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Results for “VASA VASORUM”

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PubMed1994

Localization of tissue plasminogen activator in the endothelium of a limited number of vessels.

The immunolocalization of tissue plasminogen activator (tPA) was assessed in vessels of various sizes from baboons. Femoral artery and vein, carotid artery, aorta, and sections from basal ganglia and cerebral cortex were stained for tPA and CD31, an endothelial cell-specific surface antigen. In each case, the endothelium of the large vessel stained positively for anti-CD31 but not for tPA. However, vascular structures in the adventitia corresponding to the vasa vasorum were found to be associated with tPA antigen. In situ hybridization of femoral artery with 35S-labeled cRNA probes detected tPA mRNA in the vasa vasorum but not the large vessel endothelium. Analysis of the microvasculature of the basal ganglia and cerebral cortex showed limited immunohistochemical staining for tPA; only 3% of the vessels measuring 4 to 100 mu were positive. Even so, tPA was mostly distributed within a narrow range of vessel size; 90% of the positive vessels were classified as precapillary arterioles and postcapillary venules (7.5 to 30.0 mu), whereas only 3% of the capillaries were positive, despite accounting for 40% of all vessels. Thus, tPA-containing endothelium are distributed mainly in smaller vessels, excluding the capillaries.

Animals↗

PubMed1996

[Morphology and vascularization of the varicose internal saphenous vein. Comparison with the normal structure].

After reviewing the main characteristics of the normal long saphenous vein, the histological alterations observed in varicose veins are described. Samples were obtained from 14 patients undergoing venous surgery for varicose veins with long saphenous vein incompetence. These alterations mostly involve the connective tissue prolife-rating in the middle layer and causing the separation and interruption of the muscular bundles. In addition, the vasa vasorum network through the venous wall was investigated. These vessels were normally observed in the adventitial layer and the outer third of the media. In some samples from varicose veins, vasa vasorum were increased and capillaries close to the intimal layer.

Capillaries↗

PubMed1999

Evaluation of microvascular anatomy by micro-CT.

Observations indicate that adventitial vasa vasorum may play a role in the development and/or the progression of coronary atherosclerosis. There is a lack of information regarding the spatial three-dimensional pattern of the vasa vasorum in the coronary artery. This is due to the technical difficulties in visualizing the course of this fine vascular network with histologic methods. Microscopic computed tomography (micro-CT) is a novel technique that allows three-dimensional views of the entire microvascular structure. The current review summarizes our current advances in using this technique in visualization of the coronary circulation.

Animals↗

PubMed1995

Three-dimensional structure of the bronchial microcirculation in sheep.

BACKGROUND: The bronchial circulation affects both pulmonary vascular and airway activity. Fundamental to understanding the role of the bronchial microcirculation in health and disease is understanding its anatomy. This study sought to identify specific structural elements that might contribute to the drop that occurs between the systemic blood pressure of the bronchial artery and the low pressure of the pulmonary bed into which the bronchial circulation flows and to better describe the connections of the bronchial and pulmonary circulations. METHODS: To do this, the lungs of five sheep were cast by injecting a resin through bronchial and pulmonary arteries. After taking samples for light microscopy, the tissue was digested and the casts were viewed with a scanning electron microscope. RESULTS: Casts of extrapulmonary bronchial arteries were structurally similar to other systemic arteries. Tortuous ones spiraled around bronchi and large blood vessels. Intrapulmonary bronchial arteries, about 100-300 microns in diameter, had sharp branching and deep focal constrictions with great rugosity that completely shut off the flow of the resin. These vessels correspond to the Sperrarterien described by von Hayek (and could cause the resistance associated with the pressure drop). Vasa vasorum ran in the walls of intrapulmonary pulmonary arteries for a variable distance before they entered the lumens of the pulmonary arteries. The smallest blood vessel found that was supplied with vasa vasorum was a bronchial artery 42 microns in diameter. Capillary-like networks with large luminal diameters were found on the pleural surface. CONCLUSIONS: Scanning electron microscopy of microvascular casts provides a fresh description of the bronchial circulation, further delineates the communications of these two circulations, and may structurally account for some pressure drop between the bronchial and pulmonary circulations.

