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Results for “VASA VASORUM”

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PubMed1991

The roles of turbulence and vasa vasorum in the aetiology of varicose veins.

Noradrenaline can dilate a canine lateral saphenous vein which at the time is constricted by noradrenaline. It does so when it is released from the vasa vasorum network of the constricted vein. By filling a limited section of the network of a normal, tonically constricted vein with endogenous noradrenaline it is possible to dilate the vein locally, in effect creating an acute experimental varicosity. These findings have led to the proposal that human varicosities are an active response of the vein to endogenous noradrenaline released from sections of its vasa vasorum network. The noradrenaline involved is part of the circulating overflow derived from normal adrenergic nerve activity. A bout of turbulence in the vein lumen is proposed as the trigger which causes a reflux of hypoxic blood and the endogenous noradrenaline in it from the vein lumen to the vasa. The size and shape of the varix reflects the mosaic pattern of a vein's vasa vasorum network. The site of the varicosity is determined by the location in the vein lumen of the bout of turbulent non-laminar flow.

Animals↗

PubMed1984

Intracranial vessels lack vasa vasorum.

A micro-corrosion technique was used to demonstrate an extensive vasa vasorum network in extracranial vessels but did not reveal this system in intracranial vessels of comparable size in three species of animals. The absence of a vasa vasorum network in cerebral vessels may result in a higher level of susceptibility to periarterial abnormalities, such as cerebral vasospasm secondary to subarachnoid hemorrhage.

Animals↗

PubMed2005

Vasa vasorum imaging: a new window to the clinical detection of vulnerable atherosclerotic plaques.

Complications of vulnerable atherosclerotic plaques (rupture, luminal and mural thrombosis, intraplaque hemorrhage, rapid progression to stenosis, spasm, and so forth) lead to heart attacks and strokes. It remains difficult to identify what plaques are vulnerable to these complications. Despite recent developments such as thermography, spectroscopy, and magnetic resonance imaging, none of them is approved for clinical use. Intravascular ultrasound (IVUS), a relatively old yet widely available clinical tool for guiding intracoronary procedures, is increasingly used for characterization of atherosclerotic plaques. However, inability of IVUS in measuring plaque activity limits its value in detection of vulnerable plaques. In this review, we present new information suggesting that microbubble contrast-enhanced IVUS can measure activity and inflammation within atherosclerotic plaques by imaging vasa vasorum density. An increasing body of evidence indicates that vasa vasorum density may be a strong marker for plaque vulnerability. We suggest that a combination of structural assessment (cap thickness, lipid core, calcification, etc) and vasa vasorum density imaging by IVUS can serve as the most powerful clinically available tool for characterization of vulnerable plaques. Due to space limitations, all IVUS images and movies are posted on the website of the Ultimate IVUS Collaborative Project: http://www.ultimateivus.com.

Albumins↗

PubMed1997

Microanatomy of the vasa vasorum of the human thoracic aorta: a study utilizing a polyester resin casting technique.

We have studied the vasa vasorum of the human thoracic aorta using a polyester resin casting technique, coupled with the tissue clearing method of Spalteholz. We found that the vasa vasorum originated from intercostal arteries. They ramified and formed networks within the aortic adventitia and the outer layers of the media. Venous networks were identified in the adventitia as wall. In addition to being a usefull research tool, the methodology utilized in this study produces specimens that can be used in teaching vascular anatomy to medical students.

Adult↗

PubMed1989

The role of vasa vasorum in atherosclerosis.

