(1) Model method Adult rats were anesthetized by intraperitoneal injection of ether or ketamine at a dose of 100 mg/kg body weight, fixed on their back, and opened abdomen along the transverse incision of the upper abdomen, and the blood vessels of the abdominal wall were cauterized to stop bleeding with an electrocoagulator. Expose the liver, cut off the falciform ligament, the coronary ligament and the interlobar ligament, expose the hepatic hilum, first ligate and cut the ventral bile duct of the scalp branch of the portal vein, expose the scalp branch of the portal vein and the accompanying hepatic artery, and ligate the scalp branch and the portal vein with 5-0 silk thread Accompanied by hepatic artery. Then carefully separate the branch of the right portal vein into the right upper and lower lobe and the accompanying hepatic artery, and ligate the right branch of the portal vein or the branch of the right upper lobe with 5-0 silk thread. It can be seen that the ligated liver lobe is in an ischemic state. Puncture the portal vein with a 5.5 gauge needle above the ligation line, and inject 10ml/kg body weight of 5% glucose sodium chloride solution or sodium lactate Ringer's solution until the liver leaves become white, and then quickly ligate with 5-0 silk thread to remove the liver. leaf. A total of 85%-95% of liver tissue was removed. After checking for no bleeding, suture the abdominal wall incision. The mental state, activity status, liver function changes and 12h survival rate of rats were observed after operation. After the operation, the rats were awakened and turned over as a sign of the successful operation. Those who were unable to wake up and stood up and died within 12 hours were considered to have failed the operation. Or healthy piglets are anesthetized by intraperitoneal injection of barbital sodium 30mg/kg body weight. The right upper limb is anesthetized, the right upper limb is established, the right upper limb is established, the nasal cannula is used for oxygen, and the supine is fixed. The upper abdominal median incision is used to enter the abdomen layer by layer, and the portal vein and right renal vein are freed. Inject 0.25 mg heparin into the portal vein, take a silicone plastic tube (length 15 cm, diameter 0.8 cm) filled with 2% heparin saline, and intubate it from the distal end of the free right renal vein to 2 to 3 cm into the inferior vena cava and fix it. One end was inserted about 1.5 cm from the proximal end of the portal vein to the distal end and fixed, then the bypass tube was opened, and the abdomen was closed after checking that there was no obvious bleeding. Two days later, a second-stage operation was performed. After entering the abdomen, all perihepatic ligaments (including the left and right triangular ligaments, coronary ligaments, sickle ligaments and hepatogastric ligaments) were cut off, the hepatic branch of the hepatic artery was sutured, and the hepatic artery and stomach were finally ligated. Diodenal artery caused complete blockage of human liver blood flow, and blood pressure was monitored by femoral artery catheterization. After 1, 4, and 7 hours after the blood flow into the liver was completely blocked, a small piece of liver tissue was removed and fixed with 10% formaldehyde and 0.25% glutaraldehyde, respectively. Then close the abdomen. During the operation, the experimental pigs were given 500ml of balanced saline and 800,000 U of penicillin intravenously. After death, they were autopsied and liver specimens were collected for examination. During the modeling process, the general condition and death time of the model animals can be dynamically observed. At the same time, whole blood is drawn to prepare serum for biochemical testing. After modeling, the animals were killed and their livers were taken for histomorphological examination.

