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PubMed1992

Polyarteritis nodosa with aortic dissection: necrotizing vasculitis of the vasa vasorum.

A 59-year-old woman was admitted to our hospital with acute onset of chest pain. She had experienced high fever, weight loss, polyarthralgia, myalgia, polyneuropathy and hallucinations for 3 years before admission. The diagnosis of polyarteritis nodosa with hepatitis B surface antigenemia was made by muscle biopsy and serological examinations, and administration of prednisolone induced remission of all the manifestations. After developing the acute attack of severe chest pain, she died suddenly. At autopsy, a DeBakey type 1 aortic dissection was found and the immediate cause of death was found to be cardiac tamponade secondary to rupture of the aortic dissection. Microscopically, necrotizing inflammatory lesions were present in the medium sized vascular arteries throughout her body. Furthermore, necrotizing vasculitis was also found in the vasa vasorum of the adventitia and media of the thoracic aorta. The dissecting lesion was seen in the outer layer of the media. Our results suggest that spontaneous dissection of the aorta may be attributed to necrotizing vasculitis of the vasa vasorum.

Aortic Dissection↗
PubMed1981

[Vasa-vasorum (author's transl)].

More than a common descriptive interest, this researches about vasa-vasorum have been carried on to give some anatomical basis, to the part acted by those vessels in arterial wall life. Microdissections, X-rays diaphanisation enable us to systematize even in human kind than in animal species, the main aspects of this vascularisation. The conception of a double irrigation, from the lumen and from the vasa of the blood vessels, and the presence of a venous and lymphatic drainage, can give us the basis of an interpretation of the beginning of the main arterial diseases.

Arteries↗
PubMed1992

The vasa vasorum and the paradox of beta-blocker therapy.

The use of beta-blockers in the treatment of angina, claudication or hypertension is a therapeutic paradox. All those conditions feature increased constrictor tone, so it appears to make little sense to treat them with drugs which block the action of vasodilators. The paradox would disappear, however, if vasodilators could be shown to have the ability to increase constrictor tone in certain circumstances. This paper argues that they have. It presents evidence that isoprenaline, a potent dilator of the dog's saphenous vein, is a powerful constrictor of the vein when it is released from the vasa vasorum of the vein. Indeed, on a molar basis, it appears to be a more powerful constrictor of the vein than exogenous noradrenaline is. Since there is no reason to suppose that isoprenaline is unique among dilators in demonstrating this type of bimodal behaviour, it is possible to justify the proposal that compounds which are normally classified as endogenous dilators may, when released from the pathological vasa vasorum which neoproliferate in atherosclerosis, be responsible for the constrictor effects associated with claudication, and some forms of hypertension and angina. If true then beta-blockade would not be a paradoxical choice of treatment for those conditions.

Adrenergic beta-Antagonists↗
PubMed2002

Lack of sumatriptan-induced aortic contraction or relaxation: 5-HT1B receptor protein detected in endothelium and smooth muscle of vasa vasorum but not aorta.

Since 5-HT1B receptor mRNA was reported in rat aorta, and 5-HT1B receptor activation has been linked to vascular contraction, we explored sumatriptan-induced contractility and immunohistochemical density of 5-HT1B receptor protein in rat aorta. Sumatriptan (up to 10(-4) M), a 5-HT1B/1D receptor agonist, did not contract the endothelial intact or denuded rat aorta, even in the presence of L-NAME or after induction of modest tone with PGF2 alpha (10(-6) M). Sumatriptan also did not relax aortic preparations precontract with PGF2 alpha (3 x 10(-6) M) or phenylephrine (3 x 10(-7) M). Using a polyclonal antibody directed against the 5-HT1B receptor, minimal 5-HT1B receptor protein was detected in either the endothelium or smooth muscle of the rat aorta. However, dense 5-HT1B receptor protein was found in the vascular smooth muscle of the vasa vasorum supplying the aorta. Thus, the 5-HT1B receptor mRNA detected in tissue extracts of the rat aorta most likely reflects 5-HT1B receptor expression in the arterioles of the vasa vasorum. These studies support the link between the 5-HT1B receptor and vascular contraction in that the aorta with low density of 5-HT1B receptors lacked responses to sumatriptan, an agonist thought to contract blood vessels via 5-HT1B/1D receptors. Furthermore, caution must be observed when using 5-HT1B receptor mRNA to suggest receptor protein in tissues since this RT-PCR product may be derived predominantly from small blood vessels.

