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PubMed2002

VEGF regulates remodeling during permanent anatomic closure of the ductus arteriosus.

Anatomic remodeling and permanent closure of the newborn ductus arteriosus appears to require the development of intense hypoxia within the constricted vessel wall. Hypoxic ductus smooth muscle cells express vascular endothelial cell growth factor (VEGF). We studied premature baboons and sheep to determine the effects of VEGF inhibition (in baboons) and VEGF stimulation (in sheep) on ductus remodeling in vivo. For study of VEGF inhibition, 13 premature newborn baboons (68% gestation) were treated with inhibitors of both prostaglandin and nitric oxide production to constrict the ductus and induce ductus wall hypoxia. Six received a neutralizing monoclonal antibody against VEGF (A.4.6.1, mAbVEGF), while seven did not. Both groups developed the same degree of ductus constriction, tissue hypoxia, and VEGF expression. The mAbVEGF treatment produced a significant (P < 0.05) reduction in ductus vasa vasorum ingrowth and neointima formation (due to both a decrease in luminal endothelial cell proliferation and a decrease in smooth muscle cell migration into the neointima). For study of VEGF stimulation, nine sheep fetuses (70% gestation) had their ductus wall injected with either VEGF (n = 6) or vehicle (n = 4) in vivo. VEGF administration produced a significant (P < 0.05) increase in vasa vasorum ingrowth and neointima formation. We conclude that VEGF plays an important role in the formation of neointimal mounds and vasa vasorum ingrowth during permanent ductus closure.

Animals↗
PubMed1983

Routes of drug delivery to the middle segment of the canine inferior vena cava in vivo.

Noradrenaline (1-3 micrograms/kg) administered into the right femoral vein caused a two-step increase in tension of the middle segment of the canine inferior vena cava, whereas noradrenaline administered into the right external jugular vein or the aortic arch caused a single-step one. The analysis of these vascular responses showed that noradrenaline administered into the femoral vein affected the inferior vena cava first from the endothelial side, distributed systemically and, then, affected the vein again from the adventitial side via the vasa vasorum. Acetylcholine (3 micrograms/kg) administered into the femoral vein caused a single-step increase in tension and could hardly reach the arterial side, while the same dose of acetylcholine administered into the aortic arch contracted the vein more largely as compared with noradrenaline. The response to noradrenaline administered topically through the vasa vasorum was augmented by administration of cocaine (2 X 10(-5) M) through the same route, while that to acetylcholine was not. These results show that acetylcholine reaches the middle segment of the inferior vena cava through the vasa vasorum in vivo more effectively than noradrenaline partly because it is not taken up by nerve terminals in the vein.

Acetylcholine↗
PubMed1996

[General principles of oxygen transport in the venous wall].

OBJECTIVE: To review the mechanisms of oxygen transport in the walls of arteries and veins and to consider whether oxygen transport might limit oxygen consumption in the venous wall. METHODS: (i) To review evidence for the contributions of transport from the vascular lumen and transport from the vasa vasorum to the supply of oxygen to the walls of arteries. (ii) To use the general principles of oxygen diffusion through tissues to extrapolate the findings of investigations of oxygen transport into arterial walls to transport into the walls of the larger veins. RESULTS AND DISCUSSION: The magnitude of oxygen transport from the vessel lumen into the vessel wall is dependent on the partial pressure of oxygen (PO2) in the vessel lumen. While luminal PO2 is constant and high in arteries, it is a physiological variable in veins of healthy people. In larger veins, there is evidence that flow in the vasa vasorum increases as PO2 in the vessel lumen falls. The extent to which this regulatory action of the vasa vasorum may be comprised by raised venous pressure and venous distension has not been defined.

Animals↗
PubMedDate not supplied

The effects of crimping on the healing of prosthetic arterial grafts.