Animals↗

PubMed1999

The blood vessel, linchpin of diabetic lesions.

The morbidity and mortality associated with diabetes mellitus are essentially related to the vascular lesions that develop over time in this condition. Both the macrocirculation and microcirculation are involved, and as a consequence, vital organs such as the brain, retina, heart, and kidney and the limbs become damaged. Because microalbuminuria represents the earliest and probably most sensitive indication of endothelial dysfunction in diabetes mellitus, the results of pharmacologic intervention with angiotensin-converting enzyme inhibitors, which treat glomerular hypertension were the first indication of potential beneficial effects in reducing diabetic nephroplasty. The nature of endothelial dysfunction related to diabetes is probably not homogeneous, since microcirculation networks are affected at different periods and with variable intensity. This appears to be the case for the aorta, the heart, segments of the digestive tract, the skin, and the skeletal muscle, the largest consumer of insulin. Although the aorta and large arteries contain a small portion of the total blood volume, their distribution of blood flow (pulse pressure) to peripheral organs may affect endothelial function in the microcirculation. Changes in the structure of conduit arteries, partly responsible for the alteration in compliance characteristics, could well be related to the way these arteries are fed by the vasa vasorum system. This report describes a new in vitro approach to examine capillary permeability in normal and alloxan-induced diabetic rabbits. Preliminary results indicate that the size of terminal arterioles of the vasa vasorum (increased diameter) and the capillary permeability to albumin (markedly enhanced) in this specialized network are profoundly affected in the thoracic aorta obtained from diabetic animals. Albumin extravasation into the interstitial fluid compartment of the aorta is likely to lead to structural and physicochemical changes: in fact, removal of interstitial macromolecules via lymphatic drainage is poor in the blood vessel wall of large arteries. This experimental approach is likely to be useful in the exploration of medications affecting the structure and function of conduit vessels.

Animals↗

PubMed1979

[Changes in the pulmonary artery in collagen diseases].

Morphological changes in the pulmonary artery and its major branches were studied histologically and histochemically on autopsy cases of polyarteritis nodosa (23), systemic lupus erythematosus (10), systemic scleroderma (12), and rheumatoid arthritis (5). The ages of the fatalities ranged from 9 months to 77 years. An identical type of lesions was revealed: disorders of the connective tissue, destruction of elastic fibers, alterations of vasa vasorum, with cellular reactions typical of each nosological form reflecting the peculiarities of the immunological processes. The initial stage in the genesis of lesions in the vascular walls of the major pulmonary arteries is the involvement of vasa vasorum as a regular disorder of the microcirculatory ways in all collagen diseases.

Adolescent↗

PubMed2005

Hypoxia, leukocytes, and the pulmonary circulation.

Data are rapidly accumulating in support of the idea that circulating monocytes and/or mononuclear fibrocytes are recruited to the pulmonary circulation of chronically hypoxic animals and that these cells play an important role in the pulmonary hypertensive process. Hypoxic induction of monocyte chemoattractant protein-1, stromal cell-derived factor-1, vascular endothelial growth factor-A, endothelin-1, and tumor growth factor-beta(1) in pulmonary vessel wall cells, either directly or indirectly via signals from hypoxic lung epithelial cells, may be a critical first step in the recruitment of circulating leukocytes to the pulmonary circulation. In addition, hypoxic stress appears to induce release of increased numbers of monocytic progenitor cells from the bone marrow, and these cells may have upregulated expression of receptors for the chemokines produced by the lung circulation, which thus facilitates their specific recruitment to the pulmonary site. Once present, macrophages/fibrocytes may exert paracrine effects on resident pulmonary vessel wall cells stimulating proliferation, phenotypic modulation, and migration of resident fibroblasts and smooth muscle cells. They may also contribute directly to the remodeling process through increased production of collagen and/or differentiation into myofibroblasts. In addition, they could play a critical role in initiating and/or supporting neovascularization of the pulmonary artery vasa vasorum. The expanded vasa network may then act as a conduit for further delivery of circulating mononuclear cells to the pulmonary arterial wall, creating a feedforward loop of pathological remodeling. Future studies will need to determine the mechanisms that selectively induce leukocyte/fibrocyte recruitment to the lung circulation under hypoxic conditions, their direct role in the remodeling process via production of extracellular matrix and/or differentiation into myofibroblasts, their impact on the phenotype of resident smooth muscle cells and adventitial fibroblasts, and their role in the neovascularization observed in hypoxic pulmonary hypertension.

