A Blood for Survival?

Platelet activation loosely begins with the binding of one or more agonists to receptors located on the thrombocyte get hold. Such agonists may typically include either thrombin or collagen. This is subsequently fol misfortunateed by the development of filopodia, granule secretion, and platelet solicitation.

Thrombin is mayhap the most important in vivo platelet agonist. Natural substrates for this serine proteolytic enzyme include fibrinogen, Factor V, Factor V, Factor VIII, and protein C. The compound is typically generated by the "sequential activation of the enzymes of the coagulation cascade." Essentially, the single-chain molecule, prothrombin, undergoes two proteolytic cleavages--at an arginine-threonine bond and an arginine-isoleucine bond--to form the protease. To activate platelets, thrombin binds to an acidic region on the platelet thrombin receptor. Upon binding, thrombin cleaves the extracellular domain of the receptor near the amino terminus. The new amino terminus then acts as a tethered ligand and subsequently triggers intracellular signalling pathways. Finally, thrombin's action on platelets is self-reinforcing: not only does the enzyme cause platelet activation, but phospholipids on the surface of activated platelets promote thrombin generation.

Collagen, in contrast, is a structural segment that exists throughout the body. With von Willebrand factor, collagen is able to associa

The activity of Substance H may be demo by in vitro incubation of whole blood and salivary gland extract. Incubation of fresh whole blood in a glass test tube generally leads to a solid clot within a matter seconds. The aggregation of platelets can generally be monitored by counting the verse of platelets combining with one another.

As platelet recruitment progresses, visibly large aggregations may appear. In contrast, the addition of Substance H to whole blood will prolong clotting sequence for up to 1 hour. Furthermore, these effects occur almost now and may be achieved with Substance H concentrations as low as 0.1 to 1.0 U/ml.

In Western countries, thromboembolic diseases are a prevalent cause of morbidity and mortality. For example, in the United States, surrounded by 300,000 and 600,000 hospitalizations are caused every year from deep vein thrombosis and pulmonary thromboembolism. Moreover, these two diseases result in approximately 50,000 to 100,000 deaths annually.

Marcus, A. J. "New Considerations in Antiplatelet Therapy for Thrombotic Diseases." In R. Hoffman et al. (eds.), Hematology: Basic Principles and Practice (pp. 1446-1450). New York, NY: Churchill Livingstone, 1991.

fibrin

te with platelets. This interaction serves as a potent initiator of platelet activation.

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