动物造模,慢性心力衰竭模型 z-bo 2021-11-17 349

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

　　 Method: 24 kinds of chronic heart failure, the method is to cut the second rib on the left side of the rat along the sternum to open the chest, and perform aortic arch stenosis (TAC) between the wrist trunk and the left common carotid artery. The establishment of the model and other large models performed sham operations on eight rats. The sham operation group included echocardiography, hemodynamics and N-terminal natriuretic precursor peptide (NT-terminal natriuretic precursor peptide, NT-terminal) after 4 weeks, 8 weeks and 12 weeks of TAC in the model group. I received a professional brain natriuretic peptide). Measure proBNP) and observe myocardial histopathology.

　　Result: In the model group, NT-proBNP increased significantly at 4 weeks after TAC, reached a peak at 8 weeks (P \u003cu003c0.05), and decreased at 12 weeks. 4 weeks after TAC, echocardiogram results showed the model group. Emission fraction (EF) and fractional shortening (FS) increased significantly, left ventricular end-systolic volume (LVESV) decreased significantly (P\u003c0.05), and EF increased significantly within 8 weeks. (P\u003c 0.05), EF decreased significantly at the 12th week, left ventricular end-diastolic volume (left ventricular end-diastolic volume, LVEDV) and LVESV significantly increased (P\u003c0.05); hemodynamic studies showed that the model The left ventricular contraction rate of the group was the largest (the maximum increase rate of left ventricular pressure after TAC). , Dp/dtmax) decreased, and the maximum left ventricular pressure closing rate (left ventricular maximum drop rate, -dp/dtmax) increased (P\u003c0.05); pathological observation showed that the model group showed cell hypertrophy and cell hypertrophy at 4 and 8 weeks after TAC dislocation. At 12 weeks, the border tissue between myocardium was proliferated and inflammatory cells infiltrated, myocardial cells were apoptosis, and collagen fibers were deposited 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 12 weeks, and it is irreversible.