Vasa vasorum: another cause of the carotid string sign.
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BACKGROUND AND PURPOSE: Our purpose was to describe a variant of the carotid string sign that may be associated with a completely occluded vessel and to consider possible pathophysiological mechanisms for this observation. METHODS: Carotid angiography was performed in three patients with suspected carotid stenosis and in a fourth with carotid dissection. Surgery was performed in one of the patients with carotid stenosis. RESULTS: On all angiograms, instead of a single linear or curvilinear contrast "string," either single or multiple serpiginous channels were seen. In one case, such a channel was seen emanating from below the origin of an occluded internal carotid stump, reconstituting the distal portion of the vessel. Surgery revealed a completely occluded lumen with a small intramural vessel bypassing the obstruction. CONCLUSION: We propose that these channels are either atherosclerotically induced neovessels connecting bridging vasa vasorum or recanalized luminal thrombus. We review the literature associated with this subject. (+info)
On the regulation of tone in vasa vasorum.
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OBJECTIVE: The vasa vasorum form a network of microvessels in and around the walls of large blood vessels and are thought to be necessary to delivery oxygenated blood to the outer parts of the vessel wall that are inadequately nourished by diffusion from luminal blood. This study was undertaken to investigate directly the mechanisms which control tone in the vasa vasorum. METHODS: Arterial vasa vasorum were dissected from the walls of porcine or bovine thoracic aorta and mounted in a tension myograph. Concentration-response curves were constructed to vasoconstrictors; endothelin-1(ET-1), noradrenaline (NA) angiotensin II (Ang II) and thromboxane A2-mimetics (U44069 or U46619) or vasodilators; substance P (SP) bradykinin (BK), calcitonin gene-related peptide (CGRP) or isoprenaline. Strips of porcine aorta were mounted in 25 ml organ baths. RESULTS: Potent concentration-dependent contraction of vasa vasorum was produced by ET-1. NA was a weak constrictor, Ang II had no effect or produced contraction that underwent tachyphylaxis and thromboxane A2-mimetics had no effect. In contrast NA, Ang II, U-44069 and ET-1 all produced potent concentration-dependent contraction of aortic strips. SP and BK produced endothelium-dependent relaxation while CGRP produced endothelium-independent relaxation of ET-1-precontracted vasa vasorum. Isoprenaline had no relaxant effect. CONCLUSIONS: We have demonstrated functional responses of arterial vasa vasorum to vasodilators and vasoconstrictors. Additionally these microvessels appear to respond to constrictors differently from the large host vessel. (+info)
Formation of new vasa vasorum in vasculitis. Production of angiogenic cytokines by multinucleated giant cells.
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Inflammation of the arterial wall in giant cell arteritis induces a series of structural changes, including the formation of new vasa vasorum. To study the regulation of neoangiogenesis in giant cell arteritis, temporal arteries were examined for the extent and localization of microvessel generation and for the production of angiogenic factors. In normal arteries, vasa vasorum were restricted to the adventitia, but in inflamed arteries, capillaries emerged in the media and the intima. These capillaries displayed a distinct topography with a circumferential arrangement in the external one-third of the intima. Neovascularization was closely correlated with the formation of lumen-obstructing intima, the fragmentation of the internal elastic lamina, and the presence of multinucleated giant cells. Comparison of tissue cytokine transcription in temporal arteries of giant cell arteritis patients with and without up-regulated neoangiogenesis identified interferon-gamma and vascular endothelial growth factor but not fibroblast growth factor-2 as mediators associated with vasa vasorum proliferation. Giant cells and CD68-positive macrophages at the media-intima junction were found to be the major cellular sources of vascular endothelial growth factor. These data demonstrate that formation of new vasa vasorum in vasculitis is regulated by inflammatory cells and not by arterial wall cells, raising the possibility that it represents a primary disease mechanism and not a secondary hypoxia-induced event. Increased neovascularization in interferon-gamma-rich arteries suggests that the formation of new vasa vasorum is determined by the nature of the immune response in the arterial wall, possibly resulting from the generation and functional activity of multinucleated giant cells. (+info)
Endothelin alters the reactivity of vasa vasorum: mechanisms and implications for conduit vessel physiology and pathophysiology.
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1 The walls of certain large blood vessels are nourished by the vasa vasorum, a network of microvessels that penetrate the adventitia and media of the vessel wall. The purpose of this study was to characterize endothelin-1 (ET-1)-mediated contraction of vasa and to investigate whether threshold concentrations of ET-1 alters the sensitivity to constrictors. Arterial vasa were dissected from the walls of porcine thoracic aorta and mounted in a tension myograph. 2 ET-1 and ETB-selective agonist, sarafotoxin 6c (S6c), produced concentration-dependent contraction. ETA receptor antagonist, BQ123 (10 microM), caused a biphasic rightward shift of ET-1 response curves. ETB receptor antagonist, BQ788 (1 microM), produced a rightward shift of response curves to ET-1 and S6c of 5- and 80 fold respectively. 3 ET-1 responses were abolished in Ca2+-free PSS but unaffected by selective depletion of intracellular Ca2+ stores. Nifedipine (10 microM), an L-type Ca2+ channel blocker, attenuated ET-1 responses by 44%. Inhibition of receptor-operated Ca2+ channels or non-selective cation entry using SKF 96365 (30 microM) and Ni2+ (1 mM) respectively, attenuated ET-1 contractions by 60%. 4 ET-1 (1-3 nM) enhanced responses to noradrenaline (NA) (4 fold) but not to thromboxane A2-mimetic, whilst K+ (10-20 mM) sensitized vasa to both types of constrictor. 5 Therefore, ET-1-induced contraction of isolated vasa is mediated by ETA and ETB receptors and involves Ca2+ influx through L-type and non-L-type Ca2+ channels. Furthermore elevation of basal tone of vasa vasorum alters the profile of contractile reactivity. These results suggest that ET-1 may be an important regulator of vasa vasorum reactivity. (+info)
Transarterial wall oxygen gradients at a prosthetic vascular graft to artery anastomosis in the rabbit.
