Structural and functional pathological characteristics of pressure-overload induced heart failure mouse model
Received:April 22, 2020  
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DOI:10. 3969 / j.issn.1005-4847. 2020. 05. 001
KeyWord:transverse aortic constriction model; disease progression; echocardiography; pathological evaluation; systolic function; diastolic function; mouse Conflicts of Interest: The authors declare no conflict of interest.
谭伟江 1.华南农业大学兽医学院,广州 ; 2. 广东省实验动物监测所,广东省实验动物重点实验室,广州
李想 广东省实验动物监测所,广东省实验动物重点实验室,广州
郑双 广东省实验动物监测所,广东省实验动物重点实验室,广州
马俊峰 广东省实验动物监测所,广东省实验动物重点实验室,广州
任学聪 广东省实验动物监测所,广东省实验动物重点实验室,广州
贺天真 广东省实验动物监测所,广东省实验动物重点实验室,广州
陈虹华 广东省实验动物监测所,广东省实验动物重点实验室,广州
陈建新 华南农业大学兽医学院,广州
杨丰华 广东省实验动物监测所,广东省实验动物重点实验室,广州
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       Objective To establish a heart failure model in mice, and to use ultrasound imaging and pathology techniques to comprehensively evaluate the characteristics of cardiac function and structural changes during disease development. Methods The transverse aortic constriction ( TAC) surgical technique was used to establish a model of pressure-overload-induced heart failure in mice. Blood flow Doppler spectra were collected to evaluate the pressure at the aortic arch stenosis before surgery and at weeks 2, 4, and 8 after it. B-mode and M-mode ultrasound images were collected to evaluate cardiac structure and systolic function. The blood flow Doppler spectrum from the mitral valve orifice and tissue Doppler spectrum from the mitral annulus were combined to evaluate cardiac diastolic function, and cardiac tissues were collected for histopathological observation. Results The ultrasound result showed that the blood pressure of the aortic arch stenosis increased significantly at weeks 2, 4, and 8 after the operation. At 2 weeks after the operation, the thickness of the left ventricular wall typically showed compensatory increases, while the inner diameter was decreased, accompanied by impaired diastolic function and myocardial fibrosis. Four weeks after the operation was the transition period, which was mainly manifested as a transition of the left ventricle from hypertrophy to dilation, decreased systolic function, continuously impaired diastolic function, and further fibrosis in the myocardium. Eight weeks after surgery, the ventricle was characterized by cavity enlargement, significant reductions of systolic and diastolic function, and cardiomyocytes being partially lysed and significantly fibrotic. Conclusions By evaluating the structure and function of the left ventricle in the three stages of compensated hypertrophy, transitional stage, and decompensated dilatation of a TAC-induced heart failure model in mice, the use of the model should advance basic research and translational medicine.
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