Thrombus Generation
Thrombus Generation - Related Videos
05:54
Intravital Fluorescence Microscopy to Study Microvascular Thrombus Formation
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2025
This video demonstrates the intravital fluorescence microscopy technique to study thrombus formation in a mouse model. The mouse is injected with a fluorophore-labeled polysaccharide to monitor blood circulation. Upon illumination with a high-intensity light, the phototoxic induction of an injury in the microvasculature of the ear leads to the formation of a thrombus, which is confirmed by visualizing the obstruction in the blood flow.
09:01
Intravital Microscopy and Thrombus Induction in the Earlobe of a Hairless Mouse
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Cited by 4 •
2017
The ear model of the hairless SKH1-Hrhr mouse enables intravital fluorescence microscopy of microcirculation and phototoxic thrombus induction without prior surgical preparation in the examined microvascular bed. Therefore, the ear of the hairless mouse is an excellent in vivo model to study the complex interactions during microvascular thrombus formation, thrombus evolution, and thrombolysis.
08:50
Thrombus Profiling Assay: A Microfluidics-Based Platform for Comprehensively Characterizing Biomechanical Thrombogenesis
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2026
This work describes a microfluidic assay that uses shear stress to trigger thrombus formation in blood and characterizes the thrombus by multiple dimensions of readout. The assay can measure the prothrombotic tendency of blood samples, and is thus useful in disease diagnosis, drug discovery, as well as basic mechanistic studies related to thrombosis.
02:05
Visualization of a Cerebral Thrombus in a Mouse Using Micro-Computed Tomography Imaging
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2025
Source: Kim, D., et. al. Combined Near-infrared Fluorescent Imaging and Micro-computed Tomography for Directly Visualizing Cerebral Thromboemboli. J. Vis. Exp. (2016)This video demonstrates visualization of cerebral thrombus in mice using micro-computed tomography (micro-CT) imaging. A cerebral thrombus mouse model is injected with fibrin-targeted gold nanoparticles acting as a contrasting agent. The mouse is placed on the bed of a micro-CT machine, and images are acquired from multiple angles.
11:18
Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice
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Cited by 29 •
2013
Here we report an experimental technique of fluorescence intravital microscopy to visualize heterotypic platelet-neutrophil interactions on the activated endothelium during vascular inflammation and thrombus formation in live mice. This microscopic technology will be valuable to study the molecular mechanism of vascular disease and to test pharmacologic agents under pathophysiological conditions.
FAQs
Two initiating conditions are emphasized: vascular injury exposes vessel components, while abnormal blood flow can activate platelets. Activated platelets adhere at the affected site, release signaling molecules, and recruit additional platelets into an aggregate. These linked responses focus clot-forming activity at the disturbed vascular region.
Thrombin connects platelet activity with clot stabilization. The coagulation cascade produces thrombin, which converts fibrinogen into fibrin. Fibrin then strengthens the platelet-based structure, helping transform an initially developing aggregate into a more stable clot. This distinction explains why thrombus formation depends on both cellular responses and coagulation chemistry.
Platelets provide the early cellular response by adhering to exposed vessel components, releasing signals, and aggregating. Coagulation supplies a reinforcing chemical pathway through thrombin and fibrin formation. Because these contributions are related but distinct, medical strategies can target platelet behavior, coagulation, or both when addressing thrombus-related disease.
Clinically important examples include deep vein thrombosis, stroke, and myocardial infarction. In these settings, a clot may obstruct blood flow rather than serve only a protective role against bleeding. Linking the clotting process to the affected disease helps medicine interpret thrombus formation as a potential cause of serious vascular complications.
The mechanism identifies two major therapeutic targets: platelet responses and the coagulation pathway. Antiplatelet therapies relate to adhesion, signaling, and aggregation, whereas anticoagulant therapies relate to coagulation activity that produces thrombin and fibrin. This mechanistic distinction supports the development and evaluation of treatments designed to limit disease-associated clot formation.
Understanding the sequence from vascular disturbance through platelet accumulation and fibrin stabilization provides a framework for recognizing clot-related disease. It informs clinical consideration of deep vein thrombosis, stroke, and myocardial infarction while also supporting research that develops and evaluates antiplatelet and anticoagulant therapies. The same process therefore connects diagnosis, disease interpretation, and treatment design.