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PURPOSE: Artery-wall hypoxia has been proposed to contribute to many kinds of artery-wall pathologic conditions, including atherosclerosis and intimal hyperplasia. Intimal hyperplasia is common at sites of arterial injury, including an anastomosis. The purpose of this study was to determine the effect of a prosthetic vascular graft (PVG)-to-artery anastomosis on the delivery of oxygen to the artery wall. METHODS: The transarterial wall oxygen gradient in the infrarenal aorta of New Zealand White rabbits 2 mm distal to a PVG-to-artery anastomosis was measured with an oxygen microelectrode. RESULTS: Oxygen tensions were significantly decreased in the outer artery wall immediately after the creation of the anastomosis and showed a further decrease in oxygen tensions at days 7 and 14, which correlated with the absence of a vasa vasorum. After day 14, the oxygen tensions gradually increased, returning to normal by postanastomosis day 42, correlating with a return of the vasa vasorum. These changes were noted without differences in blood pressure or arterial blood oxygen concentrations. CONCLUSION: The delivery of oxygen to the artery wall is altered by the creation of a PVG-to-artery anastomosis. Low arterial oxygen tensions at a PVG-to-artery anastomosis support a role for artery-wall hypoxia in the formation of intimal hyperplasia at the site of a PVG-to-artery anastomosis. (+info)
Endogenous factors involved in regulation of tone of arterial vasa vasorum: implications for conduit vessel physiology.
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The walls of conduit blood vessels are nourished by diffusion of oxygen from luminal blood and from the vasa vasorum. The vasa vasorum, or 'vessels of a vessel', form a network of microvessels that lie in the adventitia and penetrate the outer media of the host vessel wall. Although the importance of the vasa vasorum in providing nutritional support is not well defined, obstruction of blood flow through these vessels has been implicated in the pathogenesis of certain cardiovascular diseases including atherosclerosis. This review focuses on the mechanisms that regulate tone in the vasa vasorum of large arteries and the functional implications of changes in reactivity of vasa vasorum. (+info)
OBJECTIVE: Experimental hypercholesterolemia is associated with vasa vasorum neovascularization, unknown to occur before or after initial lesion formation. Thus, this study was performed to determine the temporal course of neovascularization of coronary vasa vasorum in relation to endothelial dysfunction, a hallmark of early atherosclerosis. METHODS: Female domestic pigs were fed a normal diet (Group 1), a hypercholesterolemic diet for 2 and 4 weeks (Group 2), or a hypercholesterolemic diet for 6 and 12 weeks (Group 3). In vitro analysis of relaxation response to bradykinin served as an index for epicardial endothelial function. Spatial pattern and density of coronary vasa vasorum were assessed by three-dimensional microscopic computed tomography. RESULTS: Relaxation response of coronary arteries to bradykinin was normal in both Group 1 (93+/-6%) and Group 2 (89+/-7%) but impaired in Group 3 (71+/-11%; P<0.05 vs. Group 1 and 2). In contrast, density of coronary vasa vasorum was significantly higher in both Group 2 (4.88+/-2.45 per-mm(2)) and Group 3 (4.50+/-1.37 per-mm(2)) compared to Group 1 (2.97+/-1.37 per-mm(2); P<0.05 vs. Group 2 and 3). CONCLUSION: This study demonstrates that coronary vasa vasorum neovascularization occurs within the first weeks of experimental hypercholesterolemia and prior to the development of endothelial dysfunction of the host vessel, suggesting a role for vasa vasorum neovascularization in the initial stage of atherosclerotic vascular disease. (+info)
Hypoxia-inducible factor-1alpha/vascular endothelial growth factor pathway for adventitial vasa vasorum formation in hypertensive rat aorta.
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The roles of adventitial vasa vasorum have been highlighted in vascular wall homeostasis. Vascular endothelial growth factor (VEGF) is a potent angiogenic factor in physiological and pathophysiological conditions. However, little is known regarding the changes in adventitial vasa vasorum and the mechanism of the formation in hypertensive arteries. Accordingly, endothelial cell proliferation, adventitial vasa vasorum count, and expression of VEGF signaling axis proteins were examined in the ascending aorta of hypertensive Wistar rats that underwent suprarenal aortic constriction. Hypertension not only induced medial and adventitial thickening but also significantly increased adventitial vasa vasorum count by day 28. Preceding the medial thickening, BrdU(+)-proliferative endothelial cells were observed in the adventitia but not in the media and intima after day 3; they peaked at day 7 and remained modestly increased at day 28. The BrdU(+) endothelial cells showed induction of Ets-1, a transcription factor mediating angiogenic response of VEGF. Furthermore, concomitant expression of VEGF and a hypoxia-inducible transcription factor (HIF-1alpha) was observed in the outer layers of medial smooth muscle cells at day 3 and extended to the middle layers of medial smooth muscle cells at day 7, returning to lower levels by day 28. In conclusion, adventitial vasa vasorum formation was induced by hypertension through the HIF-1alpha/VEGF/Ets-1 pathway during hypertensive remodeling. (+info)