Vasa vasorum growth in the coronary arteries of newborn pigs

Experimental studies have shown that a plexus of vasa vasorum already exists in fetal arteries. In this study we examine the further development of vasa vasorum in the newborn. Hearts from 1- and 6-month-old pigs were harvested and infused with Microfil via the aortic ostia of the coronary arteries at physiological pressure (100 mmHg). Coronary arteries (RCA, LAD, and LCX) were then isolated and scanned intact with micro-CT (20 m cubic voxel size). Using Analyze 5.0 software we digitally isolated individual vasa vasorum trees (eight from 1-month-old and eight from 6-month-old pigs) and measured geometrical data such as interbranch segmental diameters, lengths, and branching angles as well as mother-daughter branch relationships for all segments of each vasa vasorum tree structure. Also, we determined the volume of vessel wall perfused by individual vasa vasorum trees. Our results show that the vasa vasorum architecture in newborn pigs is already tree-like, and this structure as well as the volume of vessel wall perfused by it expand in concert with the growth of the host coronary artery. We give quantitative details of this growth of vasa vasorum in terms of its branching architecture and hemodynamic capacity, based on direct measurements from 3D images of this microvasculature.     

Functional anatomy and hemodynamic characteristics of vasa vasorum in the walls of porcine coronary arteries

In this study vasa vasorum in the walls of porcine coronary arteries were examined, using three-dimensional (3D) micro-CT scanning techniques. These techniques leave the 3D structure of the vasa vasorum tree intact and thus provide a much more direct view of this structure than is possible from conventional histological sections. The study demonstrates-for the first time, we believe-both the different types and the fine architecture of these vasa vasorum. Furthermore, with the use of automated tree analysis software, it was possible to obtain quantitative geometrical data on the 3D structure of vasa vasorum trees that have not previously been available. The results indicate that despite the restrictive topology of the space in which they are present, the branching architecture of the vasa vasorum trees, which we surveyed, is surprisingly similar to that of vasculature in general. The volume of vessel wall tissue perfused or drained by a vasa vasorum tree was found to correlate well with the cross-sectional area of the root segment of the vasa vasorum tree, and the luminal surface area corresponding to this volume was found to be comparable with the surface area of an early atherosclerotic lesion. This is consistent with earlier findings that the ligation or removal of vasa vasorum leads to atherogenesis.     

Human allograft vein failure: Immunohistochemical arguments supporting the involvement of an immune-mediated mechanism

The aim of this study was to search for signs suggestive of an ongoing immune-mediated reaction in failed human cryopreserved venous allografts. In 15 samples, the authors analyzed: (1) the pattern of morphological changes; (2) the density, distribution, and phenotype of leukocytic infiltrate; and (3) the expression of class II major histocompatibility complex (MHC) antigens and inducible adhesion molecules. Two groups of samples could be recognized. In samples explanted before 3 months after grafting, the structure of the vessel wall was preserved. A dense leukocytic infiltrate was present within the intima and around the numerous vasa vasorum located in medial and adventitial layers. Class II MHC antigens and cytokine-dependent molecules were induced on endothelial cells lining the vasa vasorum and on residual smooth muscle cells. In samples explanted after 3 months of evolution, the vessel wall has lost its normal structure and contained few vasa vasorum. A few leukocytes were detected around capillary vessels located in the peripheral connective tissue surrounding the graft. Class H MHC antigens and adhesion molecules were induced on endothelial cells lining the peripheral capillary vessels. These results suggest the involvement of an immune-mediated mechanism at the early stage of the evolution of failed human venous allografts.     

Vasa vasorum of the human great saphenous vein

The distribution of the vasa vasorum of the human great saphenous vein (GSV) was studied on veins taken both post-mortem and peroperatively. It was found that the stems of feeding vessels approach the venous wall at intervals of 1.5-2.5 cm; their smaller branches first passed the fascial compartments of the GSV and then entered the adventitia at intervals of 0.5-1.5 cm on both the stem and the largest tributaries of the GSV. In the stem regions vasa vasorum arteries and veins ran together but, between neighboring stems, isolated venae vasorum were regularly found which opened individually into terminal segments of the largest tributaries of the GSV. Neither by dissection nor by injection methods were venae vasorum found to open directly into the lumen of the GSV stem. The total thickness of the media ranged between 500 and 1300 micro m, according to the state of constriction of the venous wall before fixation. Two structurally different layers of GSV tunica media were present: an inner loose layer and an outer dense layer, both of similar thickness. The innermost capillaries of the vasa vasorum network were found in all cases on the border between the two layers of media. No lymphatic was found in any of the layers of GSV wall. From the findings the authors recommend extremely careful dissection of the GSV wall during in situ grafting surgery, to ensure the best viability of the venous wall.     

