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Julie Woodrum

Publications and source records attributed to Julie Woodrum.

2 recordsLinked to original sources

Experimental hypercholesterolemia differentially affects adventitial vasa vasorum and vessel structure of the left internal thoracic and coronary arteries.

OBJECTIVE: Atherosclerosis is a chronic and diffuse disease that affects all vascular beds. However, some vascular beds are more prone to atherosclerosis than others. Recent evidence suggests a role for the vasa vasorum in the atherosclerotic process. We hypothesized that there is a difference in adventitial vasa vasorum structure between the left internal thoracic artery and the coronary artery. Hence the current study was designed to characterize and compare the structure of the adventitial vasa vasorum in the left internal thoracic and coronary arteries. METHODS: Samples of vessels were obtained from female crossbred domestic pigs maintained on a normal (n = 6) or high-cholesterol (n = 6) diet for 12 weeks. The samples were scanned with micro-computed tomography, and the tomographic images were reconstructed and analyzed to obtain lumen area, vessel wall area, vasa vasorum count, vasa vasorum density, mean diameter of first- and second-order vasa vasorum, and second-order/first-order vasa vasorum ratio. RESULTS: Vasa vasorum density was significantly higher in the coronary arteries versus that seen in the left internal thoracic arteries in the normal group, as well as in the high-cholesterol group. The higher vasa vasorum density in the high-cholesterol group versus that in the normal group was significant for both vessels, being more pronounced in the left internal thoracic artery. Lumen area and second-order/first-order vasa vasorum ratio were higher in the high-cholesterol group than in the normal group only in the left internal thoracic artery. CONCLUSION: This study demonstrated that low vasa vasorum spatial density and higher lumen area observed in the left internal thoracic artery compared with that seen in the native coronary artery can be the structural background for the low incidence of atherosclerosis in this vessel.

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Adventitial vasa vasorum heterogeneity among different vascular beds.

INTRODUCTION: Different vascular beds show substantial variation in their susceptibilities for development of vascular disease like atherosclerosis, and thereby exhibit a variety of different clinical presentations. Yet, the underlying mechanism of this heterogeneity is not well defined. Recent evidence suggests a role for the vasa vasorum (VV) in vascular disease. We hypothesized that there is a differential distribution structure of adventitial VV in different vascular beds. Hence, the current study was designed to characterize and compare the structure of the adventitial VV in the coronary and the peripheral circulation. METHODS: Samples of vessels from different vascular beds were obtained from 6 female crossbred domestic pigs. The samples were scanned using micro-computed tomography, and the images reconstructed and analyzed to characterize VV architecture, including vessel wall area, VV count, VV density, intravessel spatial distribution, mean diameter of first- and second-order VVs and the ratio of second- to first-order VVs. RESULTS: There were significant differences in VV density among different vascular beds. Density was highest in coronary arteries (2.91 +/- 0.26 vessels/mm2, P <.05, vs renal, carotid, and femoral arteries), intermediate in renal arteries (1.45+/- 0.22 vessels/mm2, P <.05, vs femoral artery) and carotid arteries (0.64 +/- 0.08 vessels/mm2, P <.05, vs femoral artery), and lowest in femoral arteries (0.23 +/- 0.05 vessels/mm2 ). A similar pattern for the ratio of second- to first-order VV was also observed. Random intravessel spatial distribution of VVs was seen in all vascular beds. CONCLUSION: The current study demonstrates a differential structure of the adventitial VV in different vascular beds. This intra- and intervessel heterogeneity in VV anatomy is a phenotypic variability that might determine a differential local response to systemic risk factors and, thereby, variable propensity for vascular disease among different vascular beds.

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