(1) Method of replication: Guinea pigs weighing 300-400g were anesthetized with ether, and the abdominal cavity was opened to expose the gallbladder. The bile was aspirated out using a 1ml syringe, and 3 × 10000 Escherichia coli, or a filtered 20% fresh suspension of guinea pig feces at 0.1ml/animal, or 0.005mg/kg body weight of endotoxin were injected. The needle was immediately ligated, and the muscles and skin were sutured. After 10 days, blood was collected from the heart to prepare serum, and the gallbladder was dissected and fixed with 10% formaldehyde for pathological examination.
(2) Model features: After injecting Escherichia coli into the gallbladder for 10 days, the gallbladder mucosa of the model animals showed increased wrinkles and thickening, an increase in the number of fibrous cells in the lamina propria, thickening of fiber height, and localized focal or diffuse dense infiltration of inflammatory cells in the lamina propria. Injecting high-dose endotoxins (Escherichia coli lipopolysaccharides) into the gallbladder causes mucosal surface damage, mucosal coagulation, necrosis, bleeding, extensive fibrin deposition, and widespread mucosal loss.
(3) One of the main causes of human cholecystitis in comparative medicine is bacterial infection. The positive rate of bacterial culture in gallbladder bile during acute cholecystitis is over 80%. Its main source is through the ascending pathway of the duodenum, lymphatic or blood circulation, enterohepatic circulation, and infection from adjacent organs. Among them, Escherichia coli (enteric gram-negative bacteria) is the most common. Bacteria, under the action of enzymes, can convert bound bile acids into toxic free bile acids, thereby exacerbating tissue damage and inflammation. Pathologically, human cholecystitis is characterized by thickening, fibrosis, and contraction of the gallbladder wall. Clinically, it is commonly manifested as high fever, elevated white blood cells, jaundice, and recurrent biliary colic in the upper right abdomen. This method directly injects Escherichia coli, enteric Gram negative bacterial suspension, or Escherichia coli endotoxin into the gallbladder of animal models, causing an increase in peripheral blood white blood cells, an increase in bile duct sphincter tension, a decrease in bile flow, damage or necrosis of gallbladder tissue, fibrin deposition, and infiltration of inflammatory cells, resulting in a model similar to acute ischemic damage in non calculous cholecystitis in humans.