As discussed earlier, a break in the vessel endothelium exposes collagen and the vessel's subendothelial surface. Ruptured endothelial cells leak ADP and Serotonin, the chemical triggers that induce platelet adhesion, the next step in the sequence of hemostatic events. Circulating platelets are drawn to the area by those liberated chemical signals and begin to physically attach themselves to the rough, damaged surfaces of the breach, a process known as platelet adhesion.
As platelets continue to arrive and bind to the exposed collagen and basement membrane, a rudimentary barrier begins to form, as the platelets themselves serve to fill in the breached vessel wall. Once platelets begin to adhere to exposed surfaces, chemical signals activate changes in the shape of the platelets from discoid to a spiny sphere, which promotes platelets to adhere to one another, not just the damaged vessel endothelium. The process by which platelets bind to one another is called platelet aggregation and is vital because it allows for a platelet plug to be formed.
The platelet plug is the structure responsible for plugging the hole in the vessel wall.
