(1) Replication method Adult male rats, fasting without water for 48 hours, give acetylsalicylic acid 100mg/kg body weight, or 10mmol/L acetic acid or different concentrations of hydrochloric acid (1, 10, 10mmol/L), or Gavage the stomach with the same kind of bile or 2mmol/L taurocholic acid or 15% ethanol alone or in combination. 4 hours later, the rats were sacrificed, the abdominal section was immediately opened, the whole stomach was taken out, cut along the greater curvature of the stomach, everted, and the contents were poured out , Gently flush the residues in the stomach with cold normal saline, observe the mucosal lesions, and perform histopathological examinations with light and electron microscopy techniques.
(2) Model characteristics The common pathological feature of model animals is acute diffuse inflammation of the gastric mucosa. For example, if a mixture of hydrochloric acid and acetylsalicylic acid is given by intragastric administration, the gastric mucosa of model rats will show congestion and edema. In severe cases, there will be spotted hemorrhage spots and diffuse erosion. Under light microscope, the epithelial cells can be seen to show different degrees of degeneration and shedding. The layer and submucosa are infiltrated by neutrophils, interstitial congestion and edema.
(3) Comparative medicine Acute gastritis can be caused by physical, chemical factors and microbial infections. The common physical factors are: overeating, or the food consumed is too cold, hot, or too rough, leading to gastric mucosal congestion, edema, and sometimes erosion; chemical factors are mostly: taking certain non-steroidal anti-inflammatory drugs such as salicylic acid preparations, Certain hormones, high concentrations of ethanol, or ingestion of strong acids, strong bases, or other corrosive liquids such as hydrochloric acid and acetic acid can cause bleeding, necrosis and dissolution of the gastric mucosa. In severe cases, deep tissues and even perforations can be involved; microbial infections include: Food contaminated by microorganisms and bacterial toxins, or direct infection caused by gastric trauma. This model uses the above-mentioned pathogenic factors to induce acute gastritis in animals. Its pathological characteristics are basically the same as those in the clinic, and the method is simple and the model has a high success rate. It has been widely used.