01 Background

Heart failure (HF) refers to a series of complex clinical syndromes such as cardiac circulatory disorders caused by impaired contractile and/or diastolic functions of the heart, which cannot fully discharge venous return blood from the heart, leading to blood congestion in the venous system and insufficient blood perfusion in the arterial system. Its incidence and mortality rates are increasing year by year, seriously endangering human health.

Myocardial damage caused by any reason, such as myocardial infarction, cardiomyopathy, hemodynamic overload, inflammation, etc., can cause changes in myocardial structure and function, leading to poor ventricular pumping and/or filling function, and ultimately inducing heart failure.

The main clinical manifestations of heart failure are dyspnea, fatigue, pulmonary congestion and peripheral edema. The research on the pathogenesis and intervention treatment of heart failure is far from meeting clinical requirements, which requires the establishment of a mature and stable animal model of heart failure to understand the disease process and study new treatment methods.

02 Experimental materials and methods

 Experimental materials: 

◆ SD rats (male, 180-220g)

◆ Isoflurane

◆ Animal ventilator

◆ Universal small animal anesthesia machine

Modeling method: 1. Adaptive feeding for 7 days, using isoflurane and fat emulsion to make emulsified isoflurane, and intraperitoneally injecting anesthesia to the rats. 2. Cut the neck, bluntly separate the trachea, intubate through the mouth, connect the ventilator, and use the pre-adjusted parameters (rat respiratory rate 80, respiratory ratio 1:1, tidal volume 6.4) to bluntly separate the left chest muscles, expose the intercostal space, tear the muscles from the third and fourth intercostal spaces, expose the heart, gently tear open a little pericardium, and insert the needle between the left atrial appendage and the arterial cone with a 6-0 suture needle. The ST elevation on the electrocardiogram indicates successful ligation. Then suture the intercostal muscles and chest muscles, remove the ventilator after 5-10 minutes, and wait for the mouse to recover spontaneous breathing and place it in a cage. 3. Take the heart tissue 4-8 weeks after the modeling is completed.

Evaluation indicators: serum index ELISA test, Masson staining, HE staining.

03 Model verification

◆ Masson staining

Masson staining results: The myocardial tissue of rats in the normal group was basically red, with no obvious blue collagen fibrosis tissue. The myocardial fibrosis in the model group was more serious, with a large number of collagen fibers proliferating, and large areas of blue myocardial collagen were deposited around myocardial cells and blood vessels.

◆ HE staining

HE staining results: The myocardial fibers of rats in the normal group were arranged neatly and orderly, and the myocardial cells had normal morphology and clear outlines. The myocardial cells in the model group were hypertrophic, cytoplasmic swelling, unclear boundaries, disordered arrangement, significantly widened intercellular spaces, inflammatory cell infiltration, and capillary dilation and proliferation in the interstitium. The myocardial cells were severely damaged, showing small focal or sheet-like necrosis.

◆ Serum index ELISA detection

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