Venous architecture of the glabellar to the forehead region

The precise venous anatomy of the glabellar to the forehead region remains unknown. This study aimed to detail the venous architecture of the glabellar region to the forehead in conjunction with that of the supratrochlear artery to reduce the risk of venous congestion of flaps in this area. Fifteen fresh human cadavers were examined here. In five specimens, contrast medium was injected only into the venous system; in 10 specimens, two different types of contrast media were injected into the arterial and venous systems, respectively. A total of 30 hemifacial specimens were radiographed stereoscopically and observed microscopically. In all the cadavers, a distinct vein (termed as the “transverse nasal root vein”) connected the bilateral angular veins. One or two large ascending veins branched from the transverse nasal root or angular vein, coursing toward the forehead skin. Numerous small veins branched out from the large ascending vein(s), forming a subdermal polygonal venous network. Small ascending veins arose from this network and coursed toward the dermis, draining venous flow from the dermis. Three different‐sized valves prevented the reflux of blood in the venous pathway. The large ascending vein(s) and supratrochlear artery ran parallel only in the medial canthal area. Tiny venous vasa vasorum surrounded the adventitia of the supratrochlear artery and anastomosed with the polygonal venous network, while a few small veins from the vasa vasorum ascended toward the dermis. Understanding the venous architecture of this region is expected to facilitate the safe elevation of various flaps in the area. Clin. Anat. 2013. © 2012 Wiley Periodicals, Inc.     

Methods for Three-Dimensional Geometric Characterization of the Arterial Vasculature

Complex vascular anatomy often affects endovascular procedural outcome. Accurate quantitative assessment of three-dimensional (3D) in-vivo arterial morphology is therefore vital for endovascular device design, and preoperative planning of percutaneous interventions. The aim of this work was to establish geometric parameters describing arterial branch origin, trajectory, and vessel curvature in 3D space that eliminate the errors implicit in planar measurements. 3D branching parameters at visceral and aortic bifurcation sites, as well as arterial tortuosity were determined from vessel centerlines derived from magnetic resonance angiography data for three subjects. Errors in coronal measurements of 3D branching angles for the right and left renal arteries were 3.1 ± 3.4° and 7.5 ± 3.7°, respectively. Distortion of the anterior visceral branching angles from sagittal measurements was less pronounced. Asymmetry in branching and planarity of the common iliac arteries was observed at aortic bifurcations. The renal arteries possessed considerably greater 3D curvature than the abdominal aorta and common iliac vessels with mean average values of 0.114 ± 0.015 and 0.070 ± 0.019 mm⁻¹ for the left and right, respectively. In conclusion, planar projections misrepresented branch trajectory, vessel length, and tortuosity proving the importance of 3D geometric characterization for possible applications in planning of endovascular interventional procedures and providing parameters for endovascular device design.     

Deposition of amyloid proteins in the epicardial coronary arteries of 58 patients with primary systemic amyloidosis.

INTRODUCTION: We sought to determine the distribution and the effect of amyloid on epicardial coronary arteries in patients with primary cardiac amyloidosis. METHODS: We reviewed pathologic specimens taken after autopsy or cardiac transplantation from 58 patients with primary cardiac amyloidosis. Patients were seen from 1981 to 2000. Multiple sections of epicardial coronary arteries (left anterior descending artery, left circumflex artery, and right coronary artery) were examined to determine the degree of amyloid deposition in the intima, media, adventitia, and vasa vasorum (vasa vasorum are nutrient arteries for the coronary arteries themselves). RESULTS: In 56 of 58 patients (97%), amyloid was present in epicardial coronary arteries. Amyloid was identified in all artery layers (intima, media, and adventitia), and more patients had amyloid in the adventitia. However, amyloid did not cause intraluminal obstruction of epicardial coronary arteries in any patient. The vasa vasorum had considerable deposits and, in many patients, were obstructed by amyloid. Patients with obstruction of the vasa vasorum were significantly more likely to have obstructive intramural coronary amyloidosis than patients without vasa vasorum obstruction (P=.002). CONCLUSIONS: The epicardial coronary arteries of patients with primary cardiac amyloidosis had extensive amyloid deposition. This deposition, however, did not lead to obstruction of epicardial coronary arteries and therefore did not contribute to ischemic syndromes observed in these patients. Obstruction of the vasa vasorum was associated with obstructive intramural coronary amyloidosis.     

