动物造模,心力衰竭模型 z-bio 2021-12-22 440

　　The common causes of hypervolemia of the heart are aortic or mitral or tricuspid valve insufficiency, atrial septal, ventricular septal defect, and arteriovenous shunt. A common test method that causes the blood volume overload of the animal heart is the anastomosis of the abdominal aorta and the inferior vena cava to form an arteriovenous shunt.

　　1. Arteriovenous short circuit method

　　[Modeling mechanism] Under normal circumstances, the pressure in the arteriovenous system is higher than the pressure in the venous system. The short circuit between the artery and the vein transfers blood from the arterial system to the low-pressure venous system. The value of the shunt mainly depends on the size of the anastomosis and the pressure difference between the aorta and the inferior vena cava. Arterial and venous shunting through venous return increases the blood volume of the heart and increases the load on the heart. Long-term development can lead to heart failure.

　　[Modeling method]

　　(1) Dog: Choose a healthy dog and fix it in the supine position with sodium pentobarbital anesthesia (25 mg/kg). Aseptically, open the abdominal cavity along the midline and lift the intestinal cavity to the posterior peritoneal wall. At the branch of the renal artery, the abdominal cavity and the inferior vena cava are separated by about 4 cm. Kidneys and arteries. Vascular clamps clamp the ends of arteries and veins to prevent blood flow. Cut each container into an oval opening with 10-15 mm and use 5-0 silk thread. Cut the left and right anastomosis of the end of the blood vessel. The blood flow is blocked for 20-30 minutes. After the arteriovenous anastomosis, loosen the vascular clamp, check for bleeding, and close the abdominal cavity. About 1 week after the operation, 600,000 U of penicillin and 0.59 U of streptomycin were injected daily. After the animals have symptoms and signs of heart failure (limb edema, ascites, dyspnea after exercise, hair loss, etc.), an acute experiment is performed to measure hemodynamic indicators and perform histological and pathological examinations. (2) Rats: Male Sprague Dawley rats are used to block the blood flow in the abdominal aorta through a non-invasive vascular clip 2 mm below the start of the left renal artery of the abdominal aorta. After puncturing the abdominal aorta and inferior vein, the hippo and the puncture point were sealed with adhesive and placed in a cage for 4 weeks after the operation. The weight ratio of the rat heart increased significantly, the myocardium increased, the left ventricular end-diastolic pressure increased significantly, the left ventricular contractility was significantly impaired, and heart failure was caused. Alternatively, the rat uses an 8-gauge needle to puncture the abdominal aorta and inferior vena cava from 0.8-1.0 cm diagonally from the left kidney to create a heart failure model.

　　[Model Features] This method is reliable and has excellent clinical simulations in establishing chronic heart failure models. However, the establishment of this model requires better conditions and equipment, is more complicated to operate, and the success rate depends on the skill level.

　　[Model evaluation and application] This model is similar to clinical high-output heart failure, mainly due to changes in neuroendocrine mechanisms, water and electrolyte disturbances, renal dysfunction during CHF, and used for experimental drug research.

　　2, aortic and mitral regurgitation

　　[Modeling mechanism] The main hemodynamic change of aortic reflux is the return of blood to the left ventricle during diastole. Therefore, during diastole, the left ventricle must receive blood from the left ventricle and return from the aorta. This will cause the left ventricle to overfill and gradually expand and thicken to the left. In the compensation phase, the ventricular drainage is higher than normal. Decompensation reduces cardiac output and increases pressure in the left atrium and pulmonary arteries, which can lead to right heart failure. In mitral regurgitation, when the left ventricle contracts, blood enters the aorta and flows back to the left atrium, thereby reducing left ventricular drainage. The blood volume in the left atrium increases, the pressure increases, and the compensatory dilation and thickening of the left atrium gradually develops. The diastolic filling of the left ventricle increases, the load increases, and the left ventricle gradually expands and thickens. As the development continues, the left heart can develop. failure.

　　[Modeling method]

　　(1) Method of aortic regurgitation: Wistar rats were anesthetized in the abdominal cavity (200-300 g), sodium pentobarbital 40 mg/kg, fixed in the supine position. Separate the right common carotid artery and insert a rigid polyethylene catheter into the heart through the right common carotid artery. Repeated insertion of the catheter into the aortic valve will damage the aortic valve and cause aortic valve regurgitation. The method to detect aortic insufficiency is to measure the aortic pressure, which has a low diastolic pressure and a large pulse pressure difference.

　　(2) Mitral regurgitation: Choose healthy mongrel dogs 18-32 kg, intravenous anesthesia with sodium pentobarbital 25 mg/kg, and fix it on the back. Using aseptic technique, open the chest along the fifth intercostal space at the left end of the sternum to expose the heart and cut the bag. Cut a small opening in the left atrium, compress with the index finger to pass through the small opening, separate two or more myocardial tendons from the top of the mitral valve, and pass through the mitral valve to reach the left atrial pressure to 2.5, up to 3 of the normal valve pressure Times. The incision of the left atrium was sutured, and the thoracic cavity was sealed in layers. After surgery, large doses of penicillin and streptomycin should be given to prevent infection. Daily observation showed that the left ventricle dp/dtmax decreased, the LVEDP increased, the heart index decreased, the left ventricular function index decreased, the cardiac output decreased, and other hemodynamic indicators changed. The failure was formed. [Model Features] Certain conditions are required to establish this model, and animal mortality is relatively high. [Model evaluation and application] The arteriovenous short circuit method for establishing a chronic heart failure model is similar to that of clinical high-output heart failure. The heart failure model established by the aortic and mitral regurgitation method is similar to certain congenital heart disease or valvular diseases caused by other causes, and some of these models are not suitable for patients, you can get important information about them. If a model of aortic and mitral regurgitation is established in the same animal, it is similar to clinical valvular disease, and the etiology and pathological changes of heart failure caused by valvular heart disease are studied, which plays a role in this process. Important role.