[Animal Modeling] - Animal Model of Heart Failure and Heart Qi Deficiency Syndrome Induced by Transplanted Myocardial Infarction

  (1) Reproduction method: Adult rats were anesthetized and subjected to tracheal intubation with a ventilator for artificial respiration. The open heart was cut open and the left coronary artery was ligated approximately 1mm below the arterial cone and left atrial appendage. When the electrocardiogram showed significant elevation of the ST segment, the heart was reset in the chest cavity, and the chest wall was sutured. After observing the animal's rhythm and breathing stability, artificial respiration was stopped. Penicillin was injected continuously for three days to prevent infection. After surgery, the animals were routinely fed for one month, and cardiac function was measured. The heart index (CI) value ≤ 180ml · min-1 · kg-1 was used as an animal model of heart failure. Postoperative continuous observation of changes in animal palpitations or chest tightness, fatigue and fatigue (measured by heart rate, breathing, and exhausted swimming time), general condition (activity, hair, mental state, weight gain index, feed consumption index, etc.), cardiac dysfunction (indicated by hemodynamic indicators), vascular obstruction, and laboratory basis (indicated by electrocardiogram, fibrinogen, and maximum platelet aggregation rate).

  (2) Model characteristics: The model animals have less activity, mental exhaustion, curling up, withered, yellowish white hair, and often stand upright. When grasping, they resist lightly and do not bite, and their breathing rate is significantly increased; The incidence of postoperative ST segment elevation and abnormal Q waves significantly increased, but decreased with the prolongation of postoperative time; The plasma fibrinogen content and maximum platelet aggregation rate increased significantly from 1 to 3 days after surgery, but there was no significant difference thereafter; 30 days after surgery, the duration of exhaustive swimming was significantly shortened, and cardiac function parameters such as stroke output (SV), minute output (CO), and CI were significantly reduced.

  (3) Compared to normal and healthy animals in medicine, acute myocardial infarction and blood stasis syndrome occur due to the blockage of the coronary artery. As a result of the disease, myocardial necrosis and prolonged blood stasis damage the body and lead to heart qi deficiency. After surgery, the blood stasis syndrome in model animals changed from severe to mild, and from whole body to local; Heart rate, respiration, exhausted swimming time, and cardiac function were significantly abnormal 30 days after surgery, which became a process from normal to blood stasis as the main injury to the formation of heart qi deficiency syndrome. The animal model of heart qi deficiency syndrome caused by transplanted myocardial infarction in heart failure is a mature production model in modern experimental medicine. It uses the national unified diagnostic standard of combining traditional Chinese and Western medicine for deficiency syndrome and blood stasis syndrome, and replaces its qualitative consultation content with quantitative and equivalent testing indicators to evaluate the animal model of heart qi deficiency syndrome.