Animals↗
PubMed2003

Continued growth of and increased symptoms from a thrombosed giant aneurysm of the vertebral artery after complete endovascular occlusion and trapping: the role of vasa vasorum. Case report.

A 58-year-old woman harboring a partially thrombosed giant aneurysm of the vertebral artery (VA) presented with lower cranial nerve palsies and cerebellar ataxia. The authors initially attempted to reduce the mass effect by obliterating the lumen of the aneurysm as well as by trapping of the parent artery with coils. Although there was no angiographically demonstrated evidence of filling, the aneurysm continued to enlarge. Magnetic resonance imaging revealed a marked enhancement around the packed coils close to the neck of the aneurysm. Aneurysmectomy and removal of the coils were performed and resulted in an almost complete cure of the patient's symptoms. Interestingly, at the time of resection, a marked development of vasa vasorum on the occluded VA and the neck of the aneurysm was noted. When the occluded VA was cut, there was blood oozing through the coils packed within its lumen on the side where the aneurysm lay. Histological examination showed the presence of inflammatory cells and neovascularization of a partially organized thrombus around the packed coils in both the aneurysm and occluded VA. The proliferation of vasa vasorum was also recognized histologically. This unique case provides insight into the growth mechanisms of a partially thrombosed giant aneurysm after an apparently complete occlusion by endovascular treatment, especially the role of vaso vasorum on the occluded parent artery in the dynamic process of neovascularization in the incomplete organization of thrombus around the packed coils.

Aneurysm↗
PubMed1990

Histological framework of lymphatic vasa vasorum of major arteries: an experimental study.

We investigated the histological framework of lymphatic vasa vasorum of major arteries in the rabbit and guinea pig combining the "natural filling method" with light and transmission electron microscopy. An absorbing adventitial lymphatic network consisting of large and sparsely distributed vessels with capillary structure occupied a more external arterial wall position than blood capillaries. The latter were smaller, more numerous, densely distributed, and located closer to the arterial lumen at the media-adventitial border. Periarterial lymphatics (with the structure of absorbing lymph vessels) encircled the wall of the major arteries and formed a rich and irregular plexus. The topography and anatomic structure of these absorbing lymph vessels suggest that lymphatic drainage plays a significant role in large arterial wall homeostasis.

Animals↗
PubMed2002

Vasa vasorum hypoperfusion is responsible for medial hypoxia and anatomic remodeling in the newborn lamb ductus arteriosus.

Postnatal constriction of the full-term ductus arteriosus produces hypoxia of the muscle media. This is associated with anatomic remodeling (including smooth muscle death) that prevents subsequent reopening. We used late-gestation fetal and neonatal lambs to determine which factors are responsible for the postnatal hypoxia. Hypoxia [measured by 2-(2-nitro-1H-imidazol-1-yl)-N-(2,2,3,3,3-pentafluoropropyl) acetamide technique] and cell death (measured by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling technique) were observed in regions of the constricted ductus wall within 4 h after delivery. Although there was a decrease in ductus luminal flow during the first 6 h after delivery (measured by Doppler transducer), the amount of oxygen delivered to the ductus lumen (3070 +/- 1880 micromol O2 x min(-1) x g(-1)) far exceeded the amount of oxygen consumed by the constricted ductus (0.052 +/- 0.021 micromol O2 x min(-1) x g(-1), measured in vitro). Postnatal constriction increased the effective oxygen diffusion distance across the ductus wall to >3x the limit that can be tolerated for normal tissue homeostasis. This was owing to both an increase in the thickness of the ductus (fetus, 1.12 +/- 0.20 mm; newborn, 1.60 +/- 0.17 mm; p < 0.01) and a marked reduction in vasa vasorum flow (fetus, 0.99 +/- 0.44 mL x min(-1) x g(-1); newborn, 0.21 +/- 0.08 mL x min(-1) x g(-1); p < 0.01). These findings suggest that hypoxic cell death in the full-term ductus is caused primarily by changes in vasa vasorum flow and muscle media thickness and can occur before luminal flow has been eliminated. We speculate that in contrast with the full-term ductus, the preterm ductus is much less likely to develop the degree of hypoxia needed for vessel remodeling inasmuch as it only is capable of increasing its oxygen diffusion distance to 1.3x the maximally tolerated limit.