Experiments have shown that noradrenaline can dilate the lateral saphenous vein of the dog when that vein has been constricted by noradrenaline, at the same concentration, in the first place. This dilator action of noradrenaline occurs when the drug stimulates the constricted vein through its outer surface after it is released from the vein's vasa vasorum network. There is evidence suggesting that this effect is not unique to noradrenaline and that the effect of any agonist stimulating a blood vessel through its lumenal surface may be reversed following its release from vasa vasorum. This phenomenon may be important in the context of the known relationship there is between the severity of the symptoms of atherosclerosis and the degree to which vasa vasorum proliferate de novo in the adventitia of blood vessels affected by that disease. It is suggested that in atherosclerosis endogenous vasodilators have their actions reversed by release from these pathological vasa. This would result in the vasodilators of exercise having a constrictor action on the coronary vessels and becoming the immediate cause of angina. If vasodilators do indeed cause angina then the use of beta-blockade in this condition becomes a rational rather than an empirical method of treatment. An hypothesis is advanced to explain the phenomenon of drug action reversal.

Animals↗

PubMedDate not supplied

Blood flow through vasa vasorum of coronary arteries in atherosclerotic monkeys.

Morphologic studies and postmortem arteriograms provide qualitative evidence that atherosclerosis induces neovascularization in coronary arteries. In this study we obtained the first measurements of blood flow through vasa vasorum in atherosclerotic coronary arteries. We measured blood flow with microspheres to intima media and to adventitia in normal and atherosclerotic cynomolgus monkeys. Blood flow to adventitia was not altered by atherosclerosis. The blood flow to intima media, however, was increased more than fivefold by atherosclerosis: flow was 3 +/- 1 in normal animals and 16 +/- 5 in atherosclerotic monkeys (p less than 0.05). Blood flow was threefold greater in atherosclerotic than in normal coronary arteries during adenosine-induced vasodilatation, which suggests that proliferation of new vessels, not dilatation of existing vessels, accounts for the increase in flow through vasa in intima media. Histologic studies indicated that vasa vasorum to intima media in atherosclerotic coronary arteries originate from adventitial vasa. We conclude that: 1) there is a large increase in blood flow through vasa vasorum to intima media, but not to adventitia, in atherosclerotic coronary arteries; and 2) increased flow is produced primarily by proliferation of new vessels that originate from adventitial vasa.

Animals↗

PubMed1975

[Intravital study of the vasa vasorum by the transmural vasoscopy method].

The paper presents a method of transmural vasoscopy for intravital observation of vasa vasorum in the wall of main blood vessels in acute experiments in anesthetized dogs. The optical part of the cytoscope introduced into the vessels under study (the portal vein, vena cava or aorta) via the nearest largest branch was used as a source of light. For this purpose, a longitudinal cut 0,5 cm long was made in the vessel between two clamps put at a distance of 2-2,5 cm from one another. The part of the cytoscope was inserted through the cut, the vessel was ligated proximally to the cut and the proximal clamp was removed. Then the optical part of the cytoscope was introduced in the lumen of the vessel under study at a distance of 4-5 cm. The microscope MBS-1 mounted on a specially constructed bracket was used for visual observation and measuring morphological parameters of vasa vasorum. A special tubus was put on one of the oculars with a camera fixed to it. On filming in falling and passing light observations and focussing were performed through the free ocular.

Animals↗

PubMed1988

Blood flow through new microvessels: factors that affect regrowth of vasa vasorum.

A segment of abdominal aorta in dogs was transplanted to its original position (high PO2) or to the femoral vein (low PO2), and a segment of thoracic aorta was transplanted to its original position. Two days after grafting to each location, there was no blood flow (measured with microspheres) through vasa vasorum. After 2 and 4 wk, blood flow through vasa was restored to normal, or above normal, levels in all grafts. Vasa in grafts did not have smooth muscle, and they were not responsive to adenosine. Medial necrosis occurred in grafts of thoracic aorta but not in grafts of abdominal aorta. There was cellular degeneration and medial atrophy in grafts of abdominal aorta to the femoral vein. We conclude that 1) revascularization of the aorta by vasa vasorum is rapid; 2) new vasa do not have smooth muscle, and they are not responsive to vasoactive stimuli; and 3) medial necrosis occurs in grafts in which delivery of oxygen to media is compromised, either by low luminal PO2 or by interruption of medial vasa (in thoracic aorta), but not when the abdominal aorta is excised and reanastomosed. Absence of medial necrosis in grafts of abdominal aorta indicates that diffusion from the lumen of the vessel is adequate to nourish the vessel. This finding provides evidence that adventitial vasa, in contrast to medial vasa, are not essential for nourishment of the vessel wall.

