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Related Concept Videos

Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

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Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
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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.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000...
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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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Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

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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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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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Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

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Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
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Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets
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Coronavirus 2019, Microthromboses, and Platelet Activating Factor.

Theoharis C Theoharides1, Smaragdi Antonopoulou2, Constantinos A Demopoulos3

  • 1Laboratory of Molecular Immunopharmacology and Drug Discovery, Department of Immunology, Tufts University School of Medicine, Boston, MA, USA; School of Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, MA, USA; Department of Internal Medicine, Tufts University School of Medicine and Tufts Medical Center, Boston, MA, USA.

Clinical Therapeutics
|September 5, 2020
PubMed
Summary

Rupatadine, an anti-platelet activating factor (PAF) drug, may prevent COVID-19 complications. It inhibits PAF-induced mast cell activation, potentially reducing pulmonary microthromboses and inflammation seen in severe coronavirus 2019 (COVID-19).

Keywords:
COVID-19inflammationmast cellsplatelet-activating factorthromboses

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Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
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Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

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Area of Science:

  • Medical Research
  • Pharmacology
  • Immunology

Background:

  • Coronavirus 2019 (COVID-19) is associated with elevated coagulation markers, endothelial injury, and lung microthromboses.
  • Platelet activating factor (PAF) is a potent trigger of thrombi formation and its actions resemble COVID-19 manifestations like inflammation and microthromboses.
  • PAF may contribute to COVID-19 pathogenesis through mast cell activation.

Purpose of the Study:

  • To explore the potential repurposing of rupatadine for COVID-19 prophylaxis.
  • To investigate rupatadine's anti-PAF activity and its effect on mast cell activation.

Main Methods:

  • Review of existing literature on COVID-19, coagulation, endothelial injury, and PAF.
  • Analysis of rupatadine's pharmacological properties, including its anti-PAF activity.
  • Assessment of rupatadine's inhibitory effects on human mast cell activation by PAF.

Main Results:

  • Platelet activating factor (PAF) plays a significant role in thrombus formation and shares similarities with COVID-19 pathology.
  • Rupatadine exhibits anti-PAF activity and inhibits PAF-induced human mast cell activation.
  • These properties suggest a potential therapeutic role for rupatadine in COVID-19.

Conclusions:

  • Rupatadine's ability to inhibit PAF-mediated mast cell activation presents a promising avenue for COVID-19 prophylaxis.
  • Repurposing rupatadine could offer a novel strategy to mitigate COVID-19-related microthromboses and inflammation.