College - Author 1

College of Engineering

Department - Author 1

Biomedical Engineering Department

Degree Name - Author 1

BS in Biomedical Engineering

Date

6-2026

Primary Advisor

Trevor Cardinal, College of Engineering, Biomedical Engineering Department

Abstract/Summary

Peripheral artery disease (PAD) affects an estimated 200 million people worldwide and is characterized by arterial narrowing that reduces perfusion to the limbs. Collateral arterioles can naturally restore blood flow through a remodeling process called arteriogenesis, making it a promising therapeutic target. However, the femoral artery ligation (FAL) model used to study arteriogenesis requires surgical access deep to the inguinal fat pad, and approaches for handling the fat pad vary widely across surgeons and protocols. Since adipose tissue harbors a large population of macrophages, the immune cells that govern arteriogenesis, fat pad manipulation may introduce confounding inflammatory stimuli that disrupt vascular remodeling. To test this, C57BL/6 mice (n=24) were randomly assigned to three FAL treatment groups: minimal inguinal fat pad manipulation, significant inguinal fat pad manipulation, and significant inguinal fat pad manipulation followed by resection (n=8 per group), with the contralateral hindlimb serving as a sham-operated control. Seven days post-ligation, collateral vasodilatory function was assessed using transillumination intravital microscopy. All operated groups showed successful arteriogenesis, with maximally-dilated diameters significantly larger than sham-operated controls. However, both manipulation groups exhibited severely impaired vasodilatory capacity (22.5 ± 13.7% and 17.8 ± 8.2% change for manipulation and manipulation with resection, respectively) compared to sham controls (118.1 ± 17.0%). The minimal manipulation group showed an intermediate response (66.0 ± 33.0%) that was not significantly different from either sham or manipulation groups, suggesting that adipose tissue trauma is the primary driver of functional impairment rather than fat resection itself. These findings indicate that surgical manipulation of adipose tissue amplifies local inflammation, potentially exacerbating macrophage-driven sympathetic denervation and impairing collateral vascular function further. Beyond preclinical modeling, these results suggest that unnecessary adipose tissue manipulation during vascular surgical procedures may adversely affect postoperative outcomes, particularly in people with PAD who exhibit elevated baseline inflammation.

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