In an injured blood vessel, the platelet phase – which overlaps with the vascular phase – begins about 15-20 seconds after the onset of vascular spasm. As the blood vessel constricts, the damaged endothelial cells contract on the basement membrane. As a result, the collagen fibers in the underlying connective tissue are used for adhesion of the circulating platelets. The von Willebrand factor, a large plasma protein, stabilizes the platelet-collagen association. Once adhered, the platelets activate and develop cytoplasmic processes that extend toward nearby platelets. The activated platelets become stickier and release chemical messengers like adenosine diphosphate or ADP, calcium, serotonin, and thromboxane. ADP aggregates more platelets to stick to the damaged endothelium, while serotonin and thromboxane promote further vascular spasm. As more platelets arrive, they release more chemical messengers, stimulating further aggregation. The platelets aggregate to form a plug within a minute of injury, which, along with vascular spasm, controls blood loss. Later, this plug is converted into a more permanent clot.