[Animal Modeling - Pharmacological Evaluation] - Septicemia Mouse Animal Model

  (1) Copy method: BALB/c mice weighing 21-25g (rats weighing around 200g can also be used), regardless of gender. Animals were raised adaptively for one week and fasted for 12 hours before the experiment. After intraperitoneal injection of pentobarbital sodium at a dose of 50mg/kg body weight for anesthesia, the animal was fixed supine on a surgical plate. The abdominal surgical area was routinely disinfected and depilated. Under sterile conditions, a surgical knife was used to make a 2cm incision in the abdominal wall. The incision was made into the abdomen and separated from the distal end of the ileocecal valve. The cecum was ligated with a No. 3 silk thread. An No. 18 injection needle was used to puncture the ligation end twice, and a small amount of feces was squeezed out. Then, the peritoneum and skin were intermittently sutured with a No. 4 silk thread. At the same time, 50ml/kg body weight of physiological saline was immediately subcutaneously injected to.

  (2) After modeling, the mice gradually developed vertical hair, diarrhea, and purulent urine. The model animals showed a decrease in drinking, eating, and activity frequency. The systemic inflammatory response of the animals often peaked at 12 hours after surgery, and the activity frequency of the mice significantly decreased, and the activity lost its diurnal pattern. The application of animals for cecal ligation and perforation is the best animal model for replicating clinical sepsis models, especially gastrointestinal perforation. It can well reflect the bidirectional changes in immunology and hemodynamics during the development of sepsis.

  (3) Comparative medicine sepsis is a cascade reaction of inflammation caused by severe damage to the nervous, immune, endocrine, coagulation and other system functions of the body. Various harmful stimuli (mainly exogenous microorganisms) can activate the body's immune cells, leading to a large number of pro-inflammatory cytokines, such as tumor necrosis factor a (TNFa), interleukin-6 (IL6), and biologically active mediators, such as nitric oxide (NO) and reactive oxygen species (O-2), which play a key role in the progressive aggravation of systemic inflammatory response. At present, research on sepsis has reached the molecular level, and clinical treatment methods are becoming increasingly sophisticated. However, sepsis, septic shock, multiple organ dysfunction, and ultimately multiple organ failure remain the main causes of death in critically ill surgical patients. Therefore, animal models of abdominal infection established using this method, as well as animal models of multiple organ dysfunction and multiple organ failure replicated using other methods, still have many similarities with certain characteristics of human related diseases, and have great research and application value.