[Morphological consequenes of enclosing the aortae of dogs in siliconized membranes of synthetic rubber. Experimental interruption of the vasa vasorum].
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Vasa vasoritis, vasculitis and atherosclerosis.
Takayasu arteritis, Buerger's diseases, temporal arteritis, vascular Behcet disease and inflammatory abdominal aortic aneurysm are classified in Japan as intractable vasculitides involving mainly large vessels, because their etiologies are not yet elucidated and, therefore, treatments for them were not yet established. Recent experimental and vascular biological studies, however, have focussed on the roles of virus infection in vasa vasorum (vasa vasoritis) and on the subsequent inflammatory vascular changes through HLA and/or other autoimmune mechanisms. Several studies including ours have demonstrated that these vascular inflammatory changes progress from the adventitial side to the intimal side of the vessel, finally complicating atherosclerotic changes in the intima. These vascular inflammatory changes are also recognized during progression of atherosclerosis and these observations strongly suggest that inflammation is a serious risk factor of atherosclerosis.
Arteriosclerosis↗
Diffusional support of arteries.
The relative role of the arterial lumen, adventitial vasa vasorum, and medial vasa vasorum in nutritional support of arteries is unclear. We have used a newly developed autoradiographic method to study diffusion of metabolically inert [14C]antipyrine into arteries to determine the relative importance of different pathways in nutritional support of arteries. [14C]antipyrine was homogenously distributed across the media of small arteries within 15 s, which indicates that diffusion into the central media was rapid. In the thoracic and abdominal aorta, levels of antipyrine were higher in the inner media (P less than 0.05) than in the middle of the media. Levels of antipyrine in outer media of the thoracic aorta (which has medial and adventitial vasa) were comparable to those observed in the inner media, but antipyrine levels were lower in outer than in inner media of the abdominal aorta (which has adventitial vasa only). Ligation of intercostal arteries, which are the source of medial vasa vasorum in the thoracic aorta, decreased diffusional support to the outer media of the thoracic aorta. We conclude that 1) diffusional support is more effective in thinner muscular arteries than in the aorta, 2) both luminal and abluminal sources of nutrition are important, particularly for the aorta, 3) vasa vasorum appear to be important for adequate diffusional support of the thoracic aortic media, and 4) medial vasa vasorum may be more effective than adventitial vasa vasorum in nourishing the aorta.
Animals↗
Regulation of blood flow to the aortic media in dogs.
Morphologic observations suggest that the inner layers of the thoracic aorta in man and dog are avascular and the outer layers have vasa vasorum. It appears that vasa vasorum are essential in the thoracic aorta because their interruption produces medial necrosis. These experiments provide the first measurements of blood flow through aortic vasa vasorum and examine physiologic regulation of that flow. During control conditions the outer two-thirds of the media of the thoracic aorta received 10 ml/min per 100 g blood flow through vasa vasorum. Flow to the inner third of the aorta was 1 ml/min per 100 g. Flow to both the inner and outer media of the abdominal aorta was less than 1 ml/min per 100 g. Adenosine increased blood flow to vasa vasorum in the outer media of the thoracic aorta from 7 to 18 ml/min per 100 g, but did not increase flow to the inner layers of the aorta. Hemorrhagic hypotension decreased flow in the outer media of the thoracic aorta from 14 to 2 ml/min per 100 g. Acute hypertension failed to increase blood flow through vasa vasorum, as conductance decreased significantly. These studies indicate that vasa vasorum provide a considerable amount of blood flow to the outer layers of the thoracic aorta. The vessels are responsive to physiologic stimuli because they dilate during infusion of adenosine and constrict during both hemorrhagic hypotension and acute hypertension. We speculate that the failure of blood flow to the aortic wall to increase during acute hypertension might, if it were sustained, contribute to aortic medial necrosis.
Adenosine↗
Relations between disturbances in microcirculation and accumulation of lipids in the aortic wall.
For the purpose of unraveling the relations between disturbances in microcirculation and deposition of lipids in the aortic wall, 9 rabbits were fed a 1% cholesterol and 5% coconut oil at intervals up to 16 weeks, and 4 rabbits were used as controls. After microangiography of vasa vasorum, the same specimens were studied histochemically. The distribution of vasa vasorum became poorer on sacrifice by microangiography. However, it could not be thought that disturbances in vasa vasorum was a cause in the early deposition of lipids, because lesions were histologically mild in the greater parts of vasa vasorum. The sites of prediction for the vascular lesions were initially the branching part, and then the thoracic aorta. Thickness and numbers of the elastic lamina in the media decreased straightly in the distal direction, and the degree of intimal thickening and accumulation of lipids were parallel with the degree of the medial thickness. The intimal cells tended to be arranged radially with wide intercellular spaces in the cross section, suggesting the convenience for the passage of fluids. From the above facts, it may be reasonable to presume that the difference in severity of disturbances of microcirculation resulted in the difference in the site of predilection.