Arterial branching in various parts of the cardiovascular system

Angiographic pictures of vascular beds in various parts of the cardiovascular system were analyzed to study the geometrical structure of arterial bifurcations. The sites of arterial bifurcations were enlarged individually, and measurements were made of the branching angles and branch diameters at each site. Results from various parts of the cardiovascular system of man, and some from rabbit and pig, were compared with each other. The measurements were also compared with “optimum” values of branching angles and branch diameters which have been predicted by various theoretical studies. In general the measurements were found to give support to the theoretical premise that branching angles and branch diameters in the cardiovascular system are dictated by certain optimality principles which aim to maximize the efficiency of the system in its fluid-conducting function. In some parts of the system, however, the measured angles and diameters were found to be decidedly lower than those predicted by theory.     

Vasa vasorum of the human great saphenous vein

The distribution of the vasa vasorum of the human great saphenous vein (GSV) was studied on veins taken both post-mortem and peroperatively. It was found that the stems of feeding vessels approach the venous wall at intervals of 1.5-2.5 cm; their smaller branches first passed the fascial compartments of the GSV and then entered the adventitia at intervals of 0.5-1.5 cm on both the stem and the largest tributaries of the GSV. In the stem regions vasa vasorum arteries and veins ran together but, between neighboring stems, isolated venae vasorum were regularly found which opened individually into terminal segments of the largest tributaries of the GSV. Neither by dissection nor by injection methods were venae vasorum found to open directly into the lumen of the GSV stem. The total thickness of the media ranged between 500 and 1300 µm, according to the state of constriction of the venous wall before fixation. Two structurally different layers of GSV tunica media were present: an inner loose layer and an outer dense layer, both of similar thickness. The innermost capillaries of the vasa vasorum network were found in all cases on the border between the two layers of media. No lymphatic was found in any of the layers of GSV wall. From the findings the authors recommend extremely careful dissection of the GSV wall during in situ grafting surgery, to ensure the best viability of the venous wall. Résumé. La distribution des vasa vasorum de la veine grande saphène de l'homme a été étudiée sur des veines prélevées chez le cadavre et au cours d'interventions chirurgicales. Nous avons trouvé que les troncs des vaisseaux nourriciers gagnent la paroi veineuse à des intervalles de 1,5 à 2,5 cm. Leurs plus petites branches passent d'abord le fascia fermant le compartiment de la veine grande saphène, puis pénètre l'adventice à des intervalles de 0,5 à 1,5 cm, à la fois sur le tronc et sur les plus grands affluents de la veine grande saphène. Dans les régions des troncs, les artères et les veines cheminaient ensemble mais, entre les troncs voisins, des venae vasorum isolés étaient étagés régulièrement et s'ouvraient individuellement dans les segments terminaux des plus grands affluents de la veine grande saphène. Ni par la dissection, ni par les techniques d'injection nous n'avons trouvé des venae vasorum qui s'ouvraient directement dans la lumière du tronc de la veine grande saphène. L'épaisseur totale de la média variait de 500 à 1300 µm en fonction de l'état de constriction de la paroi veineuse avant la fixation. Il y avait dans la media de la veine grande saphène deux couches structurellement différentes, une couche interne lâche et une couche externe dense, toutes deux d'épaisseur approximativement similaire. Les capillaires les plus profonds du réseau des vasa vasorum étaient trouvés dans tous les cas à la frontière entre les deux couches de la media. Aucun lymphatique n'a été trouvé dans aucune des couches de la paroi de la veine grande saphène. A partir de leurs constatations, les auteurs recommandent la dissection la plus soigneuse de la paroi de la veine grande saphène au cours de la chirurgie de greffe veineuse in situ, pour assurer la meilleure viabilité de la paroi veineuse.     

