with a thin necrotic rim neighboring the normal myocardium. (2) Chronic 4-week cryoinjury was characterized by uniform Gd-enhancement, whereas MEMRI revealed reduced Mn(2+)enhancement. Histological examination showed replacement of the cryoinjured myocardium by scar tissue.

CONCLUSIONS

Acute cryoinjury resulted in formation of a no-reflow core embolized by erythrocytes and surrounded by a rim of necrotic tissue. Upon injury progression, the no-reflow zone shrunk and was completely replaced with scar tissue by 4 weeks after injury.

摘要

目的

利用对比增强磁共振成像(MRI)以及光学光谱和成像来研究猪的冷冻损伤进展。

方法

在 16 头猪体内产生冷冻损伤,并在急性和慢性条件下使用 Gd 和 Mn 增强 MRI、光学成像/光谱和组织学进行研究,直至损伤后 4 周。

结果

(1)急性冷冻损伤导致形成一个病变区域,心外膜下的吲哚菁绿(血管内光学流动示踪剂)通过速度严重降低。体内晚期 Gd 增强 MRI 显示约 10 毫米深的低信号区域,周围环绕着高信号环,而离体 Mn 增强 MRI(MEMRI)则检测到均匀的低信号区域。组织学和光谱检查显示在冷冻损伤区域内有栓塞的红细胞阻塞,正常心肌相邻处有一个薄的坏死环。(2)慢性 4 周冷冻损伤的特征是均匀的 Gd 增强,而 MEMRI 显示 Mn(2+)增强减少。组织学检查显示冷冻损伤的心肌被瘢痕组织取代。

结论

急性冷冻损伤导致形成一个由红细胞栓塞的无再流核心,并被坏死组织的边缘包围。随着损伤的进展,无再流区域缩小,在损伤后 4 周内完全被瘢痕组织取代。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验