Angiography↗
The absence of lymphatics in normal and atherosclerotic coronary arteries in man: a morphologic study.
It has been suggested by various investigators that the impairment of lymphatic drainage from the coronary arteries may play a role in predisposition to coronary atherosclerosis, the pathogenesis of which is certainly multifactorial. In our study, no lymphatic vessels were found in the walls of the coronary arteries (adventitia, media and intima) in 51 human hearts from patients ranging in ages from 3 months to 83 years with normal coronary arteries, coronary atherosclerosis, and cardiomyopathy. Visualized lymphatics were located solely in the periadventitial area, and these lymphatics were more irregular in hearts from older persons. With injection, histology, and electronmicroscopy methods we could not detect penetration of lymphatics into the wall of coronary trunks in normal as well atherosclerotic arteries. In all coronary arteries studied, and particularly in the atherosclerotic lesions, blood vasa vasorum could be visualized. In the atherosclerotic areas, vasa vasorum (angiogenesis) could be seen penetrating into the media and intima. Many of the thin-walled vasa vasorum could easily be mistaken for lymphatics. The absence of lymphatics draining the epicardial coronary arteries may be a predisposing factor to coronary atherosclerosis.
Adolescent↗
Contribution to the pathogenesis of radiation-induced injury to large arteries.
We report a case of a 35-year-old man who died of a brain infarct 20 months after radiotherapy for carcinoma of the tonsil with metastases to the cervical lymph nodes. Histology revealed mild atherosclerosis, necrotizing vasculitis, and occlusive thrombosis of the internal carotid artery. Significant changes were observed in the vasa vasorum: swelling and detachment of the endothelium, subendothelial oedema, hyaline change, fibrinoid necrosis of the vessel walls with mononuclear cellular infiltration, accompanied by focal haemorrhages and chronic inflammation in the periadventitial soft tissue. We believe that these changes of the vasa vasorum and necrotizing vasculitis are causally related and that vasculitis represents focal ischaemic necroses with inflammatory reaction. Our findings support the hypothesis, based on experimental studies, that injury to the vasa vasorum is an important mechanism in the development of radiation-induced vasculopathy of large arteries. They also suggest an evolution of the injury to the vasa vasorum and periadventitial tissue from the early lesions described in our patient, to late stages resulting in dense periadventitial fibrosis as reported previously. We suggest that injury to the vasa vasorum and the consequent ischaemic lesions of the arterial wall are morphological features distinguishing radiation-induced arterial injury from spontaneous atherosclerosis.
Adult↗
Intracranial arterial aneurysm vasculopathies: targeting the outer vessel wall.
The pathogenesis of intracranial arterial aneurysms (AA) remains unclear, despite their clinical importance. An improved understanding of this disease is important in choosing therapeutic options. In addition to the "classical" berry-type aneurysm, there are various other types of intracranial AA such as infectious, dissecting or giant, partially-thrombosed aneurysms. From the clinician's perspective, the hypothesis that some of these intracranial AA might be due to abluminal factors has been proposed for several years. Indeed, this hypothesis and the empirical use of anti-inflammatory drugs in giant intracranial aneurysms have been confirmed by recent studies reporting that an enzyme involved in the inflammatory cascade (5-lipoxygenase or 5-LO) promotes the pathogenesis of specific aneurysms in humans. 5-LO generates different forms of leukotrienes which are potent mediators of inflammation. Adventitial inflammation leads to a weakening of the media from the abluminal part of the vessel wall due to the release of proinflammatory factors that invade the media, thereby degrading the extracellular matrix, the elastic lamina of the vascular wall, and, finally, the integrity of the vessel lumen. This in turn results in a dilation of the vessel and aneurysm formation. Moreover, neoangiogenesis of vasa vasorum is found in close proximity to 5-LO activated macrophages. In addition to this biological cascade, we argue that repeated subadventitial haemorrhages from the new vasa vasorum play an important role in aneurysm pathogenesis, due to a progressive increase in size mediated by the apposition of new layers of intramural haematoma within the vessel wall. Intracranial giant AA can therefore be regarded as a proliferative disease of the vessel wall induced by extravascular activity. Considering certain aneurysmal vasculopathies as an abluminal disease might alter current therapeutic strategies. Therapy should not only be aimed at the intraluminal repair of the artery, but also cross the vessel wall to reach the vasa vasorum. Drug-eluting stents placed proximal to the lesion and targeted to the origin of the vasa vasorum could be considered as a potential future option. "Intelligent" MRI contrast agents (i.e., macrophage marking) could be used to detect vasa vasorum proliferation and weakening of the vessel wall in vivo.
