College - Author 1

College of Engineering

Department - Author 1

Biomedical and General Engineering Department

Degree Name - Author 1

BS in Biomedical Engineering



Primary Advisor

Trevor Cardinal


Many patients who suffer from the ischemic Peripheral Arterial Occlusive Disease (PAOD) experience intermittent claudication, which can be attributed to impaired vasodilation. Collateral vessels are the primary site of resistance to blood flow downstream; therefore maximizing vasodilation in collaterals is crucial for efficient circulation. Collaterals function as natural bypasses around the occluded arteries and the increase in flow into these vessels causes them to outwardly remodel into conduit vessels. However, functional vasodilation in the stem region of collateral vessels is impaired at day 7 following femoral ligation, which can be attributed to smooth muscle cell malfunction. However, the increase in vessel diameter in outwardly remodeled collaterals is not due to cell proliferation. One possible explanation for the diameter increase in the stem region of the collateral is that the vascular smooth muscle cells undergo mechanoadaptation to acclimate to the increase in blood flow and fluid shear stress. To test this hypothesis, outward remodeling was induced in the gracilis collateral stem via femoral artery ligation. At day 7 following surgery, maximal vasodilation in the profunda femoris artery (collateral stem) was evaluated before perfusion fixation. The profunda was then resected and immunostained before measuring smooth muscle cell length and overlap using confocal microscopy. Average SMC overlap was significantly less in the collateral artery, 43 ± 1 μm versus 51 ± 2 μm in the control artery. Also, average SMC length was significantly longer in the collateral artery 249 ± 13 μm versus 205 ± 10 μm in the control. These results indicate that mechanoadaptation occurred in the collateral stem and its correlation to impaired vasodilation suggests that the reorientation and remodeling associated with mechanoadaptation may play a causal role in vessel impairment. Further studies need to be performed to determine if mechanoadaptation causes impaired vasodilation for patients with PAOD.