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Related Concept Videos

Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

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.
Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
Coagulation01:09

Coagulation

The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

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 forms a...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

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...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

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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Related Experiment Video

Updated: Jun 20, 2026

Tracking Fibrinolysis of Chandler Loop-Formed Whole Blood Clots Under Shear Flow in An In-Vitro Thrombolysis Model
06:16

Tracking Fibrinolysis of Chandler Loop-Formed Whole Blood Clots Under Shear Flow in An In-Vitro Thrombolysis Model

Published on: April 19, 2024

The clot thickens (or not).

Steven E McKenzie1, Michael P Reilly

  • 1Thomas Jefferson University.

Blood
|August 29, 2009
PubMed
Summary
This summary is machine-generated.

Dasatinib, a multikinase inhibitor, causes bleeding in CML patients by affecting platelets. This research explores using kinase inhibitors as novel antithrombotic agents.

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Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States

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Last Updated: Jun 20, 2026

Tracking Fibrinolysis of Chandler Loop-Formed Whole Blood Clots Under Shear Flow in An In-Vitro Thrombolysis Model
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Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization

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Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
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Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States

Published on: April 1, 2015

Area of Science:

  • Hematology
  • Pharmacology

Background:

  • Chronic myeloid leukemia (CML) patients resistant to imatinib are often treated with dasatinib, a multikinase inhibitor.
  • Dasatinib's impact on platelet function contributes to observed bleeding side effects.

Discussion:

  • The study investigates the specific mechanisms by which dasatinib affects platelet activity.
  • Analysis of platelet function assays reveals dasatinib's influence on key platelet responses.

Key Insights:

  • Dasatinib significantly alters platelet function, explaining its association with bleeding complications in CML patients.
  • The research provides a mechanistic understanding of dasatinib-induced bleeding.

Outlook:

  • Kinase inhibitors, like dasatinib, show potential as a new class of antithrombotic therapies.
  • Further research could optimize kinase inhibitors for safe and effective antithrombotic use.