Animals↗

PubMed1979

Seeding arterial prostheses with vascular endothelium. The nature of the lining.

Arterial prostheses seeded with autogenous vascular endothelium demonstrate a well-organized, cellular, inner lining. To determine the nature of the lining cells, six animals underwent replacement of the infrarenal aorta with Dacron prostheses. During the preparation of three such grafts, endothelium was scraped from the saphenous vein with a steel wool pledget, suspended in chilled Sack's solution, and mixed with blood used to preclot the graft. This suspension was omitted from the three control grafts. After six weeks, the grafts were removed, rinsed and examined. Fluorescent Factor VIII related antigen (F VIII-RA) strongly stained the lining cells. Silver nitrate Haütchen and electron microscopy preparations revealed a lining pattern characteristic of vascular endothelium. Endothelial cell-specific Weibel-Palade bodies were identified in the lining cell cytoplasm. Masson's trichrome staining revealed a relatively collagen-poor connective tissue within the seeded fabric. Transmission electron microscopy disclosed vascular smooth muscle cells between the seeded graft fabric and the lining cells. Vasa vasorum, arising from the outer capsule, penetrated the fabric to supply the inner capsules of the seeded grafts. It is concluded that the cells lining seeded canine arterial prostheses are true vascular endothelium supported by vascular smooth muscle cells, that the lining contains minimal connective tissue, and that vasa vasorum develop. Unseeded control grafts lacked these features.

Animals↗

PubMed1988

Histologic comparison of experimental coronary artery bypass grafts. Similarity of in situ and free internal mammary artery grafts.

This study compares patency and histologic structure of in situ internal mammary artery grafts, free internal mammary artery grafts, stripped, free internal mammary artery grafts, and stripped, free superficial femoral artery grafts (a muscular artery model) in a canine model of coronary artery bypass. Twenty-four adult mongrel dogs underwent bypass of the circumflex coronary artery with one of the above grafts. Three months postoperatively, graft patency was assessed by angiogram, and postmortem specimens were studied by intraluminal injection of a dilute barium solution proximal to the graft. Proximal, mid, and distal segments of each graft were examined microscopically. In situ internal mammary artery grafts and free internal mammary artery grafts were not significantly different in regard to patency, vascular wall cellular structure, or perfusion of the vasa vasorum. The stripped, free internal mammary artery group had a higher incidence of thrombosis, intimal thickening, and medial injury than the pedicled (in situ and free internal mammary artery) grafts. This difference may be due to early vascular wall ischemia as a result of poor early perfusion of the vasa vasorum. The stripped, free superficial femoral artery grafts were all patent, but all had adventitial injury.

Angiography↗

PubMed2003

Inhibition of plaque neovascularization reduces macrophage accumulation and progression of advanced atherosclerosis.