Animals↗
PubMed1998

Regulation of ductus arteriosus patency by nitric oxide in fetal lambs: the role of gestation, oxygen tension, and vasa vasorum.

We hypothesized that nitric oxide (NO) production by the fetal ductus arteriosus is limited because of low fetal PO2, but that at neonatal PO2, NO might be an important regulator of ductus arteriosus tone. We exposed isolated rings of fetal lamb ductus arteriosus to elevated PO2. L-NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS), and methylene blue and 6-anilino-5,8-quinolinedione (LY83583), inhibitors of guanylate cyclase, produced constriction of the ductus arteriosus. When ductus arteriosus rings were exposed to low PO2, L-NAME had no effect, and methylene blue and LY83583 had only a small effect on ductus arteriosus tone. Sodium nitroprusside and calcium ionophore A23187 relaxed ductus arteriosus rings more than aortic rings, and relaxed ductus arteriosus rings from immature fetuses more than those from late gestation fetuses. In contrast, ductus arteriosus rings from both early and late gestation were equally sensitive to 8-bromo-cGMP. By both reverse transcriptase-polymerase chain reaction and immunohistochemistry, endothelial cell NOS and inducible calcium-independent NOS, but not nerve cell NOS, were detected in the ductus arteriosus. Inducible NOS was expressed only by endothelial cells lining the ductus arteriosus lumen; in contrast, endothelial cell NOS was expressed by both luminal and vasa vasorum endothelial cells. The role of inducible NOS in the ductus arteriosus is uncertain because the potency of a specific inducible NOS inhibitor in constricting the ductus arteriosus was negligible compared with that of an endothelial cell NOS inhibitor. We speculate that NO may be an important regulator of ductus arteriosus tone at high but not low PO2. The endothelial cell NOS isoform found in vasa vasorum may be an important source of NO because removal of ductus arteriosus luminal endothelium only partially blocks the effects of L-NAME, methylene blue, and LY83583.

Aminoquinolines↗
PubMed1988

The three-dimensional architecture of vasa vasorum in the wall of the human aorta. A computer-aided reconstruction study.

The three-dimensional architecture of vasa vasorum in the wall of aorta was studied by microcomputer-aided reconstruction from serial sections of wall tissue in two young individuals submitted to autopsy. The outer media was sparsely penetrated by special tunnels containing an arteriole and a venule, which we termed a "vascular cord" due to the broad space between neighboring cords that contained no capillary network whatsoever. A dense venular plexus was found extending along the outer surface of the media, forming a plane of low blood pressure. This characteristic pattern of vasculature appeared to provide an important basis on which to study the way the medial tissues are sustained.

Adult↗
PubMed1989

[The vasa vasorum of peripheral lymph vessels in the human].

Using the anterior inner prefascial bundle as an example the structure of the vasa vasorum of lymphatic vessels can be demonstrated. They have a one-dimensional capillary network of their own in the outer layers of the vascular wall. In humans this network is already differential in the second half of the fetal period.

Adult↗
PubMed2002

Simvastatin preserves the structure of coronary adventitial vasa vasorum in experimental hypercholesterolemia independent of lipid lowering.

