1. Animal modeling materials: Healthy Wistar rats, weighing 70-100g, regardless of gender; Medication: Lipopolysaccharides.
2. Method of modeling: The model group animals were intraperitoneally injected with 100mg/kg of lipopolysaccharide (LPS), while the control group animals were intraperitoneally injected with 1mg/kg of physiological saline.
3. Modeling principle: Lipopolysaccharides cause brain edema in animals.
4. Changes after modeling: Starting from 2 hours after intraperitoneal administration of lipopolysaccharide, the water content of the brain tissue in the modeling group significantly increased, especially at 6 and 12 hours; The EB content in brain tissue significantly increased, reaching its peak at 6 hours and lasting for 24 hours.
Capillary changes: After 6 hours of modeling, the glial protrusions around the capillaries showed slight swelling, some showed vacuolar like changes, and the swallowing vesicles were already abundant; 12 hours after modeling, endothelial cells degenerated, cytoplasmic vacuoles changed, basement membrane disappeared, and glial cell protrusions around capillaries showed severe edema.
Neurocyte degeneration changes: nucleoli disappear, chromatin is sparse, rough endoplasmic reticulum is degranulated, line stereopsis is blurry, cristae are disordered, swelling appears as vesicles, Golgi apparatus expands like vesicles, a large number of vacuolar structures appear around the cell body, high-density electronic fragments appear around the nerve felt, indicating protrusions, swelling, and degeneration appear as vacuoles.
Glial cell degeneration changes: 6 hours after modeling, the cytoplasm swells, the cell body is transparent, the organelles disperse, and the protrusions around the glial cells swell; After 12 hours of modeling, there was severe edema and vacuolization around the glial cells.