Femoral Artery Wire Injury
Femoral Artery Wire Injury - Related Videos
06:42
A Murine Model of Arterial Restenosis: Technical Aspects of Femoral Wire Injury
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Cited by 17 •
2015
The mouse femoral artery wire injury model of restenosis is technically challenging. In this protocol we show the key technical details essential for successfully performing wire injury to induce consistent neointima for studies of restenosis.
07:05
Murine Model of Femoral Artery Wire Injury with Implantation of a Perivascular Drug Delivery Patch
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Cited by 8 •
2015
We describe a surgical technique that produces wire injury in the femoral artery of mice to induce neointimal hyperplasia to serve as a model testing system for the perivascular delivery of therapeutic compounds for the inhibition of restenosis.
07:51
Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography
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Cited by 37 •
2011
An automated myography method for force measurements in isolated mesenteric arteries is described. It employs a Mulvany-Halpern Auto Dual Wire Myograph 510A to determine responses to phenylephrine and extracellular calcium. The method allows consistent determination of isometric responses to agonists in small vessels of diameters of 60 - 300 μm, independently.
03:17
An Experimental Model of Peripheral Ischemia: A Procedure to Generate Peripheral Ischemia via Femoral Artery Ligation in a Rabbit
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2025
In this video, we demonstrate a surgical procedure to induce peripheral ischemia via femoral artery ligation in a rabbit. This method provides an effective experimental model for peripheral vascular disease research.
09:40
Ultrasound Assessment of Flow-Mediated Dilation of the Brachial and Superficial Femoral Arteries in Rats
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Cited by 11 •
2016
Non-invasive assessment of endothelial function in humans can be determined by the flow-mediated dilation technique. Although thousands of studies have used this technique, no study has performed this technique non-invasively in rats. The following article describes non-invasive measurement of flow-mediated dilation in the brachial and superficial femoral arteries of rats.
FAQs
Mechanical removal of endothelial cells exposes the vessel to an injury response. The resulting sequence includes inflammation, proliferation of vascular smooth muscle cells, and development of a neointimal layer, meaning tissue that forms within the arterial wall or lumen after injury. Tracking this sequence helps investigators connect endothelial loss with later remodeling.
Endothelial recovery is an important endpoint because it indicates how the arterial lining responds after mechanical disruption. Studying recovery alongside inflammation and smooth muscle cell proliferation allows investigators to distinguish early repair from later neointimal formation. This perspective supports analysis of pathways that may influence arterial healing after vascular injury.
Neointimal formation provides a structural measure of the vessel’s response to injury. When analyzed with arterial remodeling, thrombosis, and restenosis, it helps researchers assess whether repair is accompanied by narrowing or other adverse changes. These outcomes make the model useful for linking cellular responses to clinically relevant vascular complications.
The procedure begins when researchers introduce a guidewire through the femoral artery and pass it along the vessel to mechanically remove or denude endothelial cells. Because the wire creates a defined injury, investigators can examine subsequent repair, inflammation, smooth muscle cell proliferation, and remodeling within a controlled experimental design.
The model supports testing of vascular therapies by providing a reproducible injury context in which endothelial recovery, inflammation, smooth muscle cell proliferation, neointimal formation, and remodeling can be examined. Investigators can compare how an intervention affects these responses, helping identify molecular pathways or treatment strategies relevant to vascular repair and restenosis.
Because the injury is produced by a guidewire and involves mechanical disruption of the arterial lining, the model offers a setting for studying responses relevant to endovascular treatment. Device-focused studies can examine repair, thrombosis, remodeling, and restenosis, while the model’s reproducibility supports consistent comparison across experimental investigations.