[Animal Experiment]-Phytolithic cholecystitis model

  (1) Method of replication: Rabbits, both male and female, weighing 2 to 3 kg, are injected intravenously with 3% pentobarbital sodium at a dose of 30 mg/kg body weight and placed on the operating table after being anesthetized with a sterile drape under the xiphoid process. Enter the abdomen through a midline incision of 3 to 4 cm to expose the gallbladder. Make a purse-string suture with a diameter of 4mm at the bottom of the gallbladder with 5-0 nylon undamaged sutures. Place two cholesterol stones weighing 0.15g and tighten the suture. After washing with normal saline, close the abdominal cavity and complete the modeling. Three months later, the animals were sacrificed, the liver and gallbladder were dissected and weighed, bile was extracted for analysis of bile components, and the cyst wall tissue was cut and fixed with 10% formaldehyde for pathological examination.

  (2) Model features: The wet weight of the gallbladder of the model animal increases, the cyst wall is thickened, and the mucosal folds become shorter and thicker, showing papillary or dendritic hyperplasia; there are varying degrees of cholesterol deposition in epithelial cells, and glandular epithelial hyperplasia, in the lamina propria and The muscular layer forms island-shaped alveoli; the nuclei have different morphologies and are arranged disorderly, shifting to the top of the cell, and mitotic phases can be seen; the glands are mucinous, and mucosal sinuses are more common; the muscular layer becomes thicker and smooth muscle is reduced, replaced by hyperplastic collagen Fibres; inflammatory cells are scattered or diffuse infiltration, mainly infiltration of eosinophils and neutrophils; tissue edema and hemorrhage, serosal vasodilation, exudation and proliferative inflammation coexist.

  (3) Comparative medicine Human cholecystitis is mostly caused by gallbladder stones blocking the cystic duct and secondary infection. Stones can mechanically damage the cyst wall and stimulate epithelial cells to release lysosomal phospholipase. This enzyme is the main rate-limiting factor for prostaglandin biosynthesis, and it is also an intermediary substance in the development and development of inflammation. It can promote the conversion of lecithin into lysolecithin and directly damage cell membranes. Implanting human cholesterol stones into the gallbladder of animals can not only make a model of gallstone cholecystitis, but also consistent with the pathological manifestations of humans suffering from gallstone cholecystitis. If it can be combined with the clinic, aiming at the most important pathogenic factor of cholecystitis, during the operation stage of this model, a certain amount of clinically common bile duct infection bacteria is injected into the animal's gallbladder or bile duct, then the model will be caused (calculous infectious cholecystitis Animal model) is closer to the clinic.