动物造模,慢性心力衰竭模型 zi-bio 2024-03-04 528

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

　　Method: Twenty four chronic heart failure models were established by cutting the second rib on the left side along the sternum of rats for thoracotomy, and performing transaortic constriction (TAC) between the brachiocephalic trunk and the left common carotid artery. An additional eight rats were selected for sham surgery. The sham surgery group underwent echocardiography, hemodynamic testing, and N-terminal pro-brain natriuretic peptide (NT proBNP) measurement at 12 weeks post surgery, while the model group underwent myocardial tissue pathological observation at 4, 8, and 12 weeks post TAC.

　　Result: In the model group, NT proBNP significantly increased at 4 weeks after TAC surgery, reached its peak at 8 weeks (P<0.05), and showed a decreasing trend at 12 weeks; The results of echocardiography showed that the ejection fraction (EF), short axis rate (FS), left ventricular end systolic volume (LVESV), and left ventricular end diastolic volume (LVESV) of the model group significantly increased at 4 weeks after TAC surgery (P<0.05), significantly increased at 8 weeks (P<0.05), significantly decreased at 12 weeks, and significantly increased at left ventricular end diastolic volume (LVEDV) and LVESV (P<0.05); Hemodynamic testing showed that the model group had a decrease in left ventricular pressure maximum rate of rise (dp/dtmax) and an increase in left ventricular pressure maximum rate of fall (- dp/dtmax) after TAC surgery (P<0.05); Pathological observations showed that in the model group, myocardial cells were enlarged and disordered at 4 weeks after TAC surgery, connective tissue proliferation and inflammatory cell infiltration between myocardium at 8 weeks, and myocardial cell apoptosis and collagen fiber deposition at 12 weeks.

　　Conclusion: The rat heart failure model induced by aortic arch stenosis showed compensatory hypertrophy of the myocardium at 4 weeks after TAC surgery, initial decompensated response at 8 weeks, and myocardial fibrosis at 12 weeks, leading to irreversible heart failure.