[Animal Modeling] - Acute Myocardial Infarction Model in Dogs

  1. Animal modeling material: Healthy hybrid dog, male or female, weighing 14-23kg; Medications: ketamine, vecuronium bromide; Instrument: controllable micro current stimulator.

  2. Method of modeling: Anesthetize dogs by intramuscular injection of ketamine 100-200mg. Intramuscular injection of 0.1mg vecuronium bromide relaxes the smooth muscle of the dog's trachea. After tracheal intubation, a ventilator is connected and electrocardiographic monitoring is performed. Open the chest along the left edge of the sternum between the 3rd and 4th ribs, layer by layer open to the pericardium, and create a pericardial hammock to clearly expose the anterior descending branch of the left coronary artery. At a distance of about 1.5cm from the opening of the anterior descending branch, the positive and negative stimulation electrodes were separated by 1cm and placed on the outer membrane of the anterior descending branch. The current gradually increased from small to large, stimulating the outer membrane of the blood vessel for 15-20cm with an interval of 10min. After the electrocardiogram monitoring showed that the electrocardiogram was stable, the same area was stimulated with current again for 20min until the color of the outer membrane of the blood vessel deepened. Observe the absence of severe arrhythmia or bleeding, and close the chest cavity layer by layer. Place a water sealed bottle in the chest cavity for drainage. After being anesthetized and conscious, the dog is returned to the animal room for feeding. The average stimulation current is 115 μ A. The voltage is 13.5V and the average time is 36.5 minutes.

  3. The principle of modeling is to establish a canine acute myocardial infarction model by stimulating the outer membrane of the coronary artery with a microcurrent stimulator, which leads to acute thrombosis in the coronary artery.

  4. Pathological changes after modeling: Changes in myocardial enzymes: After electrical stimulation of the coronary artery, serum creatine kinase (CK) and myocardial creatine kinase isoenzyme (CKMB) significantly increased, especially at 6 and 24 hours after electrical stimulation. The difference was significant compared to the baseline values before the experiment.

  Light microscopy observation: The myocardial fibers in the infarcted area undergo degeneration and necrosis, with swelling, rupture, and homogenization of the necrotic myocardial fibers. The longitudinal and transverse lines disappear, and there is bleeding and deposition of hemosiderin in the infarcted area, with a small amount of phagocytic cell infiltration. Transmission electron microscopy observation: Fibrous necrosis, myofilament breakage, disappearance of z-line, intercalated disc destruction, high swelling and degeneration of mitochondria, destruction and disappearance of cristae, and interstitial edema in the myocardial infarction area. Endothelial swelling of blood vessels in the infarcted area, degeneration of adjacent myocardium, disordered arrangement of myofilaments, swelling and degeneration of mitochondria, and blurry Z-line.

  5. Precautions: Surgical instruments should be strictly disinfected to prevent surgical infections. Surgical trauma should be minimized and sterile operations should be strictly carried out.