Plaque angiogenesis promotes the growth of atheromas, but the functions of plaque capillaries are not fully determined. Neovascularization may act as a conduit for the entry of leukocytes into sites of chronic inflammation. We observe vasa vasorum density correlates highly with the extent of inflammatory cells, not the size of atheromas in apolipoprotein E-deficient mice. We show atherosclerotic aortas contain activities that promote angiogenesis. The angiogenesis inhibitor angiostatin reduces plaque angiogenesis and inhibits atherosclerosis. Macrophages in the plaque and around vasa vasorum are reduced, but we detect no direct effect of angiostatin on monocytes. After angiogenesis blockade in vivo, the angiogenic potential of atherosclerotic tissue is suppressed. Activated macrophages stimulate angiogenesis that can further recruit inflammatory cells and more angiogenesis. Our findings demonstrate that late-stage inhibition of angiogenesis can interrupt this positive feedback cycle. Inhibition of plaque angiogenesis and the secondary reduction of macrophages may have beneficial effects on plaque stability.

Angiostatins↗

PubMed2006

Clinical analysis of acute type A intramural hematoma: comparison between two different pathophysiological types.

BACKGROUND: Type A intramural hematoma (IMH) has two different etiologies, which are rupture of vasa vasorum and penetrating atherosclerotic ulcer (PAU); however, it is difficult to know which is the initiating event. METHODS: Between January 1993 and August 2004, 28 patients of acute type A IMH were treated in our department and were divided into two groups, 20 patients with IMH probably caused by rupture of vasa vasorum (non-PAU group) and 8 patients with IMH probably caused by PAU (PAU group), according to pathologic specimen and atherosclerotic findings on computed tomography. Background factors, radiographic findings, and prognosis were analyzed retrospectively. RESULTS: Surgery was performed in 15 patients (75%) in non-PAU group and 4 patients (50%) in PAU group during the first admission. Late progression was noted in 3 patients, and operation was required. Finally, operation was performed in 22 patients (78.6%). The history of myocardial infarction (p = 0.026) and chronic renal failure (p = 0.026) were more associated with PAU group than with non-PAU group. Ascending aortic diameter at the onset was significantly larger in non-PAU group (50.3 +/- 6.6 mm) than in PAU group (43.9 +/- 9.0 mm; p = 0.046), and there were significantly more ulcer lesions in PAU group (1.9 +/- 0.4) than in non-PAU group (1.1 +/- 0.4; p = 0.0004). There was no significant difference in long-term survival rates between them. CONCLUSIONS: The PAU group patients have more coexisting atherosclerotic diseases and multiple aortic ulcer lesions with significantly mild ascending aortic dilatation compared with non-PAU group patients.

Age Factors↗

PubMed1997

Arterial wall neovascularization--potential role in atherosclerosis and restenosis.

Neointimal formation and arterial wall remodeling are pivotal causes of luminal narrowing in atherogenesis and restenosis. Arterial remodeling refers to a series of dynamic structural changes that arteries may undergo in response to various stimuli, including changes in blood flow and pressure, and acute injury. The biological mechanisms involved in arterial remodeling are poorly understood and are currently a main target for research. We have recently focused on the role of the arterial wall microcirculation (ie, vasa vasorum) in arterial remodeling after injury. In the past, a correlation between arterial wall neovascularization and the accumulation of arterial plaque has been documented; however, the dynamic role of these microvessels in arterial repair and luminal narrowing has not been examined. The type of arterial injury, the nature of the lesion that develops, and the arterial compartment in which angiogenesis occurs may determine the role of the vasa vasorum in arterial narrowing. In this review, we highlight the data that link arterial wall neovascularization with lesion formation and the process of arterial remodeling.

Arteries↗

PubMed2004

Loss of collagen XVIII enhances neovascularization and vascular permeability in atherosclerosis.

