动物造模,慢性心力衰竭 z-bio 2021-05-07 256

　　Objective: To observe the pathological changes of heart failure caused by aortic arch stenosis.

　　Method: The left second rib of the rat was incised along the sternum, the thoracic cavity was opened, and the aortic arch stenosis (TAC) was performed between the brachiocephalic artery and the left common carotid artery to establish 24 chronic heart failure models. Eight rats underwent sham surgery. The sham operation group received echocardiography, hemodynamics, and N-terminal brain natriuretic peptide (NT-terminal brain natriuretic peptide, NT-terminal brain natriuretic peptide) 4 and 8 weeks after TAC, and received 12 weeks later. Measure the model group (proBNP) and observe the myocardial histopathology.

　　Result: In the model group, NT-proBNP increased significantly at 4 weeks after TAC, reaching a peak at 8 weeks (P\u003c0.05), and showing a downward trend at 12 weeks. The echocardiographic results showed that it was in model group 4. After several weeks of TAC ejection fraction (EF), ejection fraction (FS) increased significantly, left ventricular end-systolic volume (LVESV) decreased significantly (P\u003c0.05), and EF increased significantly within 8 weeks (P\u003c0) .05). At 12 weeks of EF, it decreased significantly, and the left ventricular end diastolic volume (LVEDV) increased significantly (P\u003c0.05). The maximum left ventricular contraction in the model group was obtained by hemodynamic examination Rate (maximum left ventricular contraction rate) shows the ventricular pressure after TAC). , Dp/dtmax) decreased, and left ventricular maximum diastolic rate (left ventricular maximum diastolic pressure, -dp/dtmax) increased (P\u003c0.05); it showed that myocardial cells increased in 8 weeks and arranged randomly. Myocardial connective tissue hyperplasia and inflammatory cell infiltration, myocardial cell apoptosis and collagen fiber deposition at 12 weeks.

　　Conclusion: In a rat heart failure model caused by aortic arch stenosis, the myocardium develops compensatory hypertrophy 4 weeks after TAC, the initial myocardial response is decompensated for 8 weeks, and myocardial fibrosis is irreversible for 12 weeks, forming cardiac strength.