Anti-Inflammatory Agents↗
Bronchopulmonary arterial shunting without anatomic anastomosis in the dog.
The effects of bronchial arterial administration of vasoactive substances on the pulmonary circulation were studied by a new technique for selective catheterization of a bronchial artery in intact dogs. In most experiments, this technique permitted pressor agents to be distributed mainly to one lung with smaller amounts to the other lung. The intercostal arteries were avoided, and in all but 2 of 23 experiments only microscopic quantities of injected India ink could be identified in the distribution of the esophageal and mediastinal branches. These studies indicate that serotonin, angiotensin, histamine, and norepinephrine injected selectively into a bronchial artery increase lobar arterial pressure. Since blood flow was constant and left atrial pressure did not change, the increase in pressure suggests active pulmonary vasoconstriction. Additionally, the responses to bronchial and lobar arterial injections of pressor agents were similar. The contribution of bronchopulmonary shunt flow to pulmonary flow was small, since, under conditions of controlled lobar blood flow, changes in bronchial flow elicited by 65-75-mm Hg changes in bronchial arterial pressure produced little if any change in pressure in the perfused lobar artery or small vein. Bronchoconstriction contributed little to the response to bronchial administration of pressor agents, since responses were similar in the ventilated and the collapsed lobe. Injection of vasoflavine dyes into the bronchial artery showed the close proximity of bronchial and pulmonary arteries and confirmed the bronchial arterial origin of the vasa vasorum of pulmonary arteries. No vasa venorum were identified. Although no direct anatomic bronchial artery-pulmonary artery shunt was identified, ascorbic acid and 5-hydroxydopamine diffused rapidly into intrapulmonary arteries from the bronchial artery. These data suggest that the pulmonary pressor response results from passage of the vasoactive agents from the bronchial artery to the lobar artery through the vasa vasorum and by diffusion. Since no vasa venorum were found, pulmonary venoconstriction probably resulted from pressor agents reaching the veins by way of bronchopulmonary shunt flow. These results suggest a mechanism by which pressor substances present or liberated in the bronchial vascular bed can affect tone in the pulmonary vascular bed.
Angiotensin II↗
Aortitis during intraarterial chemotherapy for cervical cancer.
A 76-year-old woman with stage IIb cervical cancer with a bulky tumor experienced aortitis during continuous intraarterial cisplatin-based chemotherapy. The chemotherapy was administered through a catheter tip placed in the aorta abdominalis, utilizing an external infusion pump. During the third course of chemotherapy, she complained of left-sided lower back pain and moderate fever was observed. Elevated white blood cell count (WBC) and C-reactive protein (CRP) level were noted, and an abdominal X-ray and urgent computed tomography (CT) were performed. The catheter tip was displaced against the arterial blood flow. At this level of the aortic wall, soft tissue density surrounded the aorta completely. Aortitis caused by the intraarterial chemotherapy, was strongly suspected. It was thought that the maldistribution of drugs and changes in the drug flow occurred due to the vertebral height movement of the catheter tip against the aortic blood flow, and there, flow to the vasa vasorum may have occurred. Chemical vasculitis of the vasa vasorum due to the anticancer drugs was strongly suspected as a contributing factor of the aortitis. Because of the long-term use of an intraarterial catheter, the maldistribution of drugs and changes in the drug flow occurred physically and biologically during the course of the chemotherapy. We recommend occasional monitoring of the location of the catheter tip and a repeat evaluation with contrast medium in regard to flow to the vasa vasorum.
Aged↗
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.
Animals↗
Hypoxia-induced pulmonary artery adventitial remodeling and neovascularization: contribution of progenitor cells.
