(1) Reproduction method (1) Adult dogs, subcutaneously inject 2% mercury solution from the abdomen, the injection volume is 20 mg/kg body weight. Toxic tubular necrosis can occur 1-2 hours after injection. (2) 48 hours before the experiment, adult rats were injected subcutaneously with 1% mercury solution at a dose of 5 mg/kg body weight, and then intramuscularly injected with 1% mercury solution at a dose of 12 mg/kg body weight. Acute toxic renal tubular necrosis may occur. (3) Adult mice are injected subcutaneously with 1% mercury solution at a dose of 6 to 15 mg/kg body weight. About 4 hours after injection of mercury solution, mice will develop acute toxic kidney disease. ④In New Zealand adult rabbits, subcutaneous injection of 0.75 to 0.80 ml/dose of 1% mercury solution once a day for 5 consecutive days may cause acute toxic renal tubular necrosis in rabbits.
(2) Model features This method is used to replicate necrotizing nephropathy models. Animals may exhibit polyuria and decreased relative urine density in the early stages, but then all people may develop increased relative urine density, oliguria or anuria. For example, 1-2 hours after the mercury solution is injected, the urine volume of the test dog will increase sharply, and the maximum urine volume may be 5-10 times higher than before the test. A few hours after the test, the dog's urine output began to decrease, until the second day of modeling, it may develop oliguria or anuria, and a small amount of protein was found in the urine. Large animals still show general clinical symptoms of mercury poisoning and die within 3 to 10 days after injection of mercury solution. After the death of the model animal, pathological anatomy showed that the kidney was enlarged, the capsule was hard and soft, the kidney was pale, and there were a large number of bleeding spots on the surface. In the kidney tissue under the light microscope, you can see partial or extensive necrosis and separation of the renal tubules (depending on the time of the pathological examination), but mainly the proximal tubule epithelial injury of the kidney.
(3) Comparative Medicine Necrosis Necrosis is a comprehensive clinical manifestation of the extensive destruction of renal tubular epithelial cells caused by various reasons and the main symptoms of oliguria, urethral obstruction and acute renal failure. There are many causes of disease. In addition to renal ischemia, kidney poisoning is also the main cause. The use of acute animal poisoning to replicate animal models of necrotizing nephropathy is a commonly used research method. Currently, there are many reasons for kidney poisoning, including heavy metals, drugs, chemicals, and toxins, but the modeling principles are basically the same. The main reason is that the flow of toxic substances increases the concentration of toxic substances. The degeneration and necrosis of renal tubular epithelium and proximal tubules are the most serious. However, in the animal model of necrotizing nephropathy replicated by this method (including other methods), the degree and extent of the lesion are closely related to the drug concentration, the number of doses and the maintenance time of the drug. In other words, early acute tubular epithelial degeneration and necrosis and decreased urine output can be reversed, but late tubular necrosis is irreversible, and eventually develops into renal failure, leading to animal death, which is one of them.