BACKGROUND: Previous studies have demonstrated that experimental hypercholesterolemia leads to neovascularization in the coronary artery vasa vasorum (VV). Recent evidence suggests that HMG-CoA reductase inhibitors (statins) have beneficial effects independent of lipid lowering. We aimed to determine the effect of simvastatin on coronary VV neovascularization, in the absence of cholesterol lowering. METHODS AND RESULTS: Pigs were randomized to 3 groups fed a normal (N), high cholesterol (HC), or HC+simvastatin (HC+S) diet for 12 weeks. The proximal left anterior descending artery was isolated, scanned with micro-CT, and reconstructed. Quantification of the VV density in serial cross-sections along the vessel was then performed. LDL cholesterol was similarly increased in HC and HC+S compared with N. There was an increase in both VV density (4.7+/-0.3 versus 2.7+/-0.2 n/mm(2); P<0.05) and vessel wall area (3.1+/-0.2 versus 1.8+/-0.1 mm(2); P<0.05) in HC compared with N. The VV density in HC+S was preserved compared with HC (3.0+/-0.2 n/mm(2); P<0.05), despite similar increase in vessel wall area compared with N (2.5+/-0.1 mm(2); P<0.05). Coronary artery tissue expression of VEGF was increased in HC but not in HC+S compared with N. In parallel, immunoreactivity for HIF-1alpha, VEGF, MMP-2, and MMP-9 was accentuated in the outer media in HC but not in HC+S compared with N. CONCLUSIONS: This study demonstrates that simvastatin attenuates hypoxia in the coronary artery wall and VV neovascularization in experimental hypercholesterolemia, despite no change in plasma lipids. These data are consistent with an additional mechanism for the vascular effects of the statins, independent of cholesterol lowering.

Animals↗
PubMed1979

Aortic vasa vasorum in cyanotic congenital heart disease.

Three cases for longstanding untreated cyanotic congenital heart disease are presented. In addition to collateral circulation from bronchial, intercostal, and inferior phrenic arteries, thoracic aortic vasa vasorum were visualized. We believe this may represent an additional collateral pathway to the lungs. The angiography of these cases is presented.

Adolescent↗
PubMed2005

Correlation of vasa vasorum neovascularization and plaque progression in aortas of apolipoprotein E(-/-)/low-density lipoprotein(-/-) double knockout mice.

OBJECTIVE: We hypothesized that apolipoprotein E (apoE)(-/-)/low-density lipoprotein (LDL)(-/-) double knockout mice might develop vasa vasorum (VV) in association with advanced lesion formation. METHODS AND RESULTS: Aortas from apoE(-/-)/LDL(-/-) mice aged 16, 18, 20, or 80 weeks were infused in situ with Microfil, harvested, and scanned with micro-computed tomography (CT). We characterized plaque volume and CT "density" as well as VV luminal volume along the aorta using Analyze 6.0 software. Results were complemented by a detailed histological plaque classification according to American Heart Association guidelines. From 16 to 80 weeks, plaque volume and VV opacified lumen volume increased with age (P<0.001). The 3-dimensional micro-CT images of arterial and venous VV trees allowed perfusion territories to be delineated. The spatial location and magnitude of VV density and adventitial inflammation were strongly correlated in advanced atherosclerotic lesions (r=0.91) and identified as an independent correlate to advanced lesions. At age 80 weeks, VV luminal volume was increased 20-fold compared with animals at age 16 weeks (P<0.001). Micro-CT showed that adventitial VV communicate with intraplaque microvessels. CONCLUSIONS: Our results show that apoE(-/-)/LDL(-/-) double knockout mice develop VV and advanced atheromas along the aorta. Lesion volume was closely associated with amount of neovascularization in advanced atheromas.

Animals↗
PubMed2004

Role of vasa vasorum in transendothelial solute transport in the coronary vessel wall: a study with cryostatic micro-CT.

Using cryostatic microscopic computed tomography (micro-CT), we sought to determine the role of coronary vasa vasorum (VV) in transendothelial solute transport in arteries with normal and increased permeability due to high plasma cholesterol levels. In 6-mo-old pigs on a normal (n=23) and 2% high cholesterol (HC) diet (n=8), 2-cm segments of the proximal left anterior descending coronary arteries were removed in vivo after a selective injection of X-ray contrast solution. Harvesting of the specimens occurred at 0, 15, 25, 35, or 45 s after completion of the contrast injection. Specimens were snap frozen and scanned in our cryostatic micro-CT. The spatial distribution of contrast in the coronary artery wall was quantified using the CT images. Right coronary arteries were infused with Microfil to determine VV density (VV/mm2) and the cumulative lumen surface area (mm2/mm3). Transendothelial diffusion of contrast into the coronary vessel wall is a dynamic process starting at both the subintima and the adventitia. The subintimal opacification moves as a wave toward the adventitia, whereas the adventitial wave resolves. The coronary vessel wall in animals on a HC diet shows higher opacification than in normal coronary arteries without an increase of VV total luminal surface area. The loss of endothelial integrity in hypercholesterolemia significantly alters VV solute washin to, and washout from, the coronary artery wall.