Information is rapidly emerging regarding the important role of the arterial vasa vasorum in a variety of systemic vascular diseases. In addition, increasing evidence suggests that progenitor cells of bone marrow (BM) origin may contribute to postnatal neovascularization and/or vascular wall thickening that is characteristic in some forms of systemic vascular disease. Little is known regarding postnatal vasa formation and the role of BM-derived progenitor cells in the setting of pulmonary hypertension (PH). We sought to determine the effects of chronic hypoxia on the density of vasa vasorum in the pulmonary artery and to evaluate if BM-derived progenitor cells contribute to the increased vessel wall mass in a bovine model of hypoxia-induced PH. Quantitative morphometric analyses of lung tissue from normoxic and hypoxic calves revealed that hypoxia results in a dramatic expansion of the pulmonary artery adventitial vasa vasorum. Flow cytometric analysis demonstrated that cells expressing the transmembrane tyrosine kinase receptor for stem cell factor, c-kit, are mobilized from the BM in the circulation in response to hypoxia. Immunohistochemistry revealed an increase in the expression of c-kit+ cells together with vascular endothelial growth factor, fibronectin, and thrombin in the hypoxia-induced remodeled pulmonary artery vessel wall. Circulating mononuclear cells isolated from neonatal calves exposed to hypoxia were found to differentiate into endothelial and smooth muscle cell phenotypes depending on culture conditions. From these observations, we suggest that the vasa vasorum and circulating progenitor cells could be involved in vessel wall thickening in the setting of hypoxia-induced PH.
Animals↗
Arterial neovascularization and inflammation in vulnerable patients: early and late signs of symptomatic atherosclerosis.
BACKGROUND: Atherosclerosis is complicated by cardiovascular events such as myocardial infarction, stroke, or peripheral arterial occlusive disease. Inflammation and pathological neovascularization are thought to precipitate plaque rupture or erosion, both causes of arterial thrombosis and cardiovascular events. We tested the hypothesis that arterial inflammation and angiogenic events are increased throughout the arterial tree in vulnerable patients, ie, in patients who suffered from cardiovascular events, compared with patients who never suffered from complications of atherosclerosis. METHODS AND RESULTS: In a postmortem study, we quantified the inflammatory infiltrate and microvascular network in the arterial wall of iliac, carotid, and renal arteries. Tissue microarray technology was adapted to investigate full-thickness arterial sectors. We compared 22 patients with symptomatic atherosclerosis with 27 patients who never had suffered from any cardiovascular event. The absolute intimal macrophage content was 2- to 4-fold higher in vulnerable patients at all 3 arterial sites analyzed (P<0.05). Patients with symptomatic atherosclerosis had a denser network of vasa vasorum than patients with asymptomatic disease (33+/-2 versus 25+/-2 adventitial microvessels per 1 mm2; P=0.008). Hyperplasia of vasa vasorum was an early and macrophage infiltration was a late sign of symptomatic atherosclerosis. CONCLUSIONS: High intimal macrophage content and a hyperplastic network of vasa vasorum characterize vulnerable patients suffering from symptomatic atherosclerosis. These changes are uniformly present in different arterial beds and support the concept of symptomatic atherosclerosis as a panarterial disease.
Aged↗
Thoracic aortic aneurysm associated with aortitis--case reports and histological review.
Ten cases of post-inflammatory aneurysm of the thoracic aorta were studied morphologically using aortic wall and aortic valve tissue resected during the surgical repair of the lesions. Four cases of aortic aneurysm in Behcet's disease showed massive perivascular infiltration of the lymphocytes and plasma cells in adventitia and vasa vasorum. Fibrous obliteration of the vasa vasorum was seen, and neutrophilic infiltration was also associated in two cases with recurrent prosthetic valve failure. Three cases of aortic aneurysm associated with Takayasu's arteritis showed similar histologic features, but giant cells and histiocytic reactions were additional findings. Plasma cell infiltration was more pronounced compared to the Behcet's aortitis. One case of luetic aortitis showed a non-specific chronic inflammatory reaction with florid endothelial cell proliferation. One case of ankylosing spondylitis showed fibrous thickening at the periannular portion of the aortic valve cusps, but this finding was also seen in an aortic valve of a patient with Behcet's disease. One case without any disease association showed similar features of chronic inflammation with granuloma formation. The findings suggest that they have similar histologic features indistinguishable in terms of the clinical disease association, but a granulomatous reaction could be expected in Takayasu's arteritis.
Adult↗
Why do radial artery grafts for aortocoronary bypass fail? A reappraisal.
