College - Author 1

College of Engineering

Department - Author 1

Biomedical and General Engineering Department

Degree Name - Author 1

BS in Biomedical Engineering

Date

8-2015

Primary Advisor

Trevor Cardinal

Abstract/Summary

Peripheral arterial occlusive disease (PAOD) involves arterial occlusion due to the formation of atherosclerotic plaques. It is suggested that intermittent claudication, the most frequent clinical presentation of PAOD, is caused by impaired vasodilation. Current treatments for PAOD are not directed at improving vascular reactivity and are often insufficient. Stimulating arteriogenesis in collateral arterioles has therapeutic potential for PAOD, but because arterioles are the primary site of blood flow resistance, it is important that these treatments do not impair collateral vasodilation. Before this can be evaluated, the effects of arteriogenesis on collateral function must be studied in untreated collaterals. There is impaired functional vasodilation at the collateral stem following collateral enlargement in the mouse hindlimb ischemia model. In order to determine if a similar impairment occurs at the collateral midzone, visualization of the gracilis collateral arteriole must be improved. In this study, we tested the hypotheses that FITC-dextran injected into the intravascular space would allow visualization of the gracilis collateral arteriole using epifluorescence, and that a trans-illumination device placed deep to the gracilis muscle would allow visualization of the arteriole by backlighting the midzone. Both of these methods allowed for clear visualization of the gracilis vasculature. Additionally, the placement of the trans-illumination device did not affect vasodilation in the upstream feed artery, suggesting that collateral reactivity would also remain unaltered by the device. In future studies, both of these visualization techniques will be employed to assess functional vasodilation in the midzone of the gracilis collateral arteriole in both unoperated animals and those with ligation-induced ischemia.

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