慢性心力衰竭模型,动物造模 z-bio 2021-09-10 795

　　Purpose: To observe the pathological changes of heart failure in rats caused by aortic arch stenosis.

　　Methods: Cut the second rib on the left side of the rat along the sternum to open the chest, and perform transverse aortic constriction (TAC) between the brachiocephalic trunk and the left common carotid artery to establish 24 chronic heart failure models. Eight rats underwent sham operation. The sham operation group received echocardiography, hemodynamic testing and N-terminal pro-brain natriuretic peptide (N-terminal pro-brain natriuretic peptide) at 12 weeks postoperatively in the model group. , NT-proBNP) was measured, and myocardial histopathology was observed.

　　Results: In the model group, NT-proBNP increased significantly at 4 weeks after TAC, reached its peak at 8 weeks (P<0.05), and showed a downward trend at 12 weeks; echocardiographic results showed that the model group ejected blood at 4 weeks after TAC Ejection fraction (EF), fraction shortening (FS) were significantly increased, left ventricular end systolic volume (LVESV) was significantly reduced (P<0.05), and EF was significantly increased at 8 weeks High (P<0.05), EF significantly decreased at 12 weeks, left ventricular end diastolic volume (LVEDV), and LVESV significantly increased (P<0.05); hemodynamic testing showed that the model group was undergoing TAC surgery The left ventricular pressure maximal rate of rise (left ventricular pressure maximal rate of rise, dp/dtmax) decreased, and the left ventricular pressure maximal rate of fall (﹣dp/dtmax) increased (P<0.05); pathology Observations showed that in the model group, myocardial cells were hypertrophy and disordered at 4 weeks after TAC, connective tissue proliferation and inflammatory cell infiltration between myocardium at 8 weeks, and myocardial cell apoptosis and collagen fiber deposition at 12 weeks.

　　Conclusion: In the rat heart failure model caused by aortic arch stenosis, the myocardium develops compensatory hypertrophy at 4 weeks after TAC, the initial response of myocardial decompensation at 8 weeks, and myocardial fibrosis at 12 weeks, resulting in irreversible heart failure.