动物造模,慢性萎缩性胃炎动物模型 z-bio 2021-03-23 291

　　(1) Breeding method Adult rats fasted for 18 hours, injected pentobarbital sodium 30 mg/kg body weight intraperitoneally under anesthesia, opened the stomach, exposed the stomach and jejunum, and placed the forearm about 2 cm. Fix the pylorus and jejunum 5-7 cm away from the pylorus. First cut a 0.5-0.7 cm incision in the front stomach, carefully flush the gastric cavity with saline, then cut an incision of the same size in the corresponding small intestine, and then suture the inside and outside of the stomach and the small intestine. I will. Rotate. After closing the incision, rinse the abdominal cavity twice with normal saline, soak and dry with sterile gauze, and then inject 2-3 drops of gentamicin diluent. The muscle layer and skin were sutured in layers, the abdominal cavity was closed, 2-3 drops of gentamicin diluent were added, and the rats were fed regularly after 24 hours of fasting. After 9-13 weeks, fast for 24 hours, anesthetize the abdomen, ligate the pylorus, card door and anastomosis on both sides of the intestine, and cut the stomach in the curved direction after 15 minutes, collect the gastric juice and total gastric juice by measuring the bile acid in the stomach Measure and record the pH value. Observe the pathological changes of the gastric mucosa with the naked eye, and take samples from the fundus, antrum, the curvature of the stomach, the curvature of the stomach, and the anastomosis of the stomach and intestines for optical and electron microscopy. Alternatively, the adult dog opens the stomach under anesthesia, ligates the common bile duct, and forms an anastomosis between the bottom of the gallbladder and the body (bile reflux model), or forms an anastomosis between the jejunum and the body (the body). model). During the operation, one case of gastric antrum and one case of gastric mucosal tissue were taken as pre-model controls. Six months after the operation, the gastric mucosa was observed with a gastroscope, the same gastric antrum and gastric mucosa were photographed with an optical microscope and an electron microscope, and the curved side 2.5-3.0 cm from the pylorus was directly observed. ..

　　(2) Model characteristics: The pH value of the stomach of model rats increases, the content of bile acids increases, and most of the gastric juice turns yellow-green. The surface of the gastric mucosa is covered with a thick white film, most of which have yellow spots, congestion or hyperemia of the gastric mucosa, and obvious edema. Edema protrudes at the anastomotic site around the anastomosis and is pebble-like. The wrinkles of the body mucous membrane are reduced. Even if it disappears, the tension on the stomach wall will be greatly reduced. Gastric mucosal tissue shows obvious inflammatory cell infiltration, most of which occur in the lamina propria, and some can reach the mucosa and submucosa. Inflammatory cells are lymphocytes. , Neutrophils and a small amount of eosinophils. There are still atypical hyperplasia or gland atrophy in the mucosal tissue around the anastomosis, enlargement of the gastric cavity and intestinal metaplasia. Model dogs also showed obvious gastric mucosal inflammatory cell infiltration, gland atrophy and intestinal metaplasia. Inflammatory cells are mainly neutrophils and lymphocytes, and infiltration mainly occurs in gastric mucosal glands and indigenous areas. In the dog model of bile reflux, the epithelial cells of the gastric mucosa proliferate, some of which die and fall off, the opening of the gastric cavity is obviously deformed, and the gastric cavity becomes deeper, larger and dehiscence, and expand into shape. . The epithelial hyperplasia of the gastrointestinal mucosa is like the epithelium of the small intestine, and the surface microvilli grow in it. Dogs with biliary-pancreatic reflux disease have more severe gastric mucosal damage. Most of the epithelial cells sloughed off and formed ulcers, covered by necrosis, and the mucosal surface structure was unclear. When the inflammation heals, some glands shrink. In severe atrophic gastritis, the connection between the stomach depressions is completely broken and the mucous membrane becomes flat.

　　(3) In clinical comparison, pyloric sphincter dysfunction or gastrojejunostomy often causes intestinal reflux. The flow of bile and pancreatic juice back into the stomach increases the pH of the gastric juice, changes the structure of the mucosa and reduces the barrier function of the mucosa. At the same time, certain components of the duodenal contents, such as bile acid and lysolecithin, destroy the lipid membrane of mucosal cells, increase the permeability of the cell membrane, and promote the back diffusion of H + and pepsin to the mucosa. And caused mucosal damage. It works; bile enters the stomach and stimulates the growth of the stomach; acid secretion, bile acid combines with gastric acid. It increases the activity of acid hydrolase, destroys the lysosomal membrane, and causes cell disruption and ulcers. Lysolecithin in bile can further destroy the gastric mucosal barrier through the action of phospholipase A. pancreatic juice. Under the long-term stimulation of the above factors, the gastric tissue gradually evolved the same pathological process: gastric mucosal inflammatory cell infiltration, glandular hyperplasia or atrophy, and intestinal metaplasia. This model uses gastrointestinal anastomosis to reflux the fluid in the alkaline intestinal cavity into the stomach, causing a large amount of inflammatory cell infiltration. It mimics the pathological changes of chronic gastritis and is consistent with the characteristics of pathological structural changes. Chronic atrophic gastritis. This model also shows that bile or pancreatic juice can cause severe damage to the gastric mucosa when it enters the stomach, but the latter is more serious, and bile and pancreatic juice have a synergistic effect on the gastric mucosa. Due to its simple manufacturing method and clear pathological evolution process, this model is more suitable for studying the etiology of intestinal reflux disease of chronic atrophic gastritis and observing the efficacy of drugs.