The Structure-function remodeling in rabbit hearts of myocardial infarction.

The Structure-function remodeling in rabbit hearts of myocardial infarction.
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心肌梗死兔心脏的结构与功能重塑

DOI:
10.14814/phy2.13311
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发表时间:
2017-06
影响因子:
2.5
通讯作者:
Huo Y
Huo Y
中科院分区:
其他
文献类型:
--
作者:
Wu H;Li L;Niu P;Huang X;Liu J;Zhang F;Shen W;Tan W;Wu Y;Huo Y

文献摘要

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缺血性心力衰竭(ischemic heart failure,HF)的动物模型是研究HF发病机制的重要手段。本研究的目的是通过多支冠状动脉结扎建立家兔模型,以研究左心室(LV)和冠状动脉树的术后结构-功能重塑。在此,我们假设,在心肌梗死(MI)附近与心脏纤维化相关的冠状动脉血管变性和心室壁应力增加的相互作用加速了缺血性HF的发生和进展。超声心动图测量显示术后12周左心室短轴缩短率和射血分数从40%和73%下降至28%和58%,以及左心室腔持续扩大和轻微二尖瓣返流。显微CT和组织学测量结果显示,尽管术后6周时存在代偿性血管生长,但术后12周时MI附近同时发生与炎症相关的冠状动脉血管稀疏和心脏纤维化。这些发现验证了所提出的兔子模型,并证明了假设。MI后兔模型可作为试验各种药物治疗缺血性HF的参考。
Animal models are of importance to investigate basic mechanisms for ischemic heart failure (HF). The objective of the study was to create a rabbit model through multiple coronary artery ligations to investigate the postoperative structure‐function remodeling of the left ventricle (LV) and coronary arterial trees. Here, we hypothesize that the interplay of the degenerated coronary vasculature and increased ventricle wall stress relevant to cardiac fibrosis in vicinity of myocardial infarction (MI) precipitates the incidence and progression of ischemic HF. Echocardiographic measurements showed an approximately monotonic drop of fractional shortening and ejection fraction from 40% and 73% down to 28% and 58% as well as persistent enlargement of LV cavity and slight mitral regurgitation at postoperative 12 weeks. Micro‐CT and histological measurements showed that coronary vascular rarefaction and cardiac fibrosis relevant to inflammation occurred concurrently in vicinity of MI at postoperative 12 weeks albeit there was compensatory vascular growth at postoperative 6 weeks. These findings validate the proposed rabbit model and prove the hypothesis. The post‐MI rabbit model can serve as a reference to test various drugs for treatment of ischemic HF.