动物造模,效评价,肺心病 z-bio 2024-06-19 328

　　Method 1

　　1. Animal modeling material: Rabbits; Medication: 3% ferric chloride solution.

　　2. Modeling method: The animals in the modeling group were injected with 3% ferric chloride solution via the rabbit ear vein, starting at 0.5ml each time, three times a week, and gradually increasing to four times, with a total injection of 45-60ml. During the injection period, they were fed normally without any treatment.

　　3. Modeling principle: ferric chloride can increase blood viscosity, damage vascular intima, cause pulmonary arteriosclerosis, pulmonary hypertension caused by fibrosis, pulmonary heart disease, resulting in hypoxia, carbon dioxide retention, acidosis, etc., thus further damaging multiple organs such as heart, lung, liver, kidney, etc.

　　4. Changes in pulmonary artery pressure after modeling: The control group had systolic blood pressure of 12.88 ± 1.96, diastolic blood pressure of 5.88 ± 3.18, and average blood pressure of 9.38 ± 1.51; The systolic blood pressure in the model group was 25.11 ± 6.95, the diastolic blood pressure was 11.58 ± 7.10, and the average blood pressure was 18.31 ± 4.52. The pulmonary artery pressure in the model group was significantly higher than that in the control group. Blood gas analysis showed that the pH of the control group was 7.32 ± 4.34, venous carbon dioxide pressure (PvCO2) was 27.9 ± 3.07, partial pressure of venous oxygen (PvO2) was 90.2 ± 10.51, BE was -9.67 ± 3.21, HCO3- was 14.23 ± 2.71, and SaO2 was 95.53 ± 1.308; The pH of the model group is 7.25 ± 0.18, PvCO2 is 44.05 ± 9.92, PvO2 is 45.53 ± 16.46, BE is -7.33 ± 7.0, HCO3- is 18.73 ± 3.72, and SaO2 is 64.87 ± 21.74.

　　Method 2

　　1. Animal modeling materials: Healthy Japanese large eared rabbits, regardless of gender, weighing 2000-2500g, 3 months old; Medication: 1% ferric chloride solution.

　　2. Modeling method: The modeling group was injected with a 1% mass fraction of ferric chloride solution through the vein of the rabbit ear margin. From week 1 to 4, 0.5 ml of ferric chloride solution was injected twice a week; Twice a week from the 5th to the 6th week, 0.75ml each time; Four times a week in the seventh week, 1ml each time.

　　3. Modeling principle: ferric chloride can increase blood viscosity, damage vascular intima, cause pulmonary arteriosclerosis, pulmonary hypertension caused by fibrosis, pulmonary heart disease, resulting in hypoxia, carbon dioxide retention, acidosis, etc., thus further damaging multiple organs such as heart, lung, liver, kidney, etc.

　　4. Observation of changes after modeling under light microscopy: The tissue structure of the heart, lungs, liver, and kidney in the normal group was normal. Model group with myocardial edema and necrosis; Thickening of pulmonary artery wall and proliferation of collagen fibers; Severe edema of liver cells with punctate necrosis; Glomerular congestion, renal tubular cell swelling, renal interstitial congestion. Electron microscopy observation results: The ultrastructure of the heart, lungs, liver, and kidneys in the normal group was normal. The myocardial fibers in the model group showed large contraction bands and mitochondrial pyknosis; Significant thickening of alveolar walls, proliferation of fibrous connective tissue, partial occlusion of capillary lumens, and proliferation of fibrous connective tissue in the smooth muscle interstitium of pulmonary arterioles; Hepatocellular edema, partial mitochondrial condensation, fibrosis between liver lobules, and infiltration of interstitial lymphocytes; Glomerular fibrosis is evident, with membrane bodies visible in some renal tubular lumens.

　　45 days after injection, the incidence of pulmonary heart disease in rabbits was over 50%.

　　On the basis of low-dose ferric chloride, nebulization with 0.1% cadmium chloride physiological saline solution for 10 consecutive days resulted in a pulmonary heart disease formation rate of 45.5%. Its pathological changes are similar to human pulmonary heart disease.