(1) Reproduction method Anesthetize New Zealand male rabbits by conventional methods, enter the abdominal cavity through a midline incision under the xiphoid process, puncture the proximal portal vein with an indwelling needle, and measure the pressure of the portal vein through an indwelling needle cannula to perform digital subtraction angiography. A suspension of white let (Bletilla striata) and physiological saline was slowly injected into the portal vein at a dose of 4 ml and a concentration of 0.4%. Measure the pulse pressure of the portal vein again and perform digital subtraction angiography. After 3 to 4 weeks, the portal pressure was measured by the same method, the liver volume and ascites changes were observed, the pathological section of the liver biopsy was performed, and a part of the liver was poured into the portal vein. The experimental results showed that after 4 weeks, the portal vein pressure increased by 40% on average, the liver shrank by about 20%, and the embolization site was dark red. The pathological section showed that the liver cells in the embolized area were locally necrotic and inflamed. Cells are infiltrated and not absorbed by tissues. The white particles that are colorless, refracted and not stained with eosin show more combined tissue hyperplasia and typical post-necrotic liver fibrosis. The results of vascular casting showed that the embolized area accounted for 20% of the peripheral blood vessel volume of the liver.
(2) Model features This model belongs to portal sinus obstruction. The main feature of this model is the formation of typical necrotizing liver fibrosis when the portal hypertension model is formed. By using selective intubation techniques and understanding the concentration of white lettuce, you can control the extent and extent of the disease. Compared with other animal models of portal hypertension, the method is simple and easy to implement, has stable effects, good reproducibility, safety and reliability.
(3) Comparative medicine Brechila embolization can affect coagulation factors, shorten coagulation time, increase the activity of platelet factor III, shorten the production time of thromboplastin, and inhibit the activity of plasmin. Portal sinus obstruction is because when injected through the portal vein to the distal end of its branch, it can quickly form an artificial embolus and exert an embolization effect. The fiber component of Bletilla striata is not absorbed by the tissue and can be used as a long-lasting permanent embolic agent. The cause of portal hypertension is the obstruction of the blood vessels around the portal vein and the increase of vascular resistance. The portal vein and hepatic vein are compressed by hepatic fibrosis and hyperplastic connective tissue, which changes the path and reduces the vascular bed area. Many portal vein-hepatic artery anastomoses are open. Liver cells are damaged, monoamine oxidase activity is reduced, and amines cause spastic obstruction of the intrahepatic venous bed. The main factors leading to the reduction of portal pressure are: portal vein blood flow through the coronary veins of the stomach, and shunt other collateral and hepatic veins. Therefore, the level of portal pressure depends on the combined effect of the above two factors. Three to four weeks after the injection of white let (Bletilla striata), the two maintained a relative dynamic balance, and there was no significant change in portal pressure. After the portal vein is blocked, liver cells will undergo necrosis, inflammation and other pathological changes, which will eventually lead to stable destruction and liver fibrosis. Therefore, this model is very similar to the clinical portal hypertension of liver fibrosis.