The purpose of this study was to determine whether the crimping of arterial prostheses affected their healing. In ten dogs, 6 mm knitted Dacron grafts were implanted in the infrarenal aortas; 6 grafts were crimped, 4 uncrimped. Each was seeded with venous endothelium to produce a cellular lining. The grafts were removed a month after implantation and compared by light microscopy as to the (1) thickness of the inner lining, (2) completeness of endothelial healing, and (3) patterns of vasa vasorum. (1) and (3) were assessed using H & E sections and (2) by AgNO3 Häutchen preparations. The lining in uncrimped grafts was thinner and more uniform than in crimped grafts: 50.1 +/- 45.7 vs 263 +/- 183 mu, p < 0.001. While the completeness of healing was similar for both groups, 4 crimped grafts had unhealed areas in the centers of the crimps, corresponding to the thicker areas of the linings. In both kinds of grafts, vasa vasorum communicated with vascular channels parallel to the axis of flow and near the perigraft fat. In the uncrimped grafts, the smaller secondary vasa also were directed along the axis of flow, in contrast to crimped grafts in which they were circumferential to the graft and parallel to the crimps. In all instances vasa penetrated within 500 mu of the lumen. We conclude that crimping causes a change in the pattern of development of vasa vasorum in healing fabric grafts and a thicker inner lining associated with areas of delayed healing which may increase the risk of thrombosis.

Animals↗
PubMed1995

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 II 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.

Cell Adhesion Molecules↗
PubMed1991

The human penis: an unusual penetration of NPY-immunoreactive nerves within the medial muscle coat of the deep dorsal vein.

The deep dorsal penile vein was obtained from seven patients undergoing surgery for erectile dysfunction. The veins were studied histologically and immunohistochemically for serotonin, dopamine beta-hydroxylase, vasoactive intestinal polypeptide, neuropeptide Y, substance P, calcitonin gene-related peptide, somatostatin, and [Leu]- and [Met]enkephalin. Histologically, the deep dorsal vein was found to be a large muscular vein with a thin endothelial lining. The tunica media was composed of an inner longitudinally and an outer circularly arranged smooth muscle layer. Numerous vasa vasorum (up to 30 in a single transverse section) were found in the tunica adventitia. The greatest density of nerves supplying the deep dorsal vein and vasa vasorum were neuropeptide Y-immunoreactive nerves followed (in a decreasing order) by vasoactive intestinal polypeptide- and dopamine beta-hydroxylase-immunoreactive nerves. Substance P-, calcitonin gene-related peptide- and somatostatin-immunoreactive nerves, but not serotonin-, [Leu]- and [Met]enkephalin-immunoreactive nerves, were occasionally found around the deep dorsal vein. All these nerve fibers were confined to the adventitial-medial border except neuropeptide Y-immunoreactive nerves which in addition penetrated the tunica media to the subendothelial layer of the deep dorsal vein. In contrast, neuropeptide Y-immunoreactive nerves supplying the vasa vasorum were always confined to the adventitial-medial border. The possible function of the medial innervation of the deep dorsal vein by neuropeptide Y-immunoreactive nerves is discussed.

Adult↗
PubMed2000

Expression of leptin receptor (Ob-R) in human atherosclerotic lesions: potential role in intimal neovascularization.

Neovascularization of the adventitial vasa vasorum with extension into the intima of atherosclerotic lesions is frequently observed, but its pathophysiological significance is still subject to debate. Recently, leptin, the product of the Ob gene, was identified. Leptin, via activation of the endothelial receptor (Ob-R), generates a growth signal involving a tyrosine kinase-dependent intracellular pathway and promotes angiogenic processes. We hypothesized that a high concentration of leptin within vasa vasorum and plaque itself, may influence inflammatory and vascular neovascularization coupling with functional upregulation of the vascular endothelial growth factor (VEGF). Microscopic computerized tomography was utilized for the spatial distribution of vasa vasorum and intimal neovascularization from atherosclerotic human coronary arteries. Atherosclerotic coronary arteries showed a dense plexus of microvessels in the adventitia and plaque itself. Microscopic analysis from human atherosclerotic aortas revealed an increase in the intimal thickness with neovascularization. The immunoreactivity for Ob-R, VEGF and matrix metalloproteinase (MMP) increased in atherosclerotic plaque, predominantly in the endothelial lining of the intimal neovessel and macrophages/foam cells. Our observation of a prominent colocalization between Ob-R, VEGF and MMP supports this hypothesis and these factors participate in the neovascularization of atherosclerotic lesions. The present study is the first report on vascular tissue and it opens a promising perspective concerning future investigations of leptin-dependent modulation of atherogenesis and vascular neovascularization under pathophysiolgical conditions.

