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Hemostasis is the natural process of stopping blood flow or loss of blood during an injury (hemo = blood; stasis = standing). During hemostasis, blood will change from a liquid to a solid state.
MECHANICS OF HEMOSTATIS
Hemostasis includes three steps that occur in a rapid sequence: (1) vascular spasm, vasoconstriction , or intense contraction of blood vessels; (2) formation of a platelet plug; and (3) blood clotting or coagulation, which reinforces the platelet plug with fibrin threads that act as a "molecular glue". Once the flow of blood has been stopped, tissue repair can begin.
Angiogenesis Generates New Blood Vessels
Blood vessel with an erythrocyte (red blood cell) within its lumen, endothelial cells forming its tunica intima or inner layer, and pericytes forming its tunica adventitia (outer layer).
Intact blood vessels are central to moderating blood's tendency to clot. The endothelial cells of intact vessels prevent blood clotting with a heparin-like molecule and thrombomodulin and prevent platelet aggregation with nitric oxide and prostacyclin. When endothelial injury occurs, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete von Willebrand factor, which initiates the maintenance of hemostasis after injury.
FORMATION OF A PLATELET PLUG
Platelets are a large factor in the hemostatic process. They allow for the creation of the "platelet plug" that forms almost directly after a blood vessel has been ruptured. Within twenty seconds of an injury, resulting in the blood vessel's epithelial wall being disrupted, coagulation is initiated. It takes approximately sixty seconds until the first fibrin strands begin to intersperse among the wound. After several minutes, the platelet plug is completely formed by fibrin.
Contrary to popular belief, clotting of a cut on the skin is not initiated by air or drying out, but by platelets adhering to and being activated by collagen in the blood vessels' endothelium. The activated platelets then release the contents of their granules, which contain a variety of substances that stimulate further platelet activation and enhance the hemostatic process.
When the lining of a blood vessel breaks and endothelial cells are damaged, revealing collagen proteins in the vessel wall, platelets swell, grow spiky extensions, and start clumping together. They start to stick to each other and the walls of the vessel. This continues as more platelets congregate and undergo these same transformations. This process results in a platelet plug that seals the injured area. If the injury is small, the platelet plug may be able to form and close it within several seconds.
FORMATION OF A BLOOD CLOT
If the platelet plug is not enough to stop the bleeding, the third stage of hemostasis begins: the formation of a blood clot. Platelets contain secretory granules. When they stick to the proteins in the vessel walls, they degranulate, thus releasing their products, which include ADP (adenosine diphosphate), serotonin, and thromboxane A2.
First, blood changes from a liquid to a gel. At least 12 substances called clotting factors take part in a series of chemical reactions that eventually create a mesh of protein fibers within the blood. Each of the clotting factors has a very specific function. We will discuss just three of these substances: prothrombin, thrombin, and fibrinogen. Prothrombin and fibrinogen are proteins that are produced and deposited in the blood by the liver.
When blood vessels are damaged, vessels and nearby platelets are stimulated to release a substance called prothrombin activator, which in turn activates the conversion of prothrombin, a plasma protein, into an enzyme called thrombin. This reaction requires calciumions. Thrombin facilitates the conversion of a soluble plasma protein called fibrinogen into long, insoluble fibers or threads of the protein, fibrin. Fibrin threads wind around the platelet plug at the damaged area of the blood vessel, forming an interlocking network of fibers and a framework for the clot. This net of fibers traps and helps hold platelets, blood cells, and other molecules tight to the site of injury, functioning as the initial clot. This temporary fibrin clot can form in less than a minute, and usually does a good job of reducing the blood flow.
Next, platelets in the clot begin to shrink, tightening the clot and drawing together the vessel walls. Usually, this whole process of clot formation and tightening takes less than a half hour.
The use of adsorbent chemicals, such as zeolites, and other hemostatic agents, are also being explored for use in sealing severe injuries quickly.
Microvessel showing an erythrocyte (E), a tunica intima of endothelial cells, and a tunica adventitia of pericytes.
stopping blood flow or loss from injury, intensely contracting a blood vessel, forming a plug, clotting blood to reinforce plug, changing blood from liquid to gel to solid, and keeping blood flow in equilibrium