　　(2) Model features Rats wake up quickly after surgery and can stand up and move around. However, liver failure appears after 1 to 2 hours. After 12 hours, liver coma appears one after another, which is manifested as listlessness, body curling up, erect rat hair, and reduced activity. Refusal to drink or eat, yellow urine. The 12-hour survival rate of the model animals that underwent 85% liver tissue resection was 93% and all died at 48 hours; the 12-hour survival rates of the model animals that underwent 95% liver tissue resection were 92%, 75%, 58%, and 50, respectively. %, all died in 24h. The model piglets died within 12 to 16 hours after the blood flow of the human liver was completely blocked. 12h after operation, the levels of alanine aminotransferase (ALT), blood ammonia (NH3), and total bilirubin (TBIL) increased, and the blood glucose (GLU) level decreased. After the hepatic blood flow of model piglets is blocked, alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), Amm, urea nitrogen (BUN), creatinine (CRE), Prothrombin time (PT) gradually increased, albumin (ALB) and fibrinogen (FIB) gradually decreased. When the rats were sacrificed 12 hours after the operation, the remaining liver tissue was dark red in color, the capsule was swollen, and the surface was oozing blood. Under the microscope, it can be seen that the structure of the liver lobules is destroyed, the hepatocytes are extensively degenerated and necrotic, the cytoplasm is loose, the necrotic area is infiltrated by inflammatory cells, the liver sinusoids are dilated, showing a mesh shape, and congestion and bleeding can be seen. One hour after the model piglet’s hepatic blood flow was completely blocked, the structure of liver lobules and the arrangement of hepatocytes were still normal, the Disch gap was slightly expanded, the liver cells were turbid and swollen, but the nuclear membrane and nucleoli were still clear; 4 hours later, it was visible under a light microscope The structure of liver lobules still exists, the arrangement of liver cells has not been disordered, the structure of the liver plate is present, the space between the livers is significantly enlarged, the central vein collapses, the intrahepatic vacuolar degeneration, the nucleus shrinks, and the nucleolus disappears; the cytoplasm can be seen under the electron microscope Glycogen granules are homogenized, rough endoplasmic reticulum is degranulated, mitochondrial edema, ridges are blurred, some mitochondria are dissolved, microvilli of bile ducts between cells are significantly reduced, nuclear chromatin accumulates, nuclear deformation, and nuclear pseudo-inclusion bodies form. The 7h posterior microscope showed that the structure of liver lobules was disordered, the arrangement of liver cells was disordered, the liver plate was dissociated, the Diel space was expanded more obviously, the turbid swelling and vacuolar degeneration in the liver cytoplasm were more pronounced, the nuclear chromatin was marginalized, and some liver cell membranes were not. Complete and showing signs of dissolution and necrosis. Upon death due to liver failure and immediate liver microscopy, it was found that the structure of the liver lobules of the model pigs was unrecognizable, hepatocytes were reduced, the arrangement was disordered, the liver plate was dissociated, and the Disch gap was dilated, and there were focal and spot-like extensive livers. Cell necrosis.

　　(3) Comparative Medicine Acute liver failure is a syndrome of diffuse hepatocyte necrosis and/or sudden severe damage to liver function caused by multiple factors. The fatality rate of patients can be as high as 75%. The etiology is mainly caused by hepatitis virus, and can also be caused by one-time or repeated trauma, overdose of drugs or poisons. At present, there are two main categories of acute liver failure animal models: surgical operation and drug-toxic liver injury. Among them, total liver or partial liver resection is the most classic and commonly used method of modeling. Total hepatectomy can undoubtedly lead to liver failure, but the characteristics of this model are far from the pathological process of clinical acute liver failure, such as irreversible disease course, short hepatic coma, and no damaged or dead liver cells in the circulation. As a result, the toxic substances continuously released and the abnormal liver function will only be manifested 2 to 4 hours before the death of the model animal. In view of these shortcomings, people have studied and established a partial hepatectomy acute liver failure animal model to replace it. Under normal circumstances, when the liver function is normal, the animal can tolerate liver resection of 70%-75% or less. If the liver resection exceeds 75%, fatal liver failure will occur. When the liver resection exceeds 85%, additional treatment is required. The door shunted into one cavity, and almost 100% of the animals died within 48 hours. This model underwent partial hepatectomy to remove 85%-95% of liver tissue. After 6 to 12 hours, the animal’s liver and kidney function was abnormal and progressively worsened, and hepatic coma appeared successively. Histomorphological examination showed that the structure of liver lobules Disorders, hepatocellular reduction, liver plate dissociation, and obvious dilation of Disse's space, extensive hepatocyte necrosis in focal and spot forms, and all animals died within 24 to 48 hours after surgery. Compared with the model of total hepatectomy, partial hepatectomy has physiological and pathological characteristics closer to the clinic and may be reversed. For example, for 90% hepatectomy rats, intrasplenic transplantation of hepatocytes for 3 consecutive days before surgery, the survival period of 40% models can exceed 28 days. So far, people have successfully replicated and established a variety of animal partial hepatectomy models, such as rats, rabbits, dogs and pigs. Among them, small animal models are more suitable for studying the pathophysiological process of acute liver failure and the influence of drug interference on the process, while large animal models are more accustomed to evaluating the efficacy and safety of artificial liver technology. The animal model of liver failure by subtotal hepatectomy has its unique advantages. The replication cycle is short, the liver resection can be quantified, and the remaining liver tissue has no specific pathological changes. The animal symptoms and related blood index changes are consistent with the clinical manifestations of liver failure. The model is repeatable and reliable. Good stability and high success rate.