The reasons for the high failure rate of radial artery grafts for aortocoronary bypass (ACB) are appraised. Each of 11 dogs received four types of grafts: femoral arteries were grafted to carotid arteries, and jugular veins were grafted to femoral arteries bilaterally. One of each pair of grafts was wrapped in a plastic sheet in order to interfere with the regeneration of vasa vasorum. The grafts were examined 2 months later. The results suggest that although operative trauma and intraluminal pressure change play important roles, the thick-walled artery appears to depend more on vasa vasorum for its integrity than does the thin-walled vein. A free radical artery graft, with vasa vasorum disrupted at both ends, cannot regenerate readily from the adjacent tissue, as is the case at the ACB position, and is therefore more vulnerable to subintimal hyperplasia and occlusion than either the vein graft or the internal mammary artery graft; both of these grafts are thinner, and the internal mammary artery graft remains undisrupted at one end.
Animals↗
Uptake of low molecular weight materials in an in situ preparation of the rabbit thoracic aorta.
1. An in situ preparation of the rabbit thoracic aorta is described in which the integrity of the intimal endothelium is shown to be preserved. An extensive system of vasa vasorum and lymphatic vessels distributed throughout the adventitia, but not penetrating the media, are demonstrated using resin casts and lead chromate precipitation techniques and are shown to be patent in this preparation. 2. The role of the vasa vasorum in the medial uptake of low molecular weight materials is investigated as a function of luminal hydrostatic pressure and perfusion time. Comparison of uptake in vessels with and without patent vasa vasorum indicates that at physiological pressures medial uptake of 125I ions is dominated by entry from the adventitial surface. Analysis of the transmural distribution of 125I demonstrates that iodide is not retarded at the endothelial surface but a barrier exists within the intima which is tentatively identified as the internal elastic lamina. Qualitative studies show that Patent Blue V whose coloured anion has a molecular weight of 500 is able, at longer perfusion times, to penetrate this barrier. There is no circumferential variation in intimal uptake, but in contrast, adventitial uptake is rather patchy and generally more intense on the dorsal surfaces of the aorta. 3. Iodide transport across the intimal surface is argued to be predominantly diffusive in short duration experiments with an effective diffusion coefficient of (1.6 +/- 0.9) X 10(-6) cm2 min-1.
Animals↗
Diffusional support of the thoracic aorta in atherosclerotic monkeys.
We have demonstrated previously that there is increased blood flow through vasa vasorum in the aorta of atherosclerotic monkeys. In this study, a new method was used to examine diffusional support to the wall of blood vessels. Our goal was to determine whether proliferation of vasa vasorum in the outer media contributes to increased diffusional support of the atherosclerotic aorta and whether there are focal or homogeneous increases in diffusion to the aortic wall. Cynomolgus monkeys were fed normal or atherogenic diet for 1.5 or 4 years. Diffusional support of the thoracic aorta was determined by measuring the concentration of iodo[14C]antipyrine in the aortic media. The findings suggest that: 1) vasa vasorum provide only minimal nutritional support to the thoracic aorta of normal monkeys and monkeys with moderately severe atherosclerosis, and 2) in monkeys with severe atherosclerosis, diffusional support to the thoracic aorta is strikingly heterogeneous, ranging from minimal to large. We speculate that minimal diffusional support to the outer layers of the thickened atherosclerotic aorta may contribute to development of focal medial necrosis.
Animals↗
Early changes in dissected small vessels: experimental study on rat arteries and veins.
This study was undertaken to investigate the cause of the early endothelial damage that is seen at sites of microvascular anastomosis and in particular to study the possibility of a connection between damage to the vasa vasorum and subsequent endothelial denudation. Rat femoral vessels were subjected to a variety of experimental injuries, including simple dissection, clamping, and ligation. The vessels were examined in longitudinal section by light microscopy at intervals ranging from 5 minutes to 1 day. The endothelial cells were counted and the numbers were analyzed statistically. In addition, the anatomy of the vasa vasorum was studied using india ink perfusion. Simple dissection of the femoral vessels and excision of the vasa vasorum without interruption of blood flow were followed by ischemic lesions of the tunica media with subendothelial edema and ballooning and exfoliation of endothelial cells. Endothelial denudation reached a maximum level in 30 minutes. Adherence of leukocytes was found on damaged endothelial cells. Mural thrombi were seen in 13.6 percent of arteries and in 40 percent of veins following simple dissection.
Animals↗