Neutrophil and endothelial cell activation in the vasa vasorum in vasculo-Behçet disease

AIM: The aim of this study was to analyse the immunopathological mechanisms of vasculo-Beh?et disease, which were also compared to cases of Takayasu's arteritis and inflammatory aneurysm to evaluate differences in inflammatory mechanisms. METHOD AND RESULTS: We reviewed six cases of vasculo-Beh?et disease, four of Takayasu's arteritis and seven inflammatory aneurysms which underwent surgical repair. Immunohistochemical studies were performed on paraffin-embedded tissue using a labelled streptavidin-biotin method, as was in-situ hybridization for Epstein-Barr virus. Microscopically, neutrophils and lymphocytes accumulated around the vasa vasorum. Neutrophils were prominent as compared to Takayasu's arteritis and inflammatory aneurysm. Elastic fibres were not severely destroyed. Endothelial cells (ECs) of most vasa vasorum expressed HLA-DR. The number of vasa vasorum around which inflammatory infiltrating cells were observed in vasculo-Beh?et disease was significantly greater than in inflammatory aneurysms and Takayasu's arteritis (P < 0.001). The cytokines IL-1alpha, TNF-beta and IFN-gamma were expressed in neutrophils and lymphocytes which were distributed around vasa vasorum, as well as neutrophils adherent to HLA-DR positive ECs. CONCLUSION: Our results suggest that vasculo-Beh?et disease should be classified as a neutrophilic vasculitis targeting the vasa vasorum. Aneurysm formation may be related to degeneration of arterial wall caused by inflammation of the vasa vasorum.     

The microcirculation of cerebral arteries: A morphologic and morphometric examination of the major canine cerebral arteries

A morphologic and morphometric examination of the major cerebral blood vessels in the dog was carried out to determine whether there were vasa vasorum in these arteries and what features might be associated with them. True vasa vasorum confined to the media were not seen in any of the vessels examined. Microvessels confined to the adventitia, however, were found in the internal carotid and vertebral arteries but not in the basilar, middle cerebral, or anterior spinal arteries. Animal size, vessel size as determined by adventitial and medial area, and the number of smooth muscle cell lamellae were not associated with the presence of these adventitial vessels; they occurred only in arteries with both an intra- and extradural portion. It therefore appears that most canine cerebral arteries do not have vasa vasorum.     

Vasa vasorum quantification in human varicose great and small saphenous veins

Recent research regarding saphenous vasa vasorum (VV) has focused on two main topics: the VV during varicogenesis in chronic venous insufficiency and the VV in saphenous grafts used in reconstructive vascular surgery. Our aim has been (i) to establish a technique for the histological quantification of the VV in human varicose great and small saphenous veins and (ii) to describe the density and distribution of the vasa vasorum within varicose veins. Great (n=11) and small (n=5) saphenous veins (length, 15-40cm) were collected from 12 patients who were undergoing venous stripping due to chronic venous insufficiency (Clinical-Etiology-Anatomy-Pathophysiology class 2-3). The veins were divided into 5-cm long segments. In total, 92 tissue blocks were collected to trace the variability of the density and distribution of the vasa vasorum in the proximo-distal direction. The endothelium was detected by immunohistochemistry using the von Willebrand factor. We quantified the number of microvessel profiles per section area and the relative distance of the microvessels from the outer border of the adventitia. The VV did not exhibit a preferential orientation in the varicose veins. VV density profiles were highest in the middle third of the venous wall and lowest in the inner third of the venous wall. Both the density and distribution of VV were uniform along the veins, and no differences were observed between the great and small saphenous veins. The VV density was statistically independent of the relative distance from the adventitia. The usability of this technique for perioperative frozen sections remains to be tested.     

Roots and calibers of the human coronary arteries

The anatomical structure of the coronary-aortic junctions in humans is studied by using corrosion casts of the coronary network. A model is proposed for the specification of these junctions in terms of vessel diameters and branching angles, and the model is used to produce morphological data on these junctions which hitherto have not been available. This anatomical model correlates poorly with the accepted theoretical model of arterial bifurcations in the cardiovascular system. The results suggest that the structure of the coronary-aortic junctions is very different from the structure of typical arterial bifurcations and, by implication, that the flow conditions under which they function are very different. A good understanding of these junctions is important in coronary bypass surgery, where the coronary-aortic junctions are emulated by creating a new anastomosis for the graft at the base of the ascending aorta, and in coronary artery disease, where atherosclerotic lesions occur not far from the coronaiy-aortic junctions.     

