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PubMed2005

Computer vision analysis of collagen fiber bundles in the adventitia of human blood vessels.

Numerical simulations, which are based on reliable biomechanical models of blood vessels, can help to get a better understanding of cardiovascular diseases such as atherosclerosis, and can be used to develop optimal medical treatment strategies.The adventitia is the outer most layer of blood vessels and its mechanical properties are essentially determined by the three-dimensional, structural arrangement of collagen fibre bundles embedded in the tissue. Global information such as the orientation statistics of the fibre bundles as well as detailed information as the crimp of the single fibres within the bundles is of particular interest in biomechanical modeling.In order to obtain a sufficiently large amount of data for biomechanical modeling, a fully automatic method for the structural analysis of the soft tissue is required. In this contribution we present methods based on computer vision to fulfill this task. We start by discussing proper tissue preparation and imaging techniques that have to be used to obtain data, which reliably represents the real three-dimensional tissue structure. The next step is concerned with algorithms that robustly segment the collagen fibre bundles and cope with various kinds of artifacts. Novel segmentation techniques for robust segmentation of individual fibril bundles and methods for estimation of their parameters, such as location, shape, mean fibril orientation, crimp of fibrils, etc, is discussed. The proposed algorithms are based on novel perceptual grouping methods operating on the extracted orientation data of fibrils.Finally, we demonstrate the results obtained by our fully automatic method on real data. In addition, for a more quantitative assessment, we introduce a generative structural model that enables the synthesis of three-dimensional fibre bundles with well-defined characteristics.

Adventitia↗
PubMed1982

The origin of lipid phagocytes in the central nervous system: II. The adventitia of blood vessels.

The source of the lipid phagocytes that occupy a cerebral infarct has been determined by light and electron microscopy in the brains of rodents and by light microscopy only in the brains of primates. The infarcts (in neocortex, hippocampus, and thalamus) were the consequence of hypoxia-ischemia of various types. Hemorrhagic infarcts were excluded. After in vivo perfusion-fixation, paraffin- and celloidin-embedded material was used for light microscopy. Semithin plastic sections from the neocortex and thalamus were studied with the light microscope and ultrastructural studies were confined to the same regions. In all animals after about 2 days there was evidence of phagocytic activity in the fibroblasts in the adventitia of the remaining large vessels and also proliferation by mitotic division. At 5-7 days fibroblasts appeared to migrate from the vessels in a semifluid or fluid milieu and to give rise to typical phagocytes. These increased in size and number but signs of degeneration became apparent after 10 days and they had largely disappeared by 32 days. Smooth muscle cells and pericytes showed evidence of degeneration and phagocytic activity was never seen in the latter.

Animals↗
PubMed1996

Two hypothetical proteins of human aortic adventitia, with Ig kappa, collagenous, and aromatic-rich motifs.

Two of five clones, selected from an expression library of aortic adventitia, encode unique hypothetical proteins sharing sequences of Ig kappa, gly/pro rich (collagenous) motifs, and aromatic motifs that occur in several proteins of the extracellular matrix. Both proteins have a similar domain structure with at least 8 regions: (1) Ig kappa (84-120 residues in length); (2) ser/thr-rich motif (44-63); (3) a second Ig kappa motif (9-12); (4) either a possible calcium-binding motif or a gly/pro rich sequence (35-43); (5) an aromatic rich sequence (6-7); (6) another gly/pro rich sequence (62-72); (7) a third Ig kappa sequence (26-28); and (8) a C-terminal 68-70 residue sequence with another aromatic motif.

Amino Acid Sequence↗
PubMed1984

Experimental measurements of elastic properties of media and adventitia of bovine carotid arteries.

An experimental procedure is described which has been developed to measure the elastic properties of the outer (adventitial) and inner (medial) layers of excised bovine carotid arteries. The data analysis is based on a two-layered arterial wall model and the theory of large elastic deformations. The energy density functions for both layers are exponentials. The results show that the media and the adventitia are anisotropic; that the media is stiffer, more non-linear, and subjected to higher stresses than commonly assumed; and that both layers are stiffer in the axial direction than in the tangential direction.

Animals↗
PubMed1992

Effect of experimentally-induced hypertension on angiotensin converting enzyme activity in the aortic endothelium and smooth muscle cum adventitia of the Sprague Dawley rat.

The effect of experimentally-induced hypertension on the angiotensin converting enzyme (ACE) activity in the endothelium and smooth muscle cum adventitia of the Sprague Dawley rats was investigated. The ACE activity in both tissues of the 1-clip 2-kidney renovascular hypertensive rats and the deoxycorticosterone acetate/salt hypertensive rats were significantly higher than those of the normotensive control. These findings (i) support the suggestion that the 1-clip 2-kidney renovascular hypertensive rat represents a model of renin- and angiotensin-dependent hypertension and that the increased vascular ACE activity could play a role in the maintenance of hypertension (ii) provide new information regarding the association of increased vascular ACE activity and hypertension in the mineralocorticoid/salt treated hypertensive rats which may account for the finding by others that captopril is effective in preventing the development of hypertension in this low renin model of hypertension. On the other hand, the data also bring forth the possibility that the observed increase in vascular ACE activity could be the result of hypertension.

