Physiological hemostasis is one of the important protective mechanisms of the body. When a blood vessel is damaged, on the one hand, it is required to form a hemostatic plug quickly to avoid blood loss; on the other hand, it is necessary to limit the hemostatic response to the damaged part and maintain the fluid state of the blood in the systemic blood vessels. Therefore, physiological hemostasis is the result of a variety of factors and mechanisms interacting to maintain a precise balance. Clinically, small needles are often used to puncture the earlobe or fingertips to allow the blood to flow out naturally, and then measure the duration of bleeding. This period is called bleeding time (bleeding time), and normal people do not exceed 9 minutes (template method). The length of bleeding time can reflect the state of physiological hemostatic function. When the physiological hemostatic function is weakened, hemorrhage tends to occur, and hemorrhagic diseases occur; while the overactivation of the physiological hemostatic function can lead to pathological thrombosis.

Basic process of physiological hemostasis
The physiological hemostasis process mainly includes three processes: vasoconstriction, platelet thrombus formation and blood coagulation.

1 Vasoconstriction Physiological hemostasis is firstly manifested as the contraction of the damaged blood vessel and nearby small blood vessels, which reduces the local blood flow and is beneficial to reduce or prevent bleeding. The causes of vasoconstriction include the following three aspects: ① Injury stimulus reflex causes vasoconstriction; ② Damage to the vascular wall causes local vascular myogenic contraction; ③ Platelets adhering to the injury release 5-HT, TXA₂, etc. to constrict blood vessels. substances that cause vasoconstriction.

2 Formation of platelet-wise hemostatic thrombus After blood vessel injury, due to the exposure of subendothelial collagen, a small amount of platelets adhere to the subendothelial collagen within 1-2 seconds, which is the first step in the formation of hemostatic thrombus. Through the adhesion of platelets, the injury site can be "identified", so that the hemostatic plug can be positioned correctly. Adhered platelets further activate platelet signaling pathways to activate platelets and release endogenous ADP and TXA₂, which in turn activate other platelets in the blood, recruit more platelets to adhere to each other and cause irreversible aggregation; local damaged red blood cells release ADP and local The thrombin generated during the coagulation process can make the platelets flowing near the wound continuously adhere and gather on the platelets that have been adhered and fixed to the subendothelial collagen, and finally form a platelet hemostatic plug to block the wound and achieve preliminary hemostasis, also known as primary hemostasis (irsthemostasis). Primary hemostasis mainly depends on vasoconstriction and the formation of platelet hemostatic plug. In addition, the reduction of PGI₂ and NO production in the damaged vascular endothelium is also beneficial to the aggregation of platelets.

3 Blood coagulation Damaged blood vessels can also activate the blood coagulation system, and local blood coagulation occurs rapidly, so that the soluble fibrinogen in the plasma is converted into insoluble fibrin, and interwoven into a network to strengthen the hemostatic plug, which is called secondary hemostasis (secondary hemostasis) hemostasis) (Figure 3-6). Finally, the local fibrous tissue proliferates and grows into a blood clot to achieve permanent hemostasis.

Physiological hemostasis is divided into three processes: vasoconstriction, platelet thrombus formation, and blood coagulation, but these three processes occur successively and overlap each other, and are closely related to each other. Platelet adhesion is easy to achieve only when the blood flow is slowed down by vasoconstriction; S-HT and TXA2 released after platelet activation can promote vasoconstriction. Activated platelets provide a phospholipid surface for the activation of coagulation factors during blood coagulation. There are many coagulation factors bound to the surface of platelets, and platelets can also release coagulation factors such as fibrinogen, thereby greatly accelerating the coagulation process. The thrombin produced during blood coagulation can strengthen the activation of platelets. In addition, the contraction of platelets in the blood clot can cause the blood clot to retract and squeeze out the serum in it, making the blood clot more solid and firmly sealing the opening of the blood vessel. Therefore, the three processes of physiological hemostasis promote each other, so that physiological hemostasis can be carried out in a timely and rapid manner. Because platelets are closely related to the three links in the physiological hemostasis process, platelets play an extremely important role in the physiological hemostasis process. Bleeding time is prolonged when platelets are reduced or function is reduced.