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大鼠模型中的急性心肌炎:钆延迟增强与组织病理学相关性。

Acute myocarditis in a rat model: late gadolinium enhancement with histopathological correlation.

机构信息

Department of Diagnostic and Interventional Radiology, Johann Wolfgang Goethe University Frankfurt, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.

出版信息

Eur Radiol. 2009 Nov;19(11):2672-8. doi: 10.1007/s00330-009-1454-y. Epub 2009 May 21.

Abstract

The aim of the current study was to use an established animal model of autoimmune myocarditis and to judge the ability of cardiovascular MRI (CMR) in quantitatively measuring the extent of myocardial involvement compared with histopathological measurement of severity and extent. Experimental autoimmune myocarditis (EAM) was induced in 10 male Lewis rats. On day 21, all animals were investigated by CMR to measure the extent of late gadolinium enhancement (LGE). Subsequently, histopathological evaluation of the entire heart was performed. All animals of the experimental group fulfilled histopathological criteria of myocarditis, revealing necrosis in seven of eight cases. At reduced heart rate, area of LGE correlated highly with histologically proven area of myocarditis (r = 0.80-0.87, p < 0.05). LGE was mainly located in the anterior (range 50-62.5%) and lateral (range 62.5-75%) left ventricular wall and septum (range 25-50%) with a midwall to subepicardial accentuation. The LGE pattern found by CMR can be regarded as suggestive of EAM. With cellular necrosis being the main mechanism for LGE we were able to show high correlations between CMR examination results and histopathologically proven areas of myocarditis. Thus we think the current animal model can provide the opportunity for further fundamental research into myocarditis.

摘要

本研究旨在利用已建立的自身免疫性心肌炎动物模型,判断心血管磁共振(CMR)定量测量心肌受累程度与组织病理学严重程度和范围测量相比的能力。在 10 只雄性 Lewis 大鼠中诱导实验性自身免疫性心肌炎(EAM)。第 21 天,所有动物均接受 CMR 检查,以测量晚期钆增强(LGE)的程度。随后,对整个心脏进行组织病理学评估。实验组的所有动物均符合心肌炎的组织病理学标准,其中 7 例存在坏死。在降低心率时,LGE 区域与组织学证实的心肌炎区域高度相关(r = 0.80-0.87,p < 0.05)。LGE 主要位于左心室前壁(范围为 50-62.5%)和侧壁(范围为 62.5-75%)和室间隔(范围为 25-50%),具有中膜到心外膜的增强。CMR 发现的 LGE 模式可被视为 EAM 的提示。由于细胞坏死是 LGE 的主要机制,我们能够显示 CMR 检查结果与组织病理学证实的心肌炎区域之间存在高度相关性。因此,我们认为目前的动物模型可以为心肌炎的进一步基础研究提供机会。

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