Adult↗
PubMed1999

Histological evidence of concomitant intramyocardial and epicardial vasculitis in necropsied heart allografts: a possible relationship with graft coronary arteriosclerosis.

BACKGROUND: The significance of medial lymphocytic vasculitis in intramural coronary vessels in heart transplantation is very poorly understood. This study was designed to identify histological evidence of an association between the presence of epicardial coronary lesions and the occurrence of intramyocardial vasculitis and/or myocardial ischemia. METHODS: We analyzed the frequency of medial vasculitis and other myocardial histological alterations in a retrospective study of 24 human cardiac allografts from patients who died of ischemic heart disease and/or myocardial rejection. RESULTS: Medial lymphocytic vasculitis in the myocardium was associated with vasculitis in the vasa vasorum of the epicardial coronary arteries and the presence of microfoci of acute myocardial infarction but was independent of the occurrence of myocardial fiber rejection. Chronic graft epicardial arteriopathy revealed two patterns of lesions. One pattern was similar to that of usual atherosclerosis, compromising mainly the proximal segments of the coronary artery, and was not associated with intramural vasculitis. The other pattern demonstrated diffuse involvement of the epicardial artery associated with vasculitis of its vasa vasorum and lymphocytic vasculitis of the intramural vessels. This second type of epicardial coronary lesion seemed to evolve to fibrotic arteries with thinned walls, frequently demonstrating aneurysmal dilatation with severe fibrosis of the adventitia and poor vasa vasorum. CONCLUSION: Medial vasculitis affecting intramyocardial vessels is associated with adventitial epicardial coronary vasculitis in the transplanted heart. The process of vasculitis may be involved in the development of chronic graft arteriosclerosis and is associated with ischemic myocardial lesions, but seems independent of myocardial fiber rejection.

Acute Disease↗
PubMed1997

Possible mechanisms of collar-induced intimal thickening.

The positioning of a soft silicone collar around the rabbit carotid artery induces intimal thickening. We investigated to which extent occlusion of the vasa vasorum, damage of the perivascular nerve network, and/or changes in blood flow velocity contribute to intimal thickening. To this end, collars with different bores (diameter of inlet and outlet) were positioned around the carotid artery of male rabbits for 14 days. In another experiment, 75% of the wall of fitting collars was removed (open collar). In the midcollar region, the cross-sectional area of the intima reached a maximum (72 +/- 14 mm2/1000) when the endings of the collar fitted the artery closely. Removal of the side wall of these fitting collars reduced intimal thickening by 90%. Examination of unoperated carotid arteries never showed penetration of the adventitia or the media by vasa vasorum. The perivascular neuronal network in the region surrounded by a closed or an open collar was almost completely lost as compared with the zones outside the collar. Both the closed and open collar slightly bent the artery and increased the peak systolic velocity, measured with pulsed color Doppler after 6 hours, to a similar extent as compared with the proximal zone outside the collar. After 2 weeks, the peak systolic velocity within both the closed and open collar was partly normalized and was statistically not different from the proximal zone outside the collar. In conclusion, the geometry of the collar influenced the extent of intimal thickening, whereby more intimal thickening was obtained with a collar whose endings fit the carotid artery, rather than with a loose collar. Moreover, a closed structure was essential. The results obtained with the open collar exclude occlusion of vasa vasorum, damage of the perivascular neuronal network, kinking of the artery, and changes in blood flow velocity as major factors in the collar-induced intimal thickening. Our findings are consistent with the possibility that intimal thickening is the consequence of the combination of both vascular injury and hindrance of transmural flow by the collar. The obstruction of transmural fluid transport may then lead to retention of toxic metabolites, and/or cytokines within the segment enclosed by the collar.

Animals↗
PubMed1985

Nonreversed and in situ vein grafts. Clinical and experimental observations.

