Modeling experiments in animal models of acute respiratory distress syndrome
Modeling experiments in animal models of acute respiratory distress syndrome
Acute respiratory distress syndrome (acute respiratory distress syndrome, ARDS) is an acute respiratory failure caused by increased permeability of alveolar capillary membranes, caused by a variety of reasons, characterized by non-cardiogenic pulmonary edema and intractable hypoxemia. The diagnostic criteria for ARDS are: (1) acute onset, respiratory frequency (>28 breaths/min) or respiratory distress; (2) partial pressure of arterial oxygen/oxygen concentration (PO2/FiO2) <26.7 kPa (with or without positive end-expiratory pressure (PEP) ventilation); (3) infiltration of both lungs on X-ray chest radiographs; and (4) pulmonary artery wedge pressure (Paw) ≤2.4 kPa, or no clinical evidence of left atrial hypertension. At present, the morbidity and mortality rate of ARDS is still as high as 50%～70%, among which the morbidity and mortality rate of ARDS caused by infectious shock and sepsis are the highest. Currently, there are 2 main methods for modeling ARDS: endotoxin injection and ARDS caused by oleic acid.
Principle
The basic principle of endotoxin injection to construct an animal model of acute respiratory distress syndrome is that endotoxin can cause damage to the alveolar capillary wall, causing pulmonary edema.
Microthrombosis caused by fibrin, platelet and leukocyte aggregation, increase in pulmonary arterial pressure, release of vasoactive substances from aggregated platelets, and aggregation of neutrophils by complement activation may be involved in this change.
Operation method
Construction of an animal model of acute respiratory distress syndrome by endotoxin injection (Modeling experiments on animal models of acute respiratory distress syndrome)
Principle
The basic principle of endotoxin injection to construct an animal model of acute respiratory distress syndrome is that endotoxin can cause damage to the alveolar capillary wall, causing pulmonary edema. Microthrombosis caused by fibrin, platelet and leukocyte aggregation, increase in pulmonary arterial pressure, release of vasoactive substances from aggregated platelets, and aggregation of neutrophils by complement activation may be involved in this change.
Materials and Instruments
Equipment: Move The basic process of constructing an animal model of acute respiratory distress syndrome by endotoxin injection can be divided into the following steps:A. Rabbit, rat, dog: Domestic or imported Escherichia coli endotoxin, diluted in saline, is injected slowly intravenously. For rabbits (about 2.5 kg), use 0.6-0.8 mg/kg of endotoxin; for rats (about 250 g), use 1 mg/kg of endotoxin; for dogs (18-23 kg), use 1.5 mg/kg of endotoxin.B. After intravenous injection of endotoxin, within 4 hours, the animals showed frequent respiration, the pressure dropped to 70% of the pre-injury level, or increased and then decreased, the pulmonary artery pressure increased, the platelet and leukocyte counts decreased gradually within 4 hours, and the decrease of leukocytes was especially obvious.C. Decrease to about 1/3 of the pre-injection level for 6 hours. Tissue sections showed congestion, edema and hemorrhage in the interstitium of the lungs, aggregation of neutrophils in the pulmonary capillaries, and deposition of fibrin. Electron microscopy showed that type I and type II alveolar epithelial cells were damaged, and the number of vacuoles in vascular endothelial cells increased. For more product details, please visit Aladdin Scientific website.
① Syringe;
② Electron microscope;
③ Rabbit/rat/dog, etc.
Reagents:
① Escherichia coli endotoxin;
① Physiological saline.