动物造模,非开胸式主动脉弓狭窄心衰模型 z-bio 2022-11-02 273

　　Objective To establish a stable and reliable model of heart failure in mice by non thoracotomy aortic arch stenosis, and to analyze the pathological process of heart failure in mice.

　　Methods The heart failure model of C57BL/6J mice was established by non thoracotomy TAC. The cardiac function and the degree of heart failure were evaluated by echocardiography, left ventricular mass index, and histopathology.

　　Results The left ventricular mass index gradually increased with time. Compared with the sham operation group, there were very significant differences at 4 weeks, 8 weeks and 12 weeks after operation (P<0.01). Echocardiography showed that the left ventricular anterior wall thickness, left ventricular corrected weight, heart rate and cardiac output significantly increased at 4 weeks after TAC, compared with the sham operation group (P<0.01) Left ventricular corrected weight and left ventricular end systolic volume (LVVols) increased significantly (P<0.01), and ejection fraction and short axis rate decreased significantly (P<0.01). At 12 weeks after TAC, left ventricular end diastolic diameter, left ventricular end systolic diameter, left ventricular end diastolic volume and left ventricular end systolic volume increased significantly, and ejection fraction and short axis rate further decreased (P<0.01), At the same time, pathological examination showed that myocardial fibers were abnormal or diseased to varying degrees.

　　Conclusion The experimental results show that the establishment of a mouse heart failure model by non thoracotomy TAC is stable and feasible, and can simulate the pathophysiological process from left ventricular hypertrophy to heart failure caused by human pressure overload.