动物造模,心力衰竭模型 z-bio 2021-07-29 472

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

　　Method: 24 The model of chronic heart failure was established by incising the second rib on the left side of the rat along the sternum, and performing aortic arch stenosis (TAC) between the brachiocephalic artery and the left common carotid artery. The other eight large mice underwent sham operations. The sham operation group underwent echocardiography and hemodynamic examinations, measured NT-terminal pro-brainatriuretic peptide (NT-proBNP), and observed myocardial histopathology.

　　Result: NT-proBNP increased significantly at 4 weeks after TAC in the model group, reached a peak at 8 weeks (Pu003c0.05), and decreased at 12 weeks. The echocardiographic results showed that the TAC ejection fraction after 4 weeks in the model group. (EF), the ejection fraction (FS) increased significantly, the left ventricular end-systolic volume (LVESV) decreased significantly (Pu003c0.05), the EF increased significantly (Pu003c0.05), and the EF decreased significantly at 12 weeks , Left ventricular end-diastolic volume (LVEDV) and LVESV were significantly increased (Pu003c0.05); the maximum ventricular contraction rate (the maximum rate of increase in left ventricular pressure after TAC) in the model group was decreased in the left ventricular hemodynamics, and the left ventricle The maximum expansion rate (maximum left ventilor pressureate offall, ﹣dp/dtmax) increased (P\u003c0.05). Model group. At 12 weeks, myocardial cell infiltration, myocardial cell apoptosis and collagen fiber deposition.

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