Thrombosis Prevention
Thrombosis Prevention - Related Videos
10:37
Ferric Chloride-induced Murine Thrombosis Models
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Cited by 56 •
2016
We report a refined procedure of the ferric chloride (FeCl3)-induced thrombosis models on carotid and mesenteric artery as well as vein, characterized efficiently using intravital microscopy to monitor time to occlusive thrombi formation.
10:26
A Multicenter MRI Protocol for the Evaluation and Quantification of Deep Vein Thrombosis
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Cited by 5 •
2015
The goal of this study is to use magnetic resonance venography with long-circulating gadolinium-based contrast agent and direct thrombus imaging for quantitative evaluation of DVT volume in a multicenter, clinical trial setting. Inter- and intra-observer variability assessments were conducted, and reproducibility of the protocol was determined.
07:26
Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel
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Cited by 49 •
2015
The FeCl3 induced thrombosis model in mice is described herein. A method to monitor thrombus growth by intravital microscopy observation on a mesenteric vessel and by blood flow measurement in the carotid artery is presented.
04:34
Mouse Complete Stasis Model of Inferior Vena Cava Thrombosis
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Cited by 28 •
2011
The mouse complete stasis model of inferior vena cava thrombosis yields quantifiable amounts of vein wall tissue and thrombus. It has proven useful for evaluating interactions between the vein wall and the occlusive thrombus and in assessing the progression from acute to chronic inflammation.
06:03
Electrolytic Inferior Vena Cava Model (EIM) of Venous Thrombosis
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Cited by 39 •
2011
The electrolytic induction of endothelial activation to the internal surface of the Inferior Vena Cava results in venous type thrombus formation due to endothelial activation and partial blood stasis, two components of Virchow's triad.
FAQs
These processes offer distinct intervention points. Antiplatelet approaches focus on limiting platelet activation, while anticoagulant approaches address coagulation reactions that contribute to thrombin generation. Separating these mechanisms helps researchers match a preventive strategy to the blood-contacting setting, whether the main concern involves cellular adhesion, clotting chemistry, or both.
A material surface can influence how blood interacts with an implant or device, including whether platelets adhere and whether clot-promoting reactions develop. Bioengineering therefore treats surface behavior as a design consideration rather than an incidental property. Improving material compatibility can help limit platelet adhesion and thrombin generation on vascular grafts, stents, and other devices.
Blood flow is one of the interacting conditions that shapes clot formation, alongside platelets, coagulation reactions, and contacting surfaces. Engineers can therefore address thrombosis through improved fluid dynamics as well as pharmacological approaches or material design. Considering flow helps connect device geometry and operation with the way blood moves across engineered surfaces.
Development should consider how the material interacts with blood under physiological conditions. Relevant outcomes include whether the surface limits platelet adhesion and whether it reduces thrombin generation, while the surrounding flow environment also remains important. This evaluation links material selection and device design to the intended goal of safer blood-contacting implants.
The principles guide the development of blood-contacting biomaterials, vascular grafts, stents, and drug-delivery systems. Each application presents an opportunity to reduce platelet adhesion, thrombin generation, or unfavorable fluid-dynamic conditions. These designs aim to make implants and therapies safer while addressing the interaction between engineered systems and circulating blood.
Such studies can reveal how engineered materials interact with blood under physiological conditions and which design features may limit clot-promoting behavior. They also connect biological mechanisms with device performance, including platelet adhesion, thrombin generation, and flow. The resulting knowledge supports safer implants and therapies while improving the mechanistic understanding of blood-contacting systems.