Structure
In vivo the platelet is shaped like a porous disc and resembles a microscopic sponge. The invaginations of the surface membrane into the center of the platelet provide canals, through which components within granules of the platelet escape into the surrounding plasma during the release reaction. The platelet is covered by a plasma protein coat that is the mediator for the platelet membrane's adhesion to surfaces and allows coagulation proteins or factors to adhere to it. Neither adhesion of platelets to surfaces nor adhesion to proteins requires energy, but each process requires fibrinogen.
The membrane beneath the surface coat contains phospholipids and selectively absorbs certain coagulation factors. Below the coat and membrane are submembranous filaments made of actomyosin that cause the platelet to contract. The equator of the disc-shaped platelet contains a prominent structure composed of microtubules that maintain the platelet's disc-like shape. After the release reaction begins, the microtubules constrict concentrically. This process moves the clusters of organelles and granules toward the center of the platelet. The granules are important because they contain several constituents that take part in the release reaction, i.e., ADP, catecholamine, and serotonin. Energy for these reactions is derived primarily from glycogen storage granules, and the platelet is capable of both aerobic and anaerobic metabolism.

Glycoproteins (Gp) on the surface of the platelets mediate platelet adhesion and aggregation. These glycoproteins trigger reactions of the platelet during these processes. They also act as receptors for extracellular ligands, various proteins, and chemicals that affect platelet function. Glycoproteins have two other very important functions: they stabilize the platelet surface by contributing to the cell surface charge; they also give the platelet its antigen specificity. Immune problems arise when these antigens are directed against certain glycoproteins.


Properties and Functions of Membrane Glycoproteins of Platelets
*Mediate platelet adhesion and aggregation
*Act as receptors for extracellular ligands *Participate in recognition phenomena and phagocytosis ·
*Bind complement ·
*Give platelet its antigenic specificity
*Mediate membrane transport processes ·
*Act as enzymes or anti-proteases ·
*Stabilize platelet surface and contribute to cell surface charge

Role of Platelets in Hemostasis:
In hemostasis, platelets play three main roles:
1. They maintain the endothelial surface. Loss of circulating platelets quickly results in morphologic changes in the endothelial cells of the capillaries. These changes cause intravascular material to leak into the capillary bed.
2. They initially arrest bleeding in severed blood vessels.
3. They provide phospholipid, which acts as the catalytic surface for initiation of the coagulation process.

When platelets encounter a break in the endothelial surface, several important actions cause the bleeding to cease.

A.Adhesion occurs when they encounter collagen, membranes or non-collagenous microfibrils beneath the basement membranes. Adhesion is mediated by GP-Ib and von Willebrand Factor (vWF).
a.Receptors (especially for glycoprotein-Ib) bind vWF and facilitate adhesion.
b.vWF is an extremely large molecule (a multimer) that bridges the gap between different cells, the platelet, and subendothelial surfaces.
c.vWF is a very “sticky” protein and binds readily.
d.Besides binding GP-Ib, vWF also binds to GP-IIb-IIIa to facilitate adhesion.
e.Fibrinogen, binding to the GP IIb-IIIa complex on two separate platelets, can bridge the gap between those two platelets (this is important to a subsequent function—aggregation).
f.In the absence of these factors (or their receptors) both adhesion and aggregation are abnormal and certain types of bleeding problems can occur.

B.Platelets then undergo a "release reaction". This process involves change from a disc shape to a spherical shape, constriction of the microtubules toward the center of the platelet, and the release of contents of the granules (primarily ADP, catecholamine, and serotonin) into the open canalicular system. These platelets thus become “activated”.
a.During the release reaction, the granules within the platelets release their contents into the canicular system.
b.These granule components then leak into the plasma around the platelet.
c.The released ADP binds other circulating platelets in close proximity to activated platelets and this binding to surface receptors initiates the release reaction in these “recruited” platelets.
d.The release reaction is mediated by means of Thromboxane A2. Arachidonate is integrated in the phospholipids in the cell wall and is freed by a phospholipase, activated during the process of adhesion or by binding of certain ligands to receptors on the platelet surface.
e.Cyclo-oxygenase converts arachidonate to an intermediate, prostaglandin H2.
f.In the platelets PGH2 is acted upon by thromboxane synthetase to form thromboxane A2. Thromboxane A2 promotes the release reaction, change in shape, and aggregation. In the endothelial cell, the pathway is different from that of the platelet.
g.Following the formation of PGH2, prostacyclin synthetase produces PGI2, which inhibits adhesion, aggregation and the release reaction, forces that oppose those of Thromboxane A2.
h.Aspirin blocks cyclo-oxygenase and therefore the pathway that leads to both Thromboxane A2 and PGI2. In the platelet, the block is permanent for the life of the platelet, because the platelet does not have a nucleus to direct the formation of more cyclo-oxygenase. This yields a platelet that cannot function. Since the life of the platelet is about 7-10 days, the effect of the aspirin on bleeding will gradually decrease over a week, as new platelets replace those that were exposed to aspirin. In the endothelial cell, however, cyclo-oxygenase is regenerated.

C.Platelet aggregation occurs as platelets are "recruited" from the immediate area by the released contents, for example, ADP. This process is accomplished by fibrinogen, binding to the GP IIb-IIIa complex on separate platelets, and bridging the gap between platelets When the release of ADP, or other aggregating agents, is minimal, the local concentration of these agents do not reach a high level, this aggregation may be reversible; with higher concentrations, aggregation is irreversible.

Associated with the change of shape of the platelet and the release reaction, is the appearance of clotting promoting sites (historically referred to as platelet factor 3) on the platelet membranes. The receptor sites for the coagulation proteins serve as a catalytic site for the clotting proteins and assists in initiating the clotting mechanism. Important coagulation proteins that are bound to the surface include factors V and VIII among others.

E.Clot retraction occurs when platelets are trapped within the enlarging blood clot. During the release reaction, pseudopodia like structures are extended some distance from the surface of the platelet, and attach to similar structures on adjacent platelets. With time, these structures retract, pulling the body of the clot together, and sealing the vessel wall at the site of injury.