Thrombus Resolution
Thrombus Resolution - Related Videos
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.
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.
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
Tissue plasminogen activator, or tPA, converts plasminogen into plasmin. Plasmin then provides the fibrinolytic activity needed to dismantle the fibrin framework of a clot. This conversion is therefore a central control point for studies of how effectively an occluded vessel can regain patency after hemostasis.
Fibrin breakdown alone does not describe the entire remodeling process. Immune and inflammatory cells participate in reorganizing the fibrin-rich clot and clearing cellular debris, linking clot removal with tissue cleanup. Their contribution makes resolution relevant to vascular repair, not only to enzymatic dissolution of the clot.
Both conditions can alter clot structure and delay its resolution, creating a connection between immune activation and impaired vascular recovery. In infection-focused research, this relationship helps explain why a clot may remain problematic even when fibrinolytic mechanisms are present, and why inflammatory state must be considered when interpreting vessel injury.
A useful conceptual sequence begins after hemostasis: assess fibrinolytic conversion from plasminogen to plasmin, examine remodeling of the fibrin structure, and evaluate immune-cell clearance of cellular debris. Researchers can then relate these events to restoration of vessel patency and to inflammatory conditions that may slow or disrupt the process.
It is particularly informative when investigators examine the intersection of coagulation, innate immunity, and vascular repair. Infection and persistent inflammation can modify clot behavior, while sepsis-associated vascular injury provides a context in which delayed removal may contribute to tissue damage. The topic therefore connects clot biology with host-response research.
Evaluation must consider more than faster fibrinolysis. The desired outcome is improved clot removal and vessel patency while limiting bleeding risk, because excessive interference with coagulation could create a competing safety concern. This balance makes thrombus resolution useful for comparing approaches aimed at vascular recovery without worsening hemostatic injury.