动物模型,慢性胃溃疡 z-bo 2020-08-07 662

　　(1) Reproduction method Adult rats are anesthetized with sodium pentobarbital, the abdominal incision is made in the 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 a tuberculin syringe with a scale of 0.01 ml. When injecting, the tip of the needle should be tilted so that a small white spot appears at the injection site without acetic acid exudation and no injection into the stomach cavity. Then suture the omentum tissue and the serosal tissue of the gastric antrum wall at the injection site with a needle of No. 0 silk thread. Or use a cotton swab dipped in 100% acetic acid solution to apply to the serous surface of the stomach. Or cut the stomach cavity and apply 100% acetic acid solution to the mucosa and suture the stomach wall. After completing the above steps, put the stomach back in situ, suture the abdominal wall, and raise in a single cage. During the modeling period, observe the animal’s appetite, activity, sleep and other general activity conditions daily. After modeling, the animals were sacrificed by bloodletting, the stomach was taken by laparotomy, and the stomach cavity was cut along the greater curvature. The animal gastric ulcer and mucosal morphology were observed, and the ulcer area and In depth, cut the gastric antrum tissue including the ulcer, fix, dehydrate, embed, slice, HE stain, and observe with light microscope.

　　(2) Model features 0.05ml 100% acetic acid was injected into the anterior wall of the gastric antrum. The model animals showed decreased appetite, decreased activity, weakness of the limbs, sleepiness, lethargy, and fluffy coat after 1 to 4 days. The above symptoms gradually relieved after 5 to 7 days. , Diet and activity increase, and the coat regains its luster. Pathological observations showed that at 4 days postoperatively, the contents of the stomach of rats increased significantly, and ulcers appeared on the mucosal surface of the anterior wall of the gastric antrum, with a diameter of 0.5-0.7 cm. The ulcers were round, and the structure of the gastric antrum wall at the ulcer was obviously damaged, and the mucosal glands disappear , Necrotic tissue is seen on the surface of the mucosa, granulation tissue hyperplasia is seen below, and inflammatory cells such as neutrophils, monocytes, macrophages, lymphocytes, etc. can be seen. The muscle layer and serosa are completely destroyed, and the mucosal glands around the ulcer Interstitial congestion, edema, and new small capillaries can be seen; at 7 days, the contents of the stomach are obviously increased with dirty color and rancid odor. The diameter of the ulcer on the mucosal surface of the anterior wall of the gastric antrum is 1.0-1.2cm, and the ulcer is round in shape. The structure of the gastric antrum wall is obviously destroyed, the mucosal glands disappear, the surface necrotic tissue decreases, and the lower granulation tissue increases. There are still inflammatory fine infiltrations such as neutrophils, monocytes, macrophages, and lymphocytes, near the serosal surface There is scar tissue, and there is still hyperemia and edema in the mucosa and glands around the ulcer; at 10 days. Stomach content increased slightly, the diameter of the ulcer at the mucosal surface of the anterior wall of the gastric antrum was 0.4-0.5cm, the structure of the gastric antrum wall at the ulcer had been restored, the thickness of the gastric antrum wall increased significantly, the necrotic tissue had basically disappeared, and the weight of the mucosal glands appeared , The mesenchymal congestion and edema are reduced, the submucosal granulation tissue increases, the small blood vessel wall is thickened, and the inflammatory cells are reduced. However, no new connective tissue is found in the muscle layer or serosal surface; at 14, 21, 28 days, the stomach is ulcerated The structure of the sinus wall is gradually regenerated, and the mucosa and submucosa gradually approximate normal. The serosal structure gradually recovered intact, and the inflammatory cells and exudates gradually disappeared.

　　(3) Comparative medicine. There are many factors in the formation of gastric ulcer. Among them, the digestive effect of acidic gastric juice on the mucosa is the basic factor in the formation of ulcers. Hp infection and excessive intake of certain chemicals can destroy the normal defense of the gastric mucosa. And repair function, make the mucosa more sensitive to acid damage. This experiment mimics the condition that the H+ in gastric acid is inversely diffused into the mucosa under the condition of the absence of the gastric mucosal protective layer. Acetic acid is directly injected into the mucosal layer, or directly applied to the mucosa or serous membrane surface. As a result, ulcers appear at the irritation site of the gastric mucosa. The diameter of the ulcer surface is usually between 0.4 and 1.2 cm. The size of the ulcer directly depends on the concentration of acetic acid used and its dosage. However, if the concentration is too high or the dosage is too large, penetration or even perforation will often occur. The model is simple to replicate, the conditions are easy to control, the experiment is reproducible, and the induced ulcers are typical, very similar to human chronic gastric ulcers. The natural healing of the ulcer induced by this model takes about 60 days, but there are also patients with ulcer lesions that are still visible after 200 days. Therefore, it is more suitable as an experimental animal model for treating chronic gastric ulcers and promoting ulcer healing. Generally, drugs that promote mucosal repair and anti-pepsin drugs have significant effects on acetic ulcers, and antacids and anticholinergic drugs also have a healing effect.