Adenosine↗

PubMed1995

Age-related alterations in the morphology of femoral artery vasa vasorum in the rat.

The objective of this study was to explore any age-related morphological changes in the vasa vasorum of the rat femoral artery. Vascular corrosion casts were prepared from 2, 12 and 24-month-old rats. Examination of the casts with the scanning electron microscope revealed dramatic differences in the appearance of the vessels of young and aged rats. The vasa vasorum of 2-month-old rats consisted of a dense network of capillaries. These vessels were dramatically reduced in number by 12 months, and even fewer capillaries were present at 24 months. This reduction in capillary density is consistent with the observed age-related decreases in oxygen tension and may explain why the aged are more prone to atherosclerosis.

Aging↗

PubMed1993

[125I]-endothelin-1 binding to vasa vasorum and regions of neovascularization in human and porcine blood vessels: a possible role for endothelin in intimal hyperplasia and atherosclerosis.

The distribution of [125I]-endothelin-1 (ET-1) binding sites on human and porcine vessels was studied with in vitro receptor autoradiography. Binding to normal human saphenous veins was compared to atheromatous veins used as coronary artery bypass grafts. Binding to porcine vessels, from an experimental model of intimal hyperplasia, was also studied. There was dense binding of [125I]-ET-1 to smooth muscle of all vessels examined, as well as to the vasa vasorum and regions of neovascularization of diseased vessels. Binding to microvasculature (vasa vasorum and regions of neovascularization) is of particular interest, because ET-1 has been shown to have mitogenic activity on vascular smooth-muscle cells in culture and microvessels are extremely sensitive to the constrictor effect of ET-1. Binding of [125I]-ET-1 to vasa vasorum of normal blood vessels and to regions of neovascularization of atheromatous vessels suggests that ET-1 plays a pathophysiologic role in atherosclerosis.

Animals↗

PubMedDate not supplied

Changes in the vasa vasorum following percutaneous transluminal angioplasty in a canine model of aortic stenosis.

PURPOSE: To investigate the effects of percutaneous transluminal angioplasty on the vasa vasorum in dogs with experimentally created abdominal aortic stenoses. MATERIALS AND METHODS: Two stenoses were created in the abdominal aorta in each of 21 dogs. After 6 weeks, the more cephalic stenosis was dilated; the other stenosis served as an untreated control. Groups of three dogs were killed at 24 hours, 3 and 6 weeks, and 4, 8, 12, and 18 months after angioplasty. The aortae were studied by means of histologic examination, microangiography, scanning electron microscopy, and the Spalteholz technique. RESULTS: At nondilated stenoses, the vasa vasorum was interrupted in the outer adventitia and unchanged in the outer media. At dilated stenoses, the number of precapillary arterioles in the outer media progressively increased up to 8 months; thereafter, the number of precapillary arterioles began to decrease. At 18 months, the number was normal. CONCLUSION: Angioplasty brings about changes in the number of precapillary arterioles in the outer media of the aorta in our canine model of focal abdominal aortic stenosis.

Angioplasty, Balloon↗

PubMed1989

Vasa vasorum in the carotid sinus of atherosclerotic monkeys: implications for baroreceptor function.

