Date

9-2013

Degree Name

BS in Biomedical Engineering

Department

Biomedical and General Engineering Department

Advisor(s)

Trevor Cardinal

Abstract

Many patients suffering from peripheral arterial occlusive disease (PAOD) experience intermittent claudication, pain during locomotion. Previous studies suggest that this symptom could be explained in part by impaired vasodilation in collateral arteries. In this study, femoral ligation was performed on a murine animal model, stimulating collateral outward remodeling. The mechanism by which a collateral increases its luminal diameter in response to the increase in blood flow following occlusion warrents further investigation due to impaired vasodilation following collateral remodeling. Specifically, resting diameter is elevated in the stem region of the collateral circuit, but this increase in vessel size cannot be explained by vascular smooth muscle cell (VSMC) proliferation. Therefore, we tested the hypothesis that enlargement was due to changes in VSMC overlap and/or length, a process known as mechanoadaptation. VSMC length and overlap measurements in the profunda femoris were taken from 40x confocal images. Mean VSMC length and overlap were measured 7 and 28 days post ligation. Mean length was 222 μm ± 76 vs 229 μm ±12 in the contralateral control limb and 310 μm ± 67 vs 187 μm ± 31 in the contralateral control limb, respectively. Overlap was 23 ± 2 vs 27 ± 2 in the contralateral control limb and 30 ± 5 vs 30 ± 3 in the contralateral control limb, respectively. None of the values were significantly different. A major challenge faced included the inability of the vessel to maintain their native cylindrical shape because of the way they were flattened during storage on the microscope slides. A proposed perfusion fixation technique with 4% paraformaldehyde may allow for the excised muscle to maintain its native geometry and more VSMC overlap measurements to be taken.

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