Fatal pulmonary arterial dissection and sudden death as initial manifestation of primary pulmonary hypertension: a case report.

We report a rare case of sudden death due to cardiac tamponade following intrapericardial rupture of a main pulmonary artery dissecting aneurysm. On pathology examination, the pulmonary artery showed an intimal tear in an arterial wall area with reduced thickness. However, no degenerative, inflammatory or necrotic processes were evident within the vessel wall. Hypertrophy of the wall of vasa vasorum in the adventitia of the pulmonary artery was found, as well as bilaterally diffuse myointimal arterial hyperplasia of the lung vasculature. According to these findings, we conclude that pulmonary artery rupture occurred in a patient with chronic unrecognized primary pulmonary hypertension.     

The development of vasa vasorum of the human aorta in various conditions. A morphometric study

The developmental behavior of vasa vasorum under various conditions was studied on the wall tissues of aorta and great arteries from 29 autopsy cases, where the length density (LA) of vasa vasorum in a unit area of wall was determined by morphometry. In a control group, LA was found to increase exponentially, along with increasing wall thickness D, among arteries from various anatomic sites of patients with greatly divergent ages. The regression curve crossed the x-axis at D = 0.6 mm, showing that arteries thicker than this have an auxiliary circulation by vasa vasorum. The LA was markedly high both in neonates and in patients with cyanotic heart anomaly, ie, in conditions where medial cells were sustained under reduced oxygen supply. Thus, vasa vasorum were shown to elongate their intramural segments in response to the changes of microenvironment in which the medial cells are placed, meeting the demand by the cells for increased supply of oxygen and nutrients.     

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.     

Blood supply and drainage of the outer medulla of the rat kidney: scanning electron microscopy of microvascular casts

Blood supply and drainage of the outer medulla of the rat kidney were studied by scanning electron microscopy of vascular casts, using both arterial (n = 10) and venous (n = 10) injections of resin. Both outer and inner stripes of the outer medulla were supplied through different arterial capillary networks arising from efferent arterioles and arterial (descending) vasa recta. In contrast to previous studies using silicone rubber and light microscopy, a rich arterial capillary network supplying the outer stripe was demonstrated. Capillaries in the outer stripe and outer part of the inner stripe drained into venous vasa recta between vascular bundles, while capillaries in the inner part of the inner stripe drained into venous vasa recta within the bundles. The results indicate that each zone in the outer medulla is supplied through separate capillary networks. The demonstration of a rich capillary network in the outer stripe of the outer medulla suggests that the predilection of this zone for tubular necrosis with ischemic or toxic injury is not related to a sparse capillary blood supply.     

Calcitonin receptor immunoreactivity associated with specific cell types in diseased radial and internal mammary arteries

Aims:  To determine and quantify calcitonin receptor (CTR) immunoreactivity associated with specific cell types within, and associated with, the endothelial layers, neo-intima, media and vasa vasorum of diseased radial and internal mammary arteries.
Methods and results:  Immunohistochemistry and anti-CTR antibodies were used to identify positive cells within remnants of diseased human radial ( n  = 3) and internal mammary arteries ( n  = 4) that remained after bypass surgery. Three cell types expressed CTR, including endothelial cells, fibroblast-like cells within the neo-intima, and cellular structures aligned with the smooth muscle cells of the media. Other smaller cells within the surrounding parenchyma of the vasa vasorum of diseased vessels and blood-borne cells were also immunoreactive. Immunoquantification of CTR expression (Intensity × Proportional Area) in the endothelium ( P  < 0.05), neo-intima ( P  < 0.02) and media ( P  < 0.03) established a significant statistical correlation (Students' two-tailed t -test) with the ratio of intimal/media thickness.
Conclusions:  Increased immunoreactivity developed using anti-CTR antibodies was associated with specific cell types in the endothelial layers, neo-intima, media and vasa vasorum of diseased regions of radial and internal mammary arteries, in which there was an increased intimal/media ratio. Furthermore, CTR+, blood-borne cells present in the vessels of diseased regions suggest recruitment into these surrounding tissues.     

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.