1. Animal modeling materials: Rabbits, weighing 2.5-30kg, regardless of gender; Medications: Ethyl carbamate, heparin. Oleic acid.
2. The modeling method involves intravenous anesthesia with ethyl carbamate (1g/kg) and systemic heparinization after tracheal intubation. Insert a catheter into the right common carotid artery for blood sampling. Control group: Intravenous injection of physiological saline (0.12mg/kg). Model group: Intravenous injection of oleic acid (0.12mg/kg).
3. Modeling principle: Oleic acid causes pulmonary edema in animals.
4. Changes after modeling: The modeling group [lung coefficient (1.17 ± 0.12), lung wet weight/lung dry weight ratio (6.81 ± 2.38), and lung water content (85.3 ± 1.64)%] showed a significant increase compared to the control group [lung coefficient (0.44 ± 0.07), lung wet weight/lung dry weight ratio (4.86 ± 0.5), and lung water content (79.3 ± 1.8)%].
Visual observation: The entire lungs of the modeling group showed enlargement, swelling, and blood stasis. Pink foam overflows from the cut surface and trachea. Light microscopy: The lung tissue of the modeling group showed acute diffuse inflammatory changes and local necrosis, with neutrophil infiltration mainly in the alveolar cavity, as well as red blood cells, cellulose, and mucus. Pulmonary interstitial exudation and bleeding. Arteries show acute inflammatory changes. Electron microscopy: In the modeling group, the alveolar cavity, the space between capillaries and basement membrane, as well as the alveolar epithelial cells and their interstitium, are filled with edema fluid. The tight connections between endothelial cells in blood vessels show cracks, and the capillary lumen widens. Red blood cell aggregation. The endoplasmic reticulum of alveolar epithelial cells expands, the perinuclear space increases, and mitochondria swell. The control group showed no abnormalities in lung morphology.