The in situ saphenous vein (ISSV) graft has shown promise in distal bypass. Although improved patency has been attributed to preservation of vasa vasorum, there is no direct evidence to support this hypothesis. Femorodistal bypass was done in 33 patients using ISSV grafts (21) or nonreversed saphenous vein (NRSV) grafts (12) during an 18-month period. The NRSV were completely removed from the vein bed but were otherwise prepared in an identical fashion to the ISSV. Immediate complications including incomplete valvulotomy (one), intimal laceration (one), persistent AV communication (two), and extrinsic graft compression (one) were identified and corrected. Two grafts of 2.5 mm diameter occluded acutely. There were no deaths. Of 30 patients discharged with a patent graft, there was one late occlusion (ISSV) at 10 months. No difference in patency between ISSV and NRSV grafts was noted during follow-up extending to 24 months. Overall limb salvage was 94%. In a canine model, 60 vein segments were interposed in the carotid artery using in situ, reversed, and nonreversed techniques. Ultrastructural studies 1, 2, 3, and 6 months after implantation reveal no differences in in situ and nonreversed grafts. New vasa vasorum were identified in NRSV within 1 month. Both ISSV and NRSV grafts demonstrate excellent patency and maintenance of smooth muscle cell architecture. Factors including reduced size disparity at the proximal and distal anastomoses, physiologic distension under arterial pressure, careful handling, and meticulous technique appear to be more important than the theoretic advantages of preserving vasa vasorum.

Aged↗
PubMed1997

Venous drainage of the radial forearm and anterior tibial reverse flow flaps: anatomical and radiographic perfusion studies.

The anatomy of the venous system in the pedicles of the radial forearm and anterior tibial reverse flow flaps was investigated in fresh cadavers (n = 6) and their drainage pathways were observed in a radiographic perfusion study of the veins of 2 radial forearm and 2 anterior tibial pedicles. The venous system was found to consist mainly of three types of veins: venae comitantes, communicating veins between the venae comitantes, and vasa vasorum. Valves were identified in all three types of vein. In the venous system, including the vasa vasorum, there was no route of reverse flow that did not pass directly through valves. Valve incompetence was demonstrated in the radiographic perfusion study. However, valve incompetence did not occur in all valves and a difference in valve resistance against reverse flow pressure existed. Veins with relatively weak valve resistance became the drainage pathway. A possible cause of the difference in valve resistance was differences in the anatomy of the valve sinuses.

Forearm↗
PubMed1981

Hyperemia of the aortic wall in atherosclerotic monkeys.

The aortic wall is nourished by diffusion from the aortic lumen and from vasa vasorum in the adventitia and outer layers of media. Intimal proliferation in atherosclerosis might be expected to reduce the effectiveness of diffusion from the lumen and increase dependence on nourishment by vasa. This study was performed to determine whether there is increased perfusion of the aortic wall by vasa vasorum in atherosclerosis. We used microspheres to measure flow through vasa in normal and atherosclerotic cynomolgus monkeys. Blood flow to inner layers of the thoracic and abdominal aorta was less than 1 ml/min X 100 g in normal monkeys, and there was a minimal increase in atherosclerotic monkeys. Flow to the outer layers of the thoracic and abdominal aorta was 1.3 +/- 0.9 and 2.2 +/- 0.8 ml/min per 100 g in normal monkeys. Flow to outer layers of the thoracic and abdominal aorta was increased in atherosclerotic monkeys to 17 +/- 8.9 and 31 +/- 12 ml/min per 100 g (P less than 0.05 vs. normal). Thus there is increased perfusion of the atherosclerotic aorta, particularly in the outer layers. During maximal vasodilation induced by infusion of adenosine, flow through vasa was 3- to 8-fold greater in atherosclerotic than in normal monkeys. This finding suggests that proliferation of new vessels, rather than dilation of existing vessels, accounts for the increase in blood flow through vasa. We speculate that hyperemia of the aortic wall in atherosclerosis may be in part a compensatory response to increased oxygen requirements and possibly to ischemia produced by intimal proliferation and a resulting increase in diffusion distance.