The carotid sinus is unusually susceptible to development of severe atherosclerotic lesions. The purposes of this study were to examine effects of atherosclerosis on blood flow through vasa vasorum in the carotid sinus and to examine responses to humoral stimuli. Blood flow to vasa in the carotid sinus was measured with microspheres in 8 normal and 9 atherosclerotic cynomolgus monkeys. Blood flow to vasa in intima-media (in ml/min per 100 g) was 0.5 +/- 0.3 (mean +/- SE) in normal and 21 +/- 5 in atherosclerotic monkeys (P less than 0.05). Flow to adventitial vasa was 37 +/- 5 in normal monkeys and 50 +/- 7 in atherosclerotic monkeys (P greater than 0.05). Infusion of phenylephrine did not affect blood flow in normal or atherosclerotic monkeys. Infusion of serotonin did not affect blood flow to vasa in normal monkeys, but decreased flow to vasa in both intima-media and adventitia of atherosclerotic monkeys. In normal media, histological examination demonstrated the presence of a few vasa vasorum, which penetrated from adventitia. In atherosclerotic monkeys, medial vasa were much more frequent. Thus, (1) atherosclerosis produces marked increases in blood flow through vasa in intima-media of the carotid sinus, probably as a consequence of proliferation of vasa, and (2) in atherosclerotic monkeys, vasa constrict in response to serotonin. Based on these findings, we speculate that when serotonin is released as platelets aggregate at plaques in the carotid artery, serotonin may be delivered through vasa to nerves in the carotid sinus and thereby affect baroreceptor function.

Animals↗

PubMedDate not supplied

First experimental application of bevacizumab-eluting PC coated stent for inhibition of vasa vasorum of atherosclerotic plaque: angiographic results in a rabbit atheromatic model.

INTRODUCTION: Atheromatosis is associated with angiogenesis, through the development of a dense net of vasa vasorum. The role of vascular endothelial growth factor (VEGF) is important in this process. Bevacizumab, an antibody specific for VEGF, has recently been applied in the clinical field. We hypothesized that local delivery of bevacizumab by stent would inhibit the development of vasa vasorum at the stented arterial segment in an atheromatic rabbit model. METHODS: We used 10 New Zealand rabbits under atherogenic diet for 3 weeks. We immersed a BiodivYsio stent into a solution of 4 ml bevacizumab as in previous studies. Both eluting stents and non-eluting BiodivYsio stents were implanted in the middle segment of the 2 iliac arteries of the animals, with the same procedural characteristics. Sacrifice following repeat angiogram was scheduled after 28 days. RESULTS: In all animals the procedure of stent loading with bevacizumab and stent implantation was successful. There was no acute or subacute thrombosis. Iliac artery lumen diameters before and immediately after stent placement were similar in all stent treatment groups. At euthanasia stent lumen diameters were similar in all groups. All stents were angiographically patent at the time of euthanasia without aneurysm formation. Moreover, gross pathologic analysis did not show any evidence of vascular necrosis. CONCLUSIONS: Bevacizumab-eluting stent implantation in atheromatic rabbit iliac arteries is feasible and safe. This new approach for the treatment of stable and vulnerable plaques needs to be further investigated.

Angiogenesis Inhibitors↗

PubMed1991

Arterial wall hypoxia following thrombosis of the vasa vasorum is an initial lesion in atherosclerosis.

Pressure on the outside of arteries can cause physical and biochemical changes in the vessel wall of rabbits which are characteristic of atherosclerosis. It is hypothesized that occlusion of the vasa vasorum causes ischaemia of the arterial media which results in smooth muscle cell proliferation and cellular accumulation of cholesteryl esters. Hypoxia increases mRNA for platelet-derived growth factor in arterial wall cells and increases the activity of acyl CoA:cholesterol acyltransferase (ACAT). Such a mechanism may explain many of the anatomical, actuarial and environmental risk factors for atherosclerosis. Hypoperfusion may follow thrombosis of the vasa vasorum.

Animals↗

PubMed1990

Arterial wall hypoxia following hyperfusion through the vasa vasorum is an initial lesion in atherosclerosis.

