(1) Copy method Experimental rabbits are fixed after routine anesthesia. Take a polyethylene tube (0.5~0.7mm in diameter) and insert it from the right femoral artery to the aorta. 4 hours later, insert another polyethylene tube into the left carotid artery and use warm normal saline (37°C) for 10 minutes The blood was lavaged internally for 5 times, 20ml each time. At the same time, the left femoral vein was cut and bloodletted. After 5-10 minutes, 4% paraformaldehyde was injected again from the left carotid artery for 3 times, each time of 50ml, and the injection was completed within 5 minutes. After 24 hours, the thoracic and abdominal cavity was opened, and the aortic specimens were divided into several sections, respectively fixed with 10% formaldehyde and 2.5% glutaraldehyde (fixed at 4°C for 2 hours), and at the same time, 0.1 mol/L phosphate buffer (pH 7.4) was added. The specimens were taken out and prepared according to conventional methods, and observed under light microscope and transmission electron microscope.
(2) Model features The catheter used in clinical cardiac catheterization has a large difference in tube diameter and vascular diameter, and it is not easy to scratch the vascular endothelium. At the same time, the outer circumference of the catheter used in cardiac catheterization is coated with anticoagulant or anticoagulant in advance. Soak, thus preventing thrombosis during intubation. In recent years, the commonly used methods generally use 111In or 51Cr platelets to measure the radiation intensity of the injured area through the blood vessel, in order to infer the thrombosis, it is impossible to observe the pathology under the naked eye and the microscope, and cannot measure other indicators at the same time. This brings great limitations. This method caused persistent damage to the endothelium of the vascular wall by inserting a catheter, successfully established a rabbit aortic thrombosis model, and conducted experiments related to coagulation factors, platelets and vascular endothelial cells, and comprehensively studied its pathological aspects. .
(3) Comparative Medicine Loss of vascular endothelial cells and exposure of subendothelial structures can lead to thrombosis. Endothelial cells can be damaged by physical factors of blood flow. In this experiment, a polyethylene tube was inserted to reach the aorta. The diameter of the tube used was close to the diameter of the blood vessel, which increased the contact surface of the blood vessel wall and the friction between the two, resulting in chaos and stagnation of blood flow, resulting in extensive endothelial damage and internal damage. Subcutaneous exposure, as well as the release of intravascular thrombin and fibrin adhesion to platelets to form arterial thrombi; in vitro morphological studies of thrombosis found that fibrin is rarely present in the subendothelial layer, and there is rarely platelet adhesion, and it is continuously damaged And in the study of re-damaged blood vessel walls, fibrin can be present in the subendothelial layer. In this experiment, it can be clearly seen that the fibrin ring is adjacent to the subendothelial layer and the periphery of the platelets. Platelets can be seen adhering to the collagen fibers of the subendothelial layer, but no adhesion to the amorphous matrix. This reveals that the study of thrombosis in vitro and in vivo has certain difference.