During injury, 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. Platelets, small colorless disk-shaped particles found in the blood of mammals that play an important role in the formation of blood clots, adhere to damaged endothelium to form platelet plug (primary hemostasis) and then degranulate. Platelets play one of the biggest factors in the hemostatic process. The platelet plug temporarily seals the break in the vessel wall. As platelets adhere to the collagen fibers of a wound they become spiked and much stickier (Figure 2).
When platelets stick together and to the proteins in the vessel walls, they degranulate (i.e. release the contents of their granules). A variety of substances that stimulate further platelet activation and enhance the hemostatic process are released, which include adenosine diphosphate (ADP Figure 1), serotonin, and thromboxane A2. These chemicals are released to cause more platelets to stick to the area and release their contents and enhance vascular spasms. As more chemicals are released more platelets stick and release their chemicals. This creates a stronger and bigger platelet plug – this process continues in a positive feedback loop. Platelets alone are responsible for stopping the bleeding of unnoticed wear and tear of our skin on a daily basis.
If the injury is small, a platelet plug may be able to form and close it within several seconds. If the platelet plug is not enough to stop the bleeding, the third stage of hemostasis begins: the formation of a blood clot or coagulation, as discussed in the next section.