动物造模,药效评价,急性肺损伤 z-bio 2024-07-23 390

　　1. Modeling material animals: SD rats, male or female, weighing 250-350g; Drug: Ketamine hydrochloride; Instruments: syringes, surgical instruments.

　　2. Modeling method: 12 hours before the start of the experiment, the rats in the modeling group were fasted and not allowed to drink water. After intraperitoneal injection of 100mg/kg ketamine hydrochloride anesthesia, cecal ligation and perforation were performed in the abdomen to cause abdominal infection. The control group rats were anesthetized and only underwent open abdominal treatment. During the experiment, each group of rats was housed in clean grade rack style cages and fed with free drinking water and full nutrient pellet feed.

　　3. Modeling principle: Abdominal infection is a common clinical disease in surgery, which can easily lead to acute lung injury in severe cases.

　　4. Changes after modeling: Before the experiment, the animals were breathing steadily in a resting state with a respiratory rate of 40-60 breaths per minute. After modeling, the model showed rapid breathing at 24 and 48 hours, with an increase in respiratory rate of 90-100 breaths per minute and mild cyanosis.

　　The pulmonary capillary permeability of the model rats was significantly increased. The percentage of neutrophils in the model rats (21.00 ± 4.37)% was significantly higher than that in the normal control group (4.00 ± 1.41)%. There was no significant difference in lymphocyte percentage among the groups. The percentage of macrophages in the modeling group (69.4 ± 5.34)% was significantly lower than that in the control group (87.3 ± 2.31)%. The lung wet/dry weight ratio of the model rats significantly increased to (5.65 ± 0.73)%, while that of the control group was (3.92 ± 0.76)%.

　　The control group had uniform color of lung tissue, smooth capsule, white with a slight pink tint, and soft and elastic tissue. The lung tissue of the model is significantly swollen, appearing dark red, with patchy bruising and bleeding visible on some surfaces. Under light microscopy, there was no edema in the lung interstitium of the control group, and no inflammatory cell infiltration was observed in the lung interstitium and alveoli. There is inflammatory cell infiltration and significant pulmonary hemorrhage in the interstitial edema of the model lung. Visible atelectasis and inflammatory exudation within the alveoli. Electron microscopy observation showed that the structure of alveolar type I and II cells in the control group rats was intact, with normal endothelial cells in the alveolar walls and occasional presence of several normal red blood cells in the capillary lumen. Model rats showed interstitial and alveolar edema in the lungs, with white blood cells containing a large number of electron dense lysosomal particles filling the pulmonary capillary lumen. The white blood cells swelled and deformed, with unclear cell membranes. There were more microvilli in the cytoplasm of alveolar epithelial cells, mitochondrial swelling, more microvilli in the cytoplasm of pulmonary endothelial cells, and more severe perivascular edema.