22.20:

Formation of the Platelet Plug

JoVE Core
Anatomy and Physiology
A subscription to JoVE is required to view this content.  Sign in or start your free trial.
JoVE Core Anatomy and Physiology
Formation of the Platelet Plug

124 Views

01:22 min

July 18, 2024

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.

As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets circulating in the blood adhere to these exposed collagen fibers at the injury site.

A crucial plasma protein called the von Willebrand factor plays a pivotal role in stabilizing the bond between platelets and collagen fibers, ensuring steadfast attachment of platelets to the injury site.

Once adhered, platelets activate and become more adhesive. They release substances, such as Adenosine Diphosphate (ADP), serotonin, and thromboxane A2, which attract more platelets to the site and further promote vascular spasm. This platelet aggregation process culminates in forming a platelet plug within a minute of the injury. This plug collaborates with the vascular spasm to effectively control blood loss.

The platelet phase of hemostasis plays a vital role in averting excessive bleeding following an injury. This phase temporarily seals off the wound by forming a platelet plug, allowing the subsequent coagulation phase to create a more permanent clot. In addition, the substances released by activated platelets promote wound healing.

Several key factors limit the growth of the platelet plug. Prostacyclin, a prostaglandin released by endothelial cells, inhibitory compounds by white blood cells, and circulating plasma enzymes break down ADP near the plug to check on the platelet aggregation. Certain compounds can also inhibit plug formation when present in abundance. For instance, serotonin, at high concentrations, blocks the action of ADP. Lastly, developing a blood clot reinforces the platelet plug but isolates it from the general circulation.