Animals↗
PubMed1993

Kinetics of relaxation responses to vasorelaxants in intact and adventitia- and endothelium-denuded isolated rabbit thoracic aorta.

1. Although the relaxation responses to 5'-N-ethylcarboxamidoadenosine and sodium nitroprusside were stable, the relaxation response to isoproterenol partially desensitized as was observed by the partial regaining of tissue tension. 2. The apparent rate constant for relaxation by all three vasorelaxants was decreased in the presence of the adventitia and endothelium. 3. The magnitude of the relaxation responses for all three vasorelaxants and the apparent rate constant for isoproterenol desensitization were similar in intact and denuded tissues.

Adenosine↗
PubMed1991

Nerve growth factor receptor immunoreactivity on the tunica adventitia of intramuscular blood vessels in childhood muscular dystrophies.

Muscle tissues from cases of childhood neuromuscular disorders were examined immunohistochemically and immunoelectrophoretically using a monoclonal antibody against the human nerve growth factor receptor (NGFR). Strong NGFR immunoreactivity on the tunica adventitia of blood vessels and proliferating peripheral nerve endings in biopsied muscle specimens from muscular dystrophy patients was observed, but it was almost completely absent in specimens from non-diagnostic controls and cases of other neuromuscular disorders. This suggests a process in the sympathetic nervous system involving blood vessels in muscular dystrophies. Immunoblot analysis failed to show a band corresponding to 70-75 kd, the reported molecular size of the NGFR, but showed a clear band corresponding to 25 kd in muscular dystrophy patients, which is assumed to be a detached amino-terminal domain of the NGFR.

Adolescent↗
PubMed2005

Antifibrotic effect of adrenomedullin on coronary adventitia in angiotensin II-induced hypertensive rats.

OBJECTIVE: The extracellular matrix (ECM) determines the structural integrity of the heart and vasculature, participating in cardiovascular remodeling. We previously reported that adrenomedullin (AM) inhibited cellular proliferation and protein synthesis of cardiac fibroblasts; however, the precise mechanisms of AM actions as an antifibrotic factor remain unknown. The purpose of this study was to examine the biological actions of AM against the profibrotic factor angiotensin II (Ang II) in coronary adventitia. METHODS AND RESULTS: Rats with hypertension induced by Ang II infusion were administered 0.06 mug/kg/min recombinant human AM subcutaneously for 14 days. The AM infusion significantly (p<0.05) reduced the Ang II-induced increase of coronary adventitial fibroblasts expressing Ki-67 and alpha-smooth muscle actin (alpha-SMA) in the left ventricle, by 65%, and 62%, respectively, without affecting systolic blood pressure, left ventricle/body weight, or cross-sectional area of myocardial fibers. Collagen deposition of coronary arteries was reduced by the AM infusion (-24%, p<0.01), and these effects of AM were accompanied by significant reductions in gene expression of type 1 collagen (-49%, p<0.05) and transforming growth factor-beta1 (TGF-beta1) (-55%, p<0.01). In cultured cardiac fibroblasts, 10(-7) mol/L AM exerted an inhibitory effect on TGF-beta1-induced alpha-SMA expression (p<0.01) that was mimicked by 8-bromo-cAMP and attenuated by the protein kinase A inhibitor H-89. CONCLUSION: AM decreased Ang II-induced collagen deposition surrounding the coronary arteries, inhibiting myofibroblast differentiation and expressions of ECM-related genes in rats. The present findings further support the biological action of AM as an antifibrotic factor in vascular remodeling.

Actins↗
PubMed1995

The influence of the adventitia on the presence of smooth muscle cells and macrophages in the arterial intima.

OBJECTIVE: To test the hypothesis that atherosclerosis may be initiated by hypoperfusion or thrombotic occlusion of the adventitial vasa vasonum. DESIGN: In a new model of atherogenesis, an early atherosclerotic lesion may be initiated by removal of the adventitia from the carotid artery of the New Zealand White rabbit, wherein lie the vasa vasorum. SETTING: Animal laboratory, University Department of Surgery and Medicine. CHIEF OUTCOME MEASURES: Immunocytochemistry was undertaken to demonstrate the presence of smooth muscle cells and macrophages within the intimal lesions. Smooth muscle cells were labelled with a monoclonal antibody designated HHF35 and macrophages were labelled with a rabbit specific, macrophage specific antibody, RAM11. CHIEF RESULTS: In rabbits fed a normal diet, at day 14, the intimal lesion was composed exclusively of smooth muscle cells. By day 28, such lesions had regressed. In rabbits fed a high cholesterol diet, at day 14, the intimal lesion was composed of a mixture of macrophages and smooth muscle cells. By day 42, the pattern of cellular distribution was such that macrophages (present as foam cells) were predominant. In the presence of persistent hypercholesterolaemia these lesions did not regress. CONCLUSIONS: This new model can produce two different cellular responses that may mimic the intimal lesions seen with re-stenosis after angioplasty or in hypercholesterolaemic man and as such, might be useful in separating out these two different pathophysiologies.

