动物造模,慢性犬门静脉高压症模型 z-bio 2021-10-19 442

　　(1) The method of reproduction is an experimental dog of an adult dog. Fasting and anesthesia before surgery. Enter the abdomen through the oblique incision of the right rib, release the main portal vein, temporarily occlude it with non-invasive forceps, and then perform the "intubation irrigation method" (the 10th silk thread is pre-connected to the tube). Main portal vein → left trunk → left lateral branch and main portal vein → right trunk → right anterior branch or right posterior branch. The suture lengths are 12-16 cm and 9-12 cm, respectively, and the cannula is gradually pulled out at 2000o, and finally sutured The portal vein and fix the end of the silk thread. At this time, the portal vein has two 10-gauge silk threads, the front ends of which respectively extend to the portal vein branches of the left and right liver lobes. The main portal vein is sutured to reduce the diameter by half. Remove the portal vein occlusion clip. Threading and stenosis of the portal vein should be above the injection surface of the gastric coronary vein. Cut round liver, sickle-shaped liver, left triangle and hepatogastric ligament. Beware of fluids and antibiotics after surgery. Then, before and after the operation, the pressure of the portal vein was measured, portal vein angiography was performed, and gastroscopy was performed to record the degree of esophageal varices and gastric varices (no varicose veins were found). Protruding cavity). After 3-4 weeks, the animals were sacrificed and the portal vein, middle and lower esophagus and fundus were collected for pathological examination. The portal blood pressure rose immediately after the operation and decreased slightly after 3-4 weeks. One week after the operation, the main portal vein of the hepatic portal vein was stenosis, the portal vein above the stenosis had a filling defect, and some intrahepatic portal vein branches were not visible. Two weeks later, the main portal vein was occluded, there was no obvious hepatic collateral circulation, and the intrahepatic portal vein was almost invisible. The upper mesenteric and splenic veins are significantly dilated, esophageal varices and gastric varices appear, the formation rate exceeds 80%, and the incidence of portal hypertension and gastric disease exceeds 50%.

　　(2) Model features This model can shrink the main portal vein and use the chronic embolization of silk thread to completely occlude the portal vein two weeks after the operation, resulting in complete occlusion at one time. This problem will be solved. Commonly used experimental dogs destroy the portal vein. Break through unbearable problems. In addition, because of the embroidered main portal vein and the branches of grade 1 to grade 3 or higher, the peripheral ligament of hepatitis was cut during the operation, and secondary atrophic fibrosis of the liver occurred after the operation, and the portal vein was performed surgery. Then, it moves to the side of the liver. The establishment of branch loops improves the durability of the model. The model is simple and easy to implement, the modeling cycle is short, the success rate is high, and the model is durable. Compared with simple portal vein stenosis, this model does not affect the surgical process or the cycle of model formation, but the impact of portal vein pressure increase and varicose vein formation after modeling is greater than the latter.

　　(3) Comparative medicine In portal hypertension, in addition to the rupture of esophageal varices which can cause massive bleeding in the upper gastrointestinal tract, gastric varices can also form, leading to massive rupture, which can cause bleeding. Gastric mucosal damage caused by portal hypertension mainly includes gastric fundus varices and gastric mucosal lesions, both of which can cause fatal bleeding. The exact incidence of gastric varices has not been determined, with reports ranging from 2% to 100%. Compared with gastroesophageal varices bleeding, gastric varices bleeding is more serious because the collateral circulation of the stomach is very rich. Endoscopic sclerotherapy has a high mortality rate, and because it cannot control the rupture and bleeding of gastric fundus varicose veins and the embolization of varicose veins, surgical treatment is often required. Therefore, the rupture and bleeding of gastric fundus varices cause concern. Gastric mucosal congestion in portal hypertension is the root cause of gastric mucosal damage, gastric varices and gastric mucosal lesions. In this model, the portal vein pressure increased significantly, and obvious gastric varices were observed.