Anticoagulant and antiplatelet drugs

Anticoagulants can reduce blood coagulation, thereby preventing thrombosis or expanding drugs. Blood coagulation in the body depends on the function of blood vessels, platelets and coagulation system, and it is a complex chain reaction of proteolytic activation with the participation of various coagulation factors. Anticoagulant drugs exert anticoagulant effects by interfering with different aspects of the blood coagulation process or inhibiting a certain coagulation factor. Commonly used are heparin and vitamin K antagonist warfarin, dicoumarol and the like. Heparin works by interfering with multiple steps in the anticoagulant process. It is effective both in vivo and in vitro. Anticoagulant action occurs almost immediately after intravenous injection, which is characterized by prolonged clotting time, thrombin time and prothrombin time. . Vitamin K antagonists are indirect anticoagulants that primarily interfere with the synthesis of precursor proteins that are dependent on vitamin K-containing coagulation factors II, VII, IV, and X, and have no effect on the various coagulation factors that have been formed. Its advantages are effective oral administration and long duration of action. Anticoagulants can be used for thromboembolic diseases to prevent the formation and expansion of blood clots. Also used for disseminated intravascular coagulation, cardiovascular surgery, extracorporeal circulation, cardiac catheterization, and hemodialysis. Heparin is also used for anticoagulation in vitro, such as blood preservation and blood test specimens. Adverse reactions are mainly bleeding tendency (injectable with special antidote protamine) and allergic reactions. It should be avoided in certain blood system diseases, intracranial hemorrhage, active tuberculosis, peptic ulcer, and severe hypertension. . An antiplatelet agent that inhibits the function of platelets to inhibit platelet thrombosis. It is generally believed that platelets have multiple functions such as adhesion, aggregation, and dilution. When the blood vessel wall is damaged, the platelets may adhere to the blood vessel wall due to the exposure of collagen, and are activated by different biological factors to release various active substances and aggregate with each other to form platelet thrombus. The latter plays an important role in coronary heart disease and atherosclerosis. The anti-platelet drugs that emerged in the 1970s have attracted attention in the prevention and treatment of cardiovascular diseases, and have received increasing clinical attention. They have been widely used to prevent and treat ischemic cardiovascular and cerebrovascular diseases, atherosclerosis, and heart disease. Valve replacement, coronary artery bypass grafting, and arterial thrombosis caused by rejection after organ transplantation. Commonly used drugs are aspirin, persantin, sulfinpyrazone, dextran, prostacyction, and ticlo-pidine. Some of these drugs exert anti-platelet effects by activating platelet adenylate cyclase or inhibiting phosphodiesterase to increase the concentration of adenylate cyclase (cAMP) in platelets; some inhibit platelet adhesion. It affects the function of platelets in the damaged blood vessel wall or inhibits the release of platelets. Arterial thrombosis can be prevented by these routes. However, since anti-platelet drugs may have a bleeding tendency, those who have bleeding tendency are not suitable for use. Long-term medication should be monitored regularly for blood rheology parameters.