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Related Concept Videos

Formation of the Platelet Plug01:22

Formation of the Platelet Plug

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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...
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Structure and Function of Platelets01:18

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The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
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Introduction to Hemostasis01:05

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Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized,...
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Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

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Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
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Clot Retraction and Fibrinolysis01:16

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After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
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Microfluidics in Assessing Platelet Function
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Changes in platelet function with inflammation in patients undergoing vascular surgery.

Bartosz Olechowski1, Vikram Khanna1, Mark Mariathas1

  • 1a Wessex Cardiothoracic Centre University, University Hospital Southampton NHS Foundation Trust , Southampton , UK.

Platelets
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Aspirin

Keywords:
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Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Pharmacology

Background:

  • Platelets play a crucial role in ischemic events.
  • Aspirin is a standard antiplatelet therapy, inhibiting arachidonic acid (AA) metabolism via cyclooxygenase (COX).
  • The validity of AA-induced clotting as a measure of aspirin response is questioned due to variable patient results.

Purpose of the Study:

  • To investigate dynamic changes in AA-, ADP-, and thrombin-mediated platelet reactivity during major vascular surgery.
  • To explore AA-induced clotting modifications despite suppressed thromboxane B2 (TXB2) production, potentially via lipoxygenase pathways.
  • To assess platelet function and inflammatory markers in patients on aspirin undergoing vascular surgery.

Main Methods:

  • Forty patients undergoing major vascular surgery received aspirin and unfractionated heparin.
  • Platelet reactivity (AA-, ADP-, thrombin-induced clotting), AA metabolites (TXB2, 12-HETE), and inflammatory markers (CRP, IL-6, TNF-α, CD40) were measured pre- and post-surgery.
  • Thrombelastography assessed platelet reactivity; immunoassays and immune-turbidimetry measured metabolites and inflammatory markers.

Main Results:

  • Inflammatory markers (CRP, IL-6) transiently increased post-surgery.
  • Negligible TXB2 levels confirmed consistent aspirin response.
  • Thrombin-mediated clotting increased post-surgery, while AA- and ADP-induced clotting decreased initially, followed by a rebound effect at 3 months.

Conclusions:

  • Major vascular surgery induces dynamic changes in platelet aggregation, affecting AA-, ADP-, and thrombin-mediated pathways.
  • AA-induced whole blood clotting can be modified independently of COX-1 activity, suggesting alternative mechanisms.
  • Platelet function testing requires careful consideration of inflammatory states and potential non-COX pathways.