Rodent Thrombosis Models

Thrombosis refers to the formation of a blood clot inside a blood vessel, which obstructs the blood flow. Thrombosis may occur in veins or in arteries. Considering the widespread and critical role of thrombosis in many diseases, animal models of thrombosis are in need to explore its pathophysiology and develop more safe and effective drugs. Creative Biolabs is specialized in the field of cardiovascular diseases and we conduct contract efficacy studies in the following rodent models of thrombosis, including models for deep vein thrombosis (DVT) and arterial thrombosis.

Fig.1 Mechanism of thrombus formation. (Franchi et al. 2015)

Rodent DVT Models

Thrombosis is commonly induced in the inferior vena cava (IVC) because there the coagulation cascade generates better thrombus sized for analysis and act as a better platform for chronic thrombosis studies. Creative Biolabs offers the following rodent DVT models and analytic evaluative methods to study the disease mechanisms and to test pharmaceuticals for the treatment of this disease:

IVC Ligation Model – a useful model for studying clinical scenarios where complete occlusion and no recanalization occurs causing a severe response in the vein wall.

IVC Stenosis Model – a useful model to simulate nonocclusive clinical scenarios, either partial occlusion and/or recanalization.

Ferric Chloride-Induced Thrombosis Models

This model has played a key role in the study of the pathophysiology of thrombosis, in the discovery and validation of novel antithrombotic drugs, and in the understanding of the mechanism of action of these new agents. It is induced by topical application of ferric chloride (FeCl₃) that generates free radicals, resulting in lipid peroxidation and destruction of endothelial cells. The injury induces the expression of several adhesion molecules triggering platelet adhesion and aggregation as well as leukocytes recruitment. These leukocytes, particularly neutrophils, play a crucial role in the activation of the blood coagulation cascade leading to thrombosis.

This model has exhibited several advantages:

• This technique can be used to induce the formation of thrombi in a variety of vessels, including arteries or veins of both large diameter (e.g., carotid, femoral, vena cava) and small diameter (e.g., mesentery). The target vessel should be chosen based on the disease setting investigated and the parameters that will be measured.
• This technique is very simple to implement and is effective in both rats and mice, making it now the most commonly used thrombosis model. It can also be used to test the fibrinolytic capacities of novel drugs in vivo.
• This technique can be applied to genetically engineered mice models to study the function of a specific gene in thrombotic disorders.

Assessments

For evaluation of the efficacy of new drugs in the treatment of the diseases, we provide measurements of various parameters, including but not limited to:

• Thrombus formation by intravital microscopy or a Doppler probe.
• Histological analysis using different stains (e.g., Masson’s stain, Sirius Red stain).
• Gene expression, protein levels (ELISA, western blot), and protein activity.
• Hematology analysis (microparticles, hematology, coagulation, and markers of inflammation)

You might also be interested in:

• Rodent Atherosclerosis Models
• Rodent Diabetic Complication Models
• Rodent Heart Failure Models
• Rodent Hypertension Models
• Rodent Myocardial Infarction Models

Creative Biolabs provides the most cost- and time-effective preclinical services, with the highest standards of quality and accuracy. We take a hands-on approach and we work side-by-side with our clients to learn their specific preclinical study requirements. A group of scientists will be assigned to assist them to determine the most suitable model to use and tailor study-specific protocols to maximize the results with minimal resources. Contact our scientists to discuss your detailed research plan today.

Reference

1. Franchi, F.; Angiolillo, D. J. Novel antiplatelet agents in acute coronary syndrome[J]. Nature Reviews Cardiology, 2015, 12(1):30-47.

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