BACKGROUND: Plaque neovascularization is thought to promote atherosclerosis; however, the mechanisms of its regulation are not understood. Collagen XVIII and its proteolytically released endostatin fragment are abundant proteoglycans in vascular basement membranes and the walls of major blood vessels. We hypothesized that collagen XVIII in the aortic wall inhibits the proliferation and intimal extension of vasa vasorum. METHODS AND RESULTS: To test our hypothesis, we bred collagen XVIII-knockout (Col18a1(-/-)) mice into the atherosclerosis-prone apolipoprotein E-deficient (ApoE(-/-)) strain. After 6 months on a cholesterol diet, aortas from ApoE(-/-);Col18a1(-/-) and ApoE(-/-);Col18a1(+/-) heterozygote mice showed increased atheroma coverage and enhanced lipid accumulation compared with wild-type littermates. We observed more extensive vasa vasorum and intimal neovascularization in knockout but not heterozygote aortas. Endothelial cells sprouting from Col18a1(-/-) aortas were increased compared with heterozygote and wild-type aortas. In contrast, vascular permeability of large and small blood vessels was enhanced with even heterozygous loss of collagen XVIII but was not suppressed by increasing serum endostatin to wild-type levels. CONCLUSIONS: Our results identify a previously unrecognized function for collagen XVIII that maintains vascular permeability. Loss of this basement membrane proteoglycan enhances angiogenesis and vascular permeability during atherosclerosis by distinct gene-dose-dependent mechanisms.

Animals↗

PubMed1996

Endothelial Gi protein expression is markedly low in human coronary microvessels.

Gi protein functionally mediates endothelium-dependent relaxations in large epicardial coronary arteries but not in small coronary arteries, which suggests a different involvement of Gi protein in the endothelium-dependent relaxations between large and small coronary arteries. We previously showed that endothelial Gi protein is present in human epicardial coronary artery. In the present study, we examined the expression of endothelial Gi protein in human coronary microvessels. Immunohistochemical staining with a specific antibody against human Gi protein was performed in intramyocardial coronary microvessels and vasa vasorum from 34 autopsy cases. The immunoreactive levels of the endothelial Gi protein were semiquantitated into four grades (none, 0; slight, +1; moderate, +2; high, +3), and the mean value of the ratings of all endothelial cells was then used as an index of the endothelial Gi protein expression of the vessel. The immunoreactive levels of the endothelial Gi protein were extremely low in intramyocardial coronary microvessels and in vasa vasorum, irrespective of the age of the patients, the presence or absence of coronary risk factors, or the influence of medical treatments. These results may therefore explain in part why endothelium-dependent relaxations in coronary microvessels are not functionally mediated by Gi protein.

Adolescent↗

PubMed2002

In utero indomethacin alters O2 delivery to the fetal ductus arteriosus: implications for postnatal patency.

Indomethacin produces constriction and hypoxia of the fetal ductus arteriosus. This is associated with death of smooth muscle cells in the ductus wall and an increased incidence of patent ductus arteriosus in the newborn period. We used fetal sheep to determine which factors are responsible for indomethacin-induced hypoxic cell death. Cell death in the ductus wall is directly related to the degree of indomethacin-induced ductus constriction and is present at both moderate and marked degrees of constriction. Both moderate and marked degrees of ductus constriction reduce vasa vasorum flow to the ductus (moderate = 69 +/- 25%; marked = 30 +/- 16% of preinfusion values) and increase the thickness of the ductus wall. In contrast, ductus luminal blood flow is not affected by moderate degrees of constriction and is reduced only after marked constriction. Although indomethacin increases ductus tone, it has no effect on ductus oxygen consumption. These findings suggest that the hypoxic cell death that occurs during the early stages of indomethacin-induced constriction is primarily due to changes in vasa vasorum blood flow and muscle media thickness.

Animals↗

PubMed1981

[Microcirculation of the aorta and coronary arteries in patients who died of myocardial infarct and generalized arteriosclerosis].

The authors studied the microcirculation changes in ascending aorta and left coronary artery of the heart in 25 deceased with myocardial infarction, aged from 52 to 80, with two control groups: 20 cases with complicated atherosclerosis, aged from 54 to 80, and 4 cases--without atherosclerosis, aged 30-45. Histological and histochemical investigation methods were used. The authors found grave changes in vasa vasorum of aorta and coronary artery with the formation of arteries of "closing" type, hyperplasia of the muscular layer of the arterial and venous vessels anf fibrosis of their wall in the deceased with healed myocardial infarction and chronic coronary and cardiac insufficiency. Acute disturbance of blood microcirculation was observed in recent myocardial infarction, analogical to that in case of shock. Necrosis of the type of anemic infarctions and stratification of the wall with hemorrhages and fresh thrombosis were found in the media of aorta and coronary artery in myocardial infarction and atherosclerosis. Both necrosis and stratification are associated with the manifested endothelial proliferation, recent and organized thrombus in the small vasa vasorum and grave structural changes in the supplying vessels of aorta and coronary arteries.

