(1) The replication method involves fixing rabbits under conventional anesthesia. Take a polyethylene tube (diameter 0.5-0.7mm) and insert it from the right femoral artery to the aorta. After 4 hours, insert another polyethylene tube into the left carotid artery and wash the blood with warm physiological saline (37 ℃) for 10 minutes, a total of 5 times, with 20ml each time. At the same time, the left femoral vein was cut open for bleeding. After 5-10 minutes, 4% paraformaldehyde was injected again from the left carotid artery, a total of 3 times, with 50ml each time, and the injection was completed within 5 minutes. After 24 hours, open the chest and abdominal cavity, take the aortic specimen and divide it into several sections. Fix them with 10% formaldehyde and 2.5% glutaraldehyde (fixed at 4 ℃ for 2 hours), and add 0.1mol/L phosphate buffer solution (pH 7.4) at the same time. Take out the specimen and prepare it according to the conventional method. Observe it under light microscope and transmission electron microscope.
(2) The characteristics of the model are that the catheter used in clinical cardiac catheterization has a large difference in diameter compared to the blood vessel diameter, making it less likely to scratch the vascular endothelium. At the same time, the catheter used in cardiac catheterization is coated with anticoagulants or pre soaked with anticoagulants, which can prevent thrombosis during intubation. In recent years, commonly used methods have been to measure the radiation intensity of the damaged area through blood vessels using platelets labeled with 111In or 51Cr, in order to infer the formation of blood clots. This method cannot be observed by naked eye or microscopic pathology, nor can other indicators be measured simultaneously, thus bringing significant limitations. And this method caused sustained damage to the endothelial cells of the blood vessel wall by inserting a catheter, successfully establishing a thrombus model of the rabbit aorta, and conducting experiments related to coagulation factors, platelets, and endothelial cells, as well as comprehensive pathological studies.
(3) The loss of endothelial cells and exposure of subendothelial structures in comparative medicine can lead to thrombosis. Endothelial cells can be damaged by physical factors of blood flow. In this experiment, a polyethylene tube was inserted into the aorta with a diameter close to the diameter of the blood vessel, which increased the contact surface between the vessel wall and the friction between the two, resulting in blood flow disorder and stagnation, causing extensive endothelial damage and subendothelial exposure, as well as the release of thrombin and adhesion of fibrin to platelets in the blood vessel, leading to arterial thrombosis; In vitro morphological studies of thrombosis have found that fibrin is rarely present in the subendothelial layer and there is little platelet adhesion. However, in studies of continuously damaged and re damaged vascular walls, fibrin can be present in the subendothelial layer. In this experiment, it can be clearly seen that the fibrin ring is located in the subendothelial layer and around the platelets. Platelets can be seen to adhere to the collagen fibers in the subendothelial layer, but no adhesion to the amorphous matrix was observed, revealing that there are certain differences in the study of thrombus formation between in vitro and in vivo.