Hemostasis: Stop bleeding. When the continuity of the vessel wall is interrupted, the following four events can prevent further bleeding: vasoconstriction, platelet thrombosis, blood clotting, and mechanization.
After the continuity of the vascular wall is interrupted, the damaged part and its nearby blood vessels immediately contract, which can immediately reduce the blood flow; if the damaged mouth is not large, the bleeding process can be directly terminated. The mechanisms that mediate vasoconstriction are:
Mechanical stimulation directly leads to smooth muscle contracture of the vessel wall.
Neuroreflexion: The nerve endings of damaged blood vessels and surrounding tissues are impulsive, forming a reflex arc through pain fibers or other sensory fibers.
Peripheral damaged tissue and activated platelets release vasoconstrictor substances such as thromboxane A2.
2. Platelet thrombosis
Impaired continuity of the vessel wall will result in collagen exposure and exposed collagen activates platelets. Subsequently, platelets appear adhesion, aggregation, and release reactions, which can form platelet thrombus. At this point, the first phase of hemostasis is completed. Although the platelet thrombus is very soft, it also plays a role in limiting blood flow velocity and reducing the amount of bleeding in the early stage of bleeding, and creates conditions for the blood coagulation mechanism to be started. For small blood vessel damage, the whole hemostasis process can be completed by platelet thrombosis alone. In fact, the body has many spontaneous small blood vessel breakages every day. Therefore, under normal circumstances, platelet thrombosis also has the effect of repairing the blood vessel wall.
After the vascular endothelium is damaged, the tissue factor and collagen underneath it are exposed, and the exogenous and endogenous pathways can be activated, respectively, to initiate the coagulation mechanism. In addition, activated platelets also initiate blood clotting mechanisms by releasing multiple substances and accelerate the clotting process. The final product of the coagulation mechanism is fibrin, which forms a strong blood clot. At this point, complete the second phase of hemostasis.
Shortly after the hemostasis mechanism was initiated, the fibrinolysis mechanism was also activated, slowly dissolving the formed blood clots; the fibroblasts were gradually moved into the blood clots, and the blood clots were replaced by fibrous connective tissue to complete the repair.
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