N

Discharge of mediators

Synthesis of thromboxane A,

Chemical mediators

Blood vessels

Contraction of vascular smooth muscle

Vasoconstriction

Platelet plug

FIGURE 14-69

Sequence of events leading to formation of a platelet plug and vasoconstriction following damage to a blood-vessel wall. Note the two positive feedbacks in the pathways.

The platelet plug can completely seal small breaks in blood vessel walls. Its effectiveness is further enhanced by another property of platelets—contraction. Platelets contain a very high concentration of actin and myosin, which are stimulated to contract in aggregated platelets. This results in a compression and strengthening of the platelet plug. (When they occur in a test tube, this contraction and compression are termed "clot retraction.")

While the plug is being built up and compacted, the vascular smooth muscle in the damaged vessel is being stimulated to contract (Figure 14-69), thereby decreasing the blood flow to the area and the pressure within the damaged vessel. This vasoconstriction is the result of platelet activity, for it is mediated by throm-boxane A2 and by several chemicals contained in the platelet's secretory vesicles.

PART THREE Coordinated Body Functions

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

PART THREE Coordinated Body Functions

Blood vessel -

Collagen -

Platelet plug

pgi2

PGI2

j txa2

NO PGI2

pgi2

FIGURE 14-70

Prostacyclin (PGI2) and nitric oxide (NO), both produced by endothelial cells, inhibit platelet aggregation and therefore prevent spread of platelet aggregation from a damaged site. TXA2 = thromboxane A2.

Once started, why does the platelet plug not continuously expand, spreading away from the damaged endothelium along intact endothelium in both directions? One important reason involves the ability of the adjacent undamaged endothelial cells to synthesize and release the eicosanoid known as prostacyclin (also termed prostaglandin I2, PGI2), which is a profound inhibitor of platelet aggregation. Thus, whereas platelets possess the enzymes that produce thromboxane A2 from arachidonic acid, normal endothelial cells contain a different enzyme, one that converts intermediates formed from arachidonic acid not to throm-boxane A2 but to prostacyclin (Figure 14-70). In addition to prostacyclin, the adjacent endothelial cells also release nitric oxide, which is not only a vasodilator (Section D) but also an inhibitor of platelet adhesion, activation, and aggregation.

To reiterate, the platelet plug is built up extremely rapidly and is the primary sealer of breaks in vessel walls. In the following section, we shall see that platelets are also essential for the next, more slowly occurring, hemostatic event, blood coagulation.

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