动物造模,慢性胃溃疡动物模型 z-bio 2021-03-23 285

　　(1) Breeding method Adult rats are anesthetized with sodium pentobarbital, the abdomen is cut into a supine position, and 0.01 to 0.05 ml of 20% to 100% acetic acid is injected into the anterior wall of the gastric antrum with tuberculin. 0.01 ml graduated syringe. During injection, the needle tip should be tilted so that small white spots appear at the injection site without acetic acid leaking out or injected into the stomach cavity. Next, suture the omentum tissue and serosal tissue of the gastric antrum wall at the injection site with No. 0 silk thread. Alternatively, use a cotton swab dipped in a 100% acetic acid solution to apply it to the serous surface of the stomach. Alternatively, cut the stomach cavity, apply 100% acetic acid solution on the mucosa, and then suture the stomach wall. After completing the above steps, restore the stomach to its original position, suture the abdominal wall and place it in a single cage. During the modeling period, observe the animal's appetite, activity, sleep and other general activities every day. After modeling, the animal was put down and put to death, the stomach was excised by laparotomy, and the abdominal cavity was incised along the curvature. Measure the area and area of the ulcer by observing the gastric ulcer and mucosal morphology of the animal. Dissected, fixed, dehydrated, implanted, sliced, HE stained deep gastric antrum tissue with ulcers, and observed under an optical microscope.

　　(2) Model feature: Inject 0.05 ml of 100% acetic acid into the anterior wall of the gastric antrum. After 5 days, the model animals had poor appetite, lack of activity, weakness of limbs, lethargy and fluffy coat. -Number 7. Gradually reassured people, increased diet and exercise, and the coat regained its luster. Pathological observation revealed that the gastric contents of rats increased significantly 4 days after the operation, and ulcers with a diameter of 0.5 to 0.7 cm appeared on the mucosal surface of the anterior wall of the gastric antrum, and the ulcers were round. Ulcer obviously destroys the structure of the tissue, mucosal glands disappear, necrotic tissue can be seen on the mucosal surface, granulation tissue proliferation, neutrophils, monospheres, macrophages, lymphocytes and other inflammations can be seen below. The cells, muscle layer and serum were completely destroyed, and ulcers, edema and congestion of the mucosal space around the new small capillaries were visible. Within 7 days, the contents of the stomach increased significantly and the color became dirty. , It smells bad. The diameter of the ulcer on the mucosal surface of the anterior wall of the stomach vestibule is 1.0 to 1.2 cm, and the ulcer has a round shape. The structure of the vestibular wall of the stomach was obviously destroyed, the mucosal glands disappeared, the superficial necrotic tissue decreased, and the lower granulation tissue increased. In the vicinity of the serosal surface, neutrophils, monocytes, macrophages, lymphocytes, etc. still have good inflammatory infiltration. The mucosa and interstitial edema and scar tissue surrounding the ulcer are still hyperemic; day 10. Stomach content increased slightly. The diameter of the mucosal surface ulcer in the vestibule of the stomach is 0.4-0.5 cm. The structure of the ulcer gastric antrum has been restored. The thickness of the gastric antrum increases significantly and becomes necrotic. The tissue basically disappeared, and the mucous glands reappeared. , Mesenchyme and edema decreased, submucosal granular tissue increased, small blood vessel wall thickened, inflammatory cells decreased, but no new connective tissue was found. Muscle layer or serosal surface; on the 14, 21, 28 days, gastric ulcer, antral wall structure gradually regenerates, mucosa and submucosa gradually return to normal. The serosal structure gradually recovered intact, and the inflammatory cells and exudate gradually disappeared.

　　(3) Comparative medicine There are many factors in the formation of gastric ulcers, among which the digestive effect of acidic gastric juice on the mucosa is the basic factor in the formation of ulcers. Hp infection and overdose of certain chemicals can destroy the gastric mucosa. The normal defense and repair functions make the mucosa more sensitive to acid damage. This experiment simulates the diffusion of H+ of gastric acid back to the mucosa in the absence of a protective layer of the gastric mucosa. Acetic acid is directly injected into the mucosal layer or directly applied to the mucosal or serosal surface. As a result, ulcers appear in the inflamed area of the gastric mucosa. The surface diameter of the ulcer is usually 0.4-1.2 cm. The size of the ulcer directly depends on the concentration of acetic acid used and its dose. However, if the concentration is too high or the dose is too high, penetration and even perforation will often occur. The model is easy to replicate, the conditions are easy to control, and the experiment is reproducible. The induced ulcers are typical and very similar to human chronic gastric ulcers. The spontaneous healing of ulcers induced by this model takes about 60 days, but because some patients can still see ulcer damage after 200 days, it is more effective as an experimental animal model for treating chronic gastric ulcers and promoting ulcer repair. It fits and heals. Generally, drugs that promote mucosal repair and anti-pepsin drugs have a significant effect on acetic acid ulcers, while antacids and anticholinergic drugs also have a healing effect.