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Histological characterization of mouse carotid artery alteration following ferric chloride-induced injury

Abstract number: OC-TH-035

Eckly¹ A., Freund¹ M., Zerr Fouineau¹ M., Cazenave¹ J., Lanza¹ F., Hechler¹ B., Gachet¹ C.

¹¹UMR_S 949 INSERM-Université de Strasbourg, Etablissement Français du Sang – Alsace, Strasbourg, France

How-to-cite Eckly A, Freund M, Zerr Fouineau M, Cazenave J, Lanza F, Hechler B, Gachet C. Histological characterization of mouse carotid artery alteration following ferric chloride-induced injury. Journal of Thrombosis and Haemostasis 2009; Volume 7, Supplement 2: Abstract OC-TH-035

Ferric chloride (FeCl₃)-induced vascular injury is widely used in animal models of thrombosis. However, the precise mechanisms underlying thrombus formation are not fully characterized. The aim of the present study was to examine histological changes in the vascular wall and of blood cells, after FeCl₃ treatment. FeCl₃ (7.5%) was externally applied to the carotid artery for 2 min and histological analyses were performed. Prussian blue staining of FeCl₃ showed its diffusion through the vessel wall causing loss of the elastic lamina undulation. Electron microscopy analysis showed severe lesions in all the vessel wall layers with presence of ghost endothelial cells, burnt appearing smooth muscle cells and altered periodicity of adventitial collagen fibers. Numerous, electron dense, spherical vesicles (3 μm diameter), likely containing ferric ions, originated from the endothelium and were surrounded by a PECAM-positive membrane. Interestingly, thrombi mainly composed of degranulated platelets and fibrin were observed in close contact with these vesicles, suggesting their direct involvement in thrombus formation. The potential impact of free FeCl₃ on blood cells was evaluated in vitro by adding increasing concentrations to isolated erythrocytes and platelets. Membrane permeabilization occurred at levels (≥ 0.1%), which were well above iron levels measured in plasma by a chromogenic method after carotid application (< 0.0001%). Finally, platelet aggregation in response to FeCl₃-pretreated collagen was close to that with native collagen indicating normal reactivity of this matrix after FeCl₃ treatment. In conclusion, topical application of FeCl₃ to the carotid artery causes the formation of iron containing vesicles budding off the endothelium into the vessel lumen which are able to directly activate platelets by yet unknown mechanisms and induce thrombus formation.

Disclosure of interest: none declared.

To cite this abstract use the following format:

Journal of Thrombosis and Haemostasis 2007; Volume 5, Supplement 2: abstract number

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