Animals↗
PubMed2005

Intravascular ultrasound-based imaging of vasa vasorum for the detection of vulnerable atherosclerotic plaque.

Vulnerable plaques are dangerous atherosclerotic lesions that bear a high risk of complications that can lead to heart attacks and strokes. These plaques are known to be chronically inflamed. The vasa vasorum (VV) are microvessels that nourish vessel walls. Proliferation of VV is part of the "response to injury" phenomenon in the process of plaque formation. Recent evidence has shown strong correlations between neovessel formation and macrophage infiltration in atherosclerotic plaque, suggesting VV density as a surrogate marker of plaque inflammation and vulnerability. We have developed a novel method for imaging and analyzing the density and perfusion of VV in human coronary atherosclerotic plaques using intravascular ultrasound (IVUS). Images are taken during the injection of a microbubble contrast agent and the spatiotemporal changes of the IVUS signal are monitored using enhancement-detection techniques. We present analyses of in vivo human coronary cases that, for the first time, demonstrate the feasibility of IVUS imaging of VV.

Coronary Artery Disease↗
PubMed1992

Basic fibroblast growth factor enhances the coupling of intimal hyperplasia and proliferation of vasa vasorum in injured rat arteries.

Basic fibroblast growth factor (bFGF) is mitogenic for smooth muscle cells (SMC) and angiogenic. We examined the in vivo effects of bFGF in balloon denuded carotid arteries of laboratory rats. bFGF was administered continuously from polymer-based devices at 34 ng/d into the periadventitial space of rat carotid arteries for 2 wk. Intimal hyperplasia was not observed in the absence of injury or with lipopolysaccharide induced endothelial dysfunction. Different degrees of vascular injury produced proportionally more intimal hyperplasia. bFGF increased the intimal hyperplastic response 1.3-fold with severe vascular injury, and 2.4-fold with more mild injury. Increased cell proliferation, not extracellular matrix production, accounted for these effects. Cell density was unchanged for the control and bFGF-treated groups, and the number of proliferating intimal cells at 2 wk rose to an amount equivalent to the increase in mass; 1.9- and 4.0-fold for severe and lesser injury, respectively. The relative ability of heparin to reduce SMC proliferation was not altered by the presence of bFGF.bFGF also induced profound angiogenesis within and surrounding the polymeric releasing device, and in the vasa vasorum immediately around the injured arteries. bFGF's effect on vasa was linearly related to the amount of SMC proliferation within the blood vessel. Thus, the in vivo mitogenic and angiogenic potential of bFGF are coupled, and may be similarly modulated by the products of local injury and/or factors in the vessel wall.

Animals↗
PubMed2006

Vasa vasorum neovascularization and lesion distribution among different vascular beds in ApoE-/-/LDL-/- double knockout mice.

OBJECTIVE: To increase understanding of the substantial variation in the incidence and distribution of atherosclerotic lesions among different vascular beds. In view of some evidence that there are different distributions of adventitial vasa vasorum (VV) in different vascular beds, and that this correlates with lesion formation, we explored this possible linkage in apoE-/-/LDL-/- double knockout mice, which develop VV at age beyond 16 weeks. METHODS AND RESULTS: Samples from the aorta, coronary, pulmonary, carotid, and cerebral arteries in apoE-/-/LDL-/- double knockout mice at the age of 16-80 weeks (n=24) were scanned by micro-CT. Using those 3D images, we characterized plaque volume, vessel luminal diameter and VV luminal volume along the vessels. Results were complemented by histology. Advanced atherosclerotic lesions were found in the aorta, pulmonary artery and carotid artery. Occluded intramyocardial vessels (vessel diameter approximately 0.1mm) with concomitant myocardial infarctions were found without any evidence of adventitial VV neovascularization. VV luminal volume follows the order: aorta>pulmonary arteries>carotid arteries. VV were only observed in atherosclerotic diseased vessels with a lumen diameter>0.4mm. No atherosclerotic lesions, and no VV, were observed in cerebral arteries. CONCLUSION: The spatial heterogeneity in the development of atherosclerotic lesions among different vascular beds is linked to appearance of VV and to vessel lumen diameter.

Animals↗