动物造模,高血压肾阴虚证 zi-bio 2024-05-17 783

　　(1) Reproduction method: Adult rats were subjected to nephrectomy on one side and ligation of 2/3 of the renal artery on the other side. The tail artery blood pressure of the rats was measured 2 weeks after surgery, and those with systolic blood pressure>140mmHg (18.6kPa) were identified as hypertensive rats. Animals were euthanized at 4 time points 2 weeks, 1 month, 2 months, and 4 months postoperatively. Before euthanasia, 24-hour urine was collected and 24-hour urine protein levels were measured; Then perform cardiac blood collection to measure blood creatinine and urea nitrogen concentrations; Euthanize the animal and immediately remove the kidney, prepare a histopathological sample, and observe relevant indicators.

　　(2) Model characteristics: The blood pressure of experimental animals increased 2 weeks, 1 month, 2 months, and 4 months after surgery. At 2 and 4 months after surgery, blood creatinine, urea nitrogen concentration, and 24-hour urine protein level significantly increased, indicating serious renal function damage. One month after surgery, the glomerular capillary basement membrane (GBM) of animals slightly thickened, with focal mesangial cell proliferation and increased mesangial matrix. Two months after the operation, the mesangial matrix increased significantly, especially the blood vessels. The deposition of PAS positive substances and foam like changes were seen. The number of mesangial cells increased significantly, and crescent formation was seen in some cases. At 4 months, the number of sclerotic glomeruli increases, and glassy deposits with strong PAS staining can be seen along the vascular wall, while GBM significantly thickens. Ordinary electron microscopy shows that the mesangial area of the animal's glomerulus widens 2 weeks after surgery, with a tendency to increase the matrix. At 1 month after surgery, the mesangial matrix increases, the number of cells increases, and there is edema under the endothelial cells. The thickness of the basement membrane varies. At 2 months of disease, the basement membrane generally thickens. At 4 months after surgery, the inner skin cells become edematous and degenerate, the endothelial cell pores open, and the mesangial matrix significantly increases and hardens, with proliferation of basement membrane like substances and dense deposits, resulting in significant widening of the mesangial area. The basement membrane thickens significantly, forming small mound like protrusions towards the epithelial side, and foot process fusion can be seen. GBM significantly increased in hypertensive rats at 2 and 4 months postoperatively. Histochemical electron microscopy shows that the size of the loose layer outside the GBM of normal animals is consistent, with PEI stained particles arranged in a more regular manner (this is the location where negative charge sites exist). There is a significant increase in PEI stained particles at the junction of the basement membrane, and there are also a small number of PEI stained particles with shallow staining, inconsistent size, and irregular arrangement in the loose layer inside the basement membrane. PEI stained particles on GBM are numerous and dense. Scattered PEI stained particles can also be seen in the glomerular mesangial matrix. As the disease progresses, the number of PEI stained particles gradually decreases in model animals. After 4 months of surgery in the model animal, the number of PEI stained particles in the outer loose layer of GBM decreased significantly, with sparse arrangement and irregular arrangement caused by particle loss. The polyimide (PEI) staining particles in the glomerular mesangial matrix also gradually decrease with the progression of the disease.

　　(3) The theoretical basis of the comparative medicine model is mainly that hypertension usually presents with the syndrome of kidney yin deficiency and internal heat. This model is effective with nourishing kidney yin formula, but worsens its condition with warming kidney yang formula. Traditional Chinese medicine syndrome differentiation in clinical hypertension is often characterized by liver kidney yin deficiency syndrome or liver yang hyperactivity syndrome. This method simulates the pathogenesis of hypertension and replicates the hypertension disease model. However, whether the syndrome characteristics belong to simple kidney yin deficiency syndrome needs further evaluation, and it is difficult to determine based solely on the experimental results mentioned above.