Adenosine↗
PubMed1999

Liver microvascular architecture: an insight into the pathophysiology of portal hypertension.

Structural adaptations in the liver to constantly receive and release a large volume of circulating blood at low pressure are present at many levels; alteration of these structures can modify flow and perturb pressure gradients. Liver growth multiplies the lobule number by a factor of 4-5 after birth. Lobule configuration conforms with observations in space division, each unit being bordered by planes; curvature will impede expansibility and retractability among units. Lobular organization with hepatocytic plates and sinusoids, being radial centrally and reticular peripherally, maximizes its reversible distensibility. Resistance sites in the portal, sinusoidal, and hepatic system are subject to species variations; real portal sphincters are photographed in the frog. Small venules are demonstrably resistive. In endothelin-1-induced rat portal hypertension, the distal segment of preterminal portal venules constricts most intensely, whereas the terminal portal venules and sinusoids are flaccid. Their pericytes and arachnocytes (stellate cells, Ito cells, retinol-storing cells), respectively, possess no effective contractile machinery. In the dog, the initial sublobular veins react with venoconstriction to many stimulations. Well-developed musculature in hepatic veins, as in man and pig, can regulate flow by junctional constriction. These histoarchitectonics provide hepatic hemodynamics with high capacitance and high compliance properties. The hepatic artery supplies oxygenated blood to five stromal compartments: peribiliary vascular plexus, portal tract interstitium, portal vein vasa vasorum, hepatic capsule, and central-sublobular-hepatic vein vasa vasorum. Its role as the nutrient vessel to the veins is established, but what influence it may have in the pathophysiology of portal hypertension awaits clarification.

Animals↗
PubMed2000

Transarterial wall oxygen gradients at a prosthetic vascular graft to artery anastomosis in the rabbit.

PURPOSE: Artery-wall hypoxia has been proposed to contribute to many kinds of artery-wall pathologic conditions, including atherosclerosis and intimal hyperplasia. Intimal hyperplasia is common at sites of arterial injury, including an anastomosis. The purpose of this study was to determine the effect of a prosthetic vascular graft (PVG)-to-artery anastomosis on the delivery of oxygen to the artery wall. METHODS: The transarterial wall oxygen gradient in the infrarenal aorta of New Zealand White rabbits 2 mm distal to a PVG-to-artery anastomosis was measured with an oxygen microelectrode. RESULTS: Oxygen tensions were significantly decreased in the outer artery wall immediately after the creation of the anastomosis and showed a further decrease in oxygen tensions at days 7 and 14, which correlated with the absence of a vasa vasorum. After day 14, the oxygen tensions gradually increased, returning to normal by postanastomosis day 42, correlating with a return of the vasa vasorum. These changes were noted without differences in blood pressure or arterial blood oxygen concentrations. CONCLUSION: The delivery of oxygen to the artery wall is altered by the creation of a PVG-to-artery anastomosis. Low arterial oxygen tensions at a PVG-to-artery anastomosis support a role for artery-wall hypoxia in the formation of intimal hyperplasia at the site of a PVG-to-artery anastomosis.

Analysis of Variance↗
PubMed2002

Inner layer infarction of the coronary artery wall due to coronary thrombosis.

Cross sections of 112 coronary artery segments from 65 human hearts with coronary thromboses were investigated after postmortem coronary angiography. In almost all cases the inner layers of coronary artery walls adjacent to the obstructing thrombi or to parietal thrombi were infarcted. These infarctions followed nearly the same course as classical infarctions. From 13 hearts with segments occluded by thrombi but without atherosclerotic lesions, 19 specimens were found suitable for quantitative investigations. The 2 segments with the thinnest intima were lacking in inner layer infarctions. The other 17 specimens contained areas of inner layer necrosis of increasing diameter, depending on the thickness of the wall. In each case the media was completely preserved. The mean thickness of the noninfarcted wall tissue was 190+/-28 micro m. This noninfarcted wall tissue was supplied by vasa vasorum in the adventitia located at an average distance of approximately 40 micro m from the media. The knowledge of the supplying areas of the vasa vasorum could help us understand the pathogenesis of necroses in atherosclerotic plaques.

Aged↗