动物造模,非开胸式主动脉弓狭窄心衰 z-bio 2022-08-26 291

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

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

　　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). At 4 weeks after TAC, left ventricular anterior wall thickness, left ventricular corrected weight, heart rate, and cardiac output were significantly increased (P<0.01). End-stage volume was significantly increased (P<0.01), ejection fraction and short-axis rate were significantly decreased (P<0.01), 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 were significantly increased (P<0.01), and ejection fraction and short-axis rate were further decreased (P<0.01). 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-thoracic TAC is stable and feasible, and can simulate the pathophysiological process from left ventricular hypertrophy to heart failure caused by human pressure overload.