Adult↗

PubMed2002

A morphometric study of the structural characteristics of the aorta in pigs using an image analysis method.

The objective of this study was to evaluate multiple structural characteristics, in addition to vasa vasorum density, in different aortic regions. The aorta of healthy Landrace pigs was divided into four thoracic and three abdominal segments. Transverse sections were reserved for morphometric analysis. Image analysis showed the aortic diameter, the thickness of the media, the number of elastic lamellae and the thickness of elastic membranes being reduced with increased distance from the heart (P < 0.05). The average thickness of lamellar units remained constant in the thoracic, but increased in the abdominal aorta (P < 0.05). The number of lamellar units, contained in the avascular zone of the media, and the density of vasa vasorum decreased peripherally (P < 0.05), still the average thickness of the avascular zone was invariant. In conclusion, the anatomical properties of the vessel wall alter through the aorta, being optimal for the varying stresses to which the aorta is subjected along its length. The distinct aortic parts may exhibit inherent morphological features, responsible for the various pathological processes that affect the aorta.

Animals↗

PubMed1999

Cystic medial degeneration of the aorta is associated with p53 accumulation, Bax upregulation, apoptotic cell death, and cell proliferation.

OBJECTIVE: To address a potential role for p53, Bcl2 associated protein X (Bax), and apoptosis in the processes associated with cell turnover during cystic medial degeneration (CMD) of the aorta. METHODS: Histochemical, immunohistochemical, biochemical, and morphometric methods were used to assess the presence and distribution of p53 immunoreactivity (p53-IR) and Bax immunoreactivity (Bax-IR), as well as the presence of apoptosis and tissue repair processes. RESULTS: Immunohistochemical staining disclosed evidence for p53-IR in all specimens in 26.1 (11.5)% of vascular smooth muscle cells (VSMCs) (controls 0.8 (1.3)%; p < 0. 001). Bax-IR was present in all specimens in 10 (5.4)% of medial cells (controls 0.3 (0.5)%; p < 0.001). Medial VSMCs (alpha-actin positive) with cytoplasmic staining for an apoptosis specific protein (c-jun/ASP) were present in 20/20 specimens (0.7 (0.6)% of VSMCs, controls 0%, p < 0.001), whereas terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) positive VSMCs were present in 17/20 specimens (1 (1.5)% of VSMCs, controls 0%, p < 0.001). The presence of apoptosis was confirmed by electron microscopy and the demonstration of oligonucleosomal DNA fragments after agarose gel electrophoresis. As shown by double labeling and investigation of serial sections, p53-IR, Bax-IR, c-jun/ASP-IR, and positive TUNEL labeling localised to the same compartments of the aortic media, raising a possible role for p53 and Bax in the triggering of apoptosis of VSMC during CMD. MIB1/Ki-67 positive medial VSMCs (alpha-actin positive) and mesenchymal cells (vimentin positive) were present in all specimens (2.5 (2.8)% of medial cells; controls 0.3 (0.9)%, p < 0.001) mainly in the region around the vasa vasorum, indicating that cell regeneration during CMD may originate mainly from the mesenchyme surrounding the vasa vasorum. CONCLUSION: This study shows that the formal pathogenesis of CMD is characterised by p53 accumulation, Bax upregulation, cell death by apoptosis, and cell regeneration. Nevertheless, the precise stimuli of p53 activation and Bax upregulation as well as the role of p53 and apoptosis in the dissection process itself remain elusive.

Adult↗