Pressure on the outside of arteries can cause physical and biochemical changes in the vessel wall of rabbits which are characteristic of atherosclerosis. It is hypothesized that occlusion of the vasa vasorum causes ischaemia of the arterial media which results in smooth muscle cell proliferation and cellular accumulation of cholesteryl esters. Hypoxia increases mRNA for platelet-derived growth factor in arterial wall cells and increases the activity of acyl CoA: cholesterol acyltransferase (ACAT). Such a mechanism may explain many of the anatomical, actuarial and environmental risk factors for atherosclerosis. Hyperfusion of the vasa vasorum may follow thrombosis.

Animals↗

PubMed1986

Oxygen tension changes in the outer vascular wall supplied by vasa vasorum following adenosine and epinephrine.

We measured blood vessel wall oxygen tension (PO2) in vivo in the tissue and on the surface of dog thoracic aortas and femoral arteries. The overall mean tissue PO2 in the outer vascular wall supplied by vasa vasorum for both blood vessels was 49.4 +/- 2.6 (SE) Torr for 42 sites in 8 dogs. Changes in PO2 were measured after intravenous injections of adenosine and epinephrine. There was some tendency for the PO2 to decrease with epinephrine for both vessels. With adenosine the thoracic aorta wall tissue PO2 increased significantly (+23.2 +/- 6.0 Torr, p less than 0.025), while the femoral artery did not. One possible interpretation of these results is that the vasa vasorum of the thoracic aorta are capable of changing blood flow and oxygen supply to the outer wall to a greater degree than the femoral artery.

Adenosine↗

PubMedDate not supplied

Connective tissue proteinases and inhibitors in abdominal aortic aneurysms. Involvement of the vasa vasorum in the pathogenesis of aortic aneurysms.

Recent studies have shown that increases in proteolytic activity are associated with abdominal aortic aneurysms (AAAs). We have studied samples of the dilated aortic wall, taken during corrective surgery for AAAs, in terms of the number, type, and tissue location of connective tissue proteinases and their inhibitors. Five distinct caseinolytic serine proteinases and six gelatinolytic metalloproteinases were resolved by molecular weight by use of sodium dodecyl sulfate-substrate gel electrophoresis. Isoforms of the Mr 92,000 neutrophil gelatinase were identified by immunoprecipitation of biosynthetically labeled organ culture media. About 50% of the total radiolabeled protein secreted by AAA organ cultures was identified as the Mr 30,000 glycoprotein, tissue inhibitor of metalloproteinase (TIMP), by immunoprecipitation. Both TIMP and gelatinase were localized to the vasa vasorum by immunoperoxidase staining. However, interstitial collagenase could not be detected by any method. These results suggest the involvement of the vasa vasorum in the maintenance and possibly the genesis of AAAs.

Aorta, Abdominal↗

PubMedDate not supplied

Collateral circulation in experimental coarctation of the aorta in minipigs: a possible association with hypertrophied vasa vasorum.

Experimental coarctation of the thoracic aorta was produced in 13 adult Yucatan minipigs by placing a gradually expanding "C-shaped" occluder around the aorta. The aortic constriction was standardized by measuring the blood pressure above the coarctation, with a mean arterial pressure of 165-170mmHg as the target. The pigs were humanely killed after 8 weeks of hypertension. No deaths were associated with constriction of the aorta, and neither rear limb weakness nor neurological dysfunction was noted. The lack of clinical signs in these animals suggested the development of an extensive collateral circulation. Collateral vessels, which were verified angiographically, included intercostal arteries, muscular intercostal arteries, and the internal thoracic artery. In two of the animals in which the thoracic aorta was completely occluded, revascularization also occurred via small arterial channels. Histologically, there was a marked increase in the number of vessels as well as significant hyperplasia and hypertrophy of smooth muscle of adventitial vasa vasorum. These findings support the hypothesis that collateralization of occluded thoracic aortas may be aided by hypertrophy of the vasa vasorum. To our knowledge, these vessels have not previously been shown convincingly by histopathological methods to revascularize occluded large arteries such as the aorta.

Angiography↗