The liver receives 75% of its blood from the portal vein. The portal vein is formed by the confluence of the superior mesenteric vein and the splenic vein and begins in the capillaries of the stomach, intestines, spleen, pancreas and other viscera and ends in the hepatic blood sinuses. The portal vein normally maintains a proper pressure, too low affects the blood supply to the liver, and an increase is known as portal hypertension. Post-hepatitis cirrhosis is the most common cause of portal hypertension. Chronic hepatitis that is not treated effectively can lead to liver fibrosis and eventually to cirrhosis. In cirrhosis, the liver lobules become fibrotic, the liver parenchyma becomes stiff, the resistance in the liver sinusoids increases, the main and terminal branches of the intrahepatic vascular system (hepatic artery, hepatic vein, portal vein and lymphatic vessels) become thin, twisted and stiff, the resistance to blood flow in the lumen increases, and the portal vein pressure rises and gradually increases. If the portal vein pressure continues to rise, esophagogastric varices, splenomegaly and hypersplenism will inevitably occur. Further development of the disease will lead to primary peritonitis, recurrent ascites or intractable ascites, and even ruptured hemorrhage of esophagogastric varices and hepatic encephalopathy, endangering the life of patients. There are many treatment measures for portal hypertension, but early treatment should be mainly internal medicine, not rash surgery. In the early stage of the disease, the degree of cirrhosis is not serious, the portal vein pressure is slightly higher than normal, and there are usually no serious complications such as splenomegaly and esophagogastric fundic varices. The main measures are to treat the underlying liver disease, including antiviral, anti-inflammatory and liver preservation, and prevention and control of liver fibrosis. Once the liver inflammation is controlled and the disease no longer progresses, the portal hypertension will be relieved. If the portal vein pressure is indeed too high, targeted drug therapy may be given. Pharmacological treatment of portal hypertension focuses on the treatment of bleeding esophageal varices and the prevention of rebleeding. The medications work by reducing the pressure in the portal and variceal veins, thus decreasing the tension in the vessel walls of the varices. Current medications for the treatment of portal hypertension work primarily to regulate excessive visceral circulation, with vasoconstrictors reducing portal pressure by decreasing visceral arterial flow and vasodilators reducing portal pressure by decreasing intrahepatic and extrahepatic resistance. Commonly used vasoconstrictors include vasopressin and its analogs, growth inhibitors and their analogs, and adrenergic receptor blockers. Vasopressin and its analogues are mostly used in combination with nitroglycerin, mainly for the treatment of ruptured esophageal variceal bleeding. Growth inhibitors and their analogues include Stanozolol and Octreotide (also called Suntab), which have higher efficiency in controlling esophageal variceal bleeding and less side effects. The adrenergic receptor blockers, such as tretinoin and nadolol, are mostly used to prevent primary and reemergent bleeding in patients with varices, but the reduction of morbidity and mortality is not obvious. Commonly used vasodilators are nitrates, alpha-adrenergic receptor blockers, calcium channel blockers, etc. Nitrates are generally not used alone for acute variceal bleeding, nitroglycerin is mostly used in combination with vasopressin or insulin to reduce side effects and increase the efficacy. α-adrenergic receptor blockers such as phentolamine and prazosin can be used to prevent esophageal variceal bleeding, but they are relatively little used. Calcium channel blockers are mainly used to prevent primary and reemergence of variceal hemorrhage. Drug therapy for portal hypertension and its resulting upper gastrointestinal bleeding is effective, simple and easy to use, and suitable for long-term application. Surgical treatment should be chosen carefully, it mainly targets the serious complications of portal hypertension and cannot solve the problem of portal hypertension and esophageal varices, and may even aggravate the condition. The portal vein is an important channel through which blood from the gastrointestinal tract flows into the liver, and the various nutrients within the blood are the material basis for maintaining the normal function of the liver. The portal vein pressure is not as low as possible, but the proper pressure is maintained to ensure the blood flow to the liver. The increased portal pressure in cirrhosis is an important compensatory mechanism for the body to maintain portal venous perfusion. In this pathological state, maintaining a slightly higher than normal portal pressure is beneficial to the perfusion of the liver. Some patients underwent bypass surgery when the portal vein pressure was not excessively high, as a result of which the portal vein pressure was significantly reduced and the blood flow supply to the liver from the portal vein was drastically reduced, leading to a rapid deterioration of liver function. It is important to note that the use of drugs should also not excessively lower portal pressure, which can have equally serious consequences if it affects the blood supply to the liver. However, patients with advanced disease and others with indications for surgery should opt for surgical treatment in a timely manner and should not miss the opportunity.