Animals↗
PubMed1977

[The diagnosis of cystic degeneration of the adventitia (author's transl)].

The clinical picture of cystic degeneration of the adventitia is illustrated by two cases. This usually occurs in a portion of an artery near a joint, most commonly in the popliteal artery. The diagnosis is made in the presence of irregular, intermittent claudication associated with an "hour glass" stenosis of the popliteal artery on the arteriogram, without displacement of the vessel. The aetiology is probably related to herniation of the synovia from the adjacent joint capsule; this explains not only the variable pressure within the cyst in the arterial wall, but also the connection found at operation between the adventitial cyst in the popliteal artery and the joint capsule. Treatment consists in shelling out of the cyst. The prognosis is good and recurrences do not occur.

Arterial Occlusive Diseases↗
PubMed1997

[Cystic degeneration of the adventitia of the popliteal artery: ultrasound angiography-aided puncture].

A filiform stenosis of the popliteal artery was examined by sonography and the reason for the cystic lesion in the arterial wall was found to be an uncommon type of cystic degeneration of the adventitia. The narrow lumen could be demonstrated by sonography and the lesion was punctured under ultrasound control. A viscous secretion was removed and the patient's claudication was cured without recourse to surgery.

Arterial Occlusive Diseases↗
PubMed2006

Application to vascular adventitia of a nonviral vector for TIMP-1 gene therapy to prevent intimal hyperplasia.

Somatic gene transfer continues to have potential for the study and therapy of cardiovascular disease. We have developed a modular, self-assembling, nonviral system consisting of Lipofectin, integrin-targeting peptides, and plasmid DNA (LID) and we have applied this to a model of vascular injury, rat carotid angioplasty. Marker gene studies identified transfection of adventitial cells after vector delivery to that layer. Human tissue inhibitor of metalloproteinase-1 (hTIMP-1) was tested as a therapeutic gene product after direct application to the exposed adventitial layer. Vascular LID.hTIMP-1 transfection was confirmed by polymerase chain reaction and gene expression by immunohistochemistry at 7 days. Neointimal areas were 0.160 +/- 0.078 and 0.225 +/- 0.052 mm(2) for LID.hTIMP-1-transfected (n = 14) and LID.pCI-transfected (n = 12) vessels, respectively, at 14 days, and 0.116 +/- 0.068 mm(2) (n = 14) and 0.194 +/- 0.095 mm(2) (n = 14), respectively, at 28 days, representing a 29 and 40% reduction in neointimal hyperplasia at 14 and 28 days, respectively, after balloon dilatation. Neointima-to-media ratios were similarly reduced. In addition, expansile remodeling after balloon injury was inhibited at 14 days, the area within the external elastic lamina being 0.50 +/- 0.02 and 0.61 +/- 0.02 mm(2) in LID.hTIMP-1- and LID.pCI-transfected arteries, respectively (p < 0.0005). We have demonstrated an effective system of therapeutic gene transfer, particularly targeting the arterial adventitia, where transfer of genes involved in matrix remodeling and cell migration may be useful.

Animals↗
PubMed2004

An automated method for lumen and media-adventitia border detection in a sequence of IVUS frames.

In this paper, we present a method for the automated detection of lumen and media-adventitia border in sequential intravascular ultrasound (IVUS) frames. The method is based on the use of deformable models. The energy function is appropriately modified and minimized using a Hopfield neural network. Proper modifications in the definition of the bias of the neurons have been introduced to incorporate image characteristics. A simulated annealing scheme is included to ensure convergence at a global minimum. The method overcomes distortions in the expected image pattern, due to the presence of calcium, employing a specialized structure of the neural network and boundary correction schemas which are based on a priori knowledge about the vessel geometry. The proposed method is evaluated using sequences of IVUS frames from 18 arterial segments, some of them indicating calcified regions. The obtained results demonstrate that our method is statistically accurate, reproducible, and capable to identify the regions of interest in sequences of IVUS frames.

Algorithms↗
PubMed2002

Remodeling of the adventitia during coronary arteriogenesis.

We studied the role of the adventitia in adaptive arteriogenesis during the phase of active growth of coronary collateral vessels (CV) induced by chronic occlusion of the left circumflex coronary artery in canine hearts. We used electron microscopy and immunoconfocal (IF) labeling for bFGF, matrix metalloproteinase (MMP)-2, MMP-9, tissue-type plasminogen activator (tPA), its inhibitor (PAI-1), fibronectin (FN), and Ki-67. Proliferation of smooth muscle cells and adventitial fibroblasts was evident. Quantitative IF showed that adventitial MMP-2, MMP-9, and FN were 9.2-, 7.5-, and 8.6-fold, bFGF was 5.1-fold, and PAI-1 was 3.4-fold higher in CV than in normal vessels (NV). The number of fibroblasts was 5-fold elevated in CV, but the elastic fiber content was 25-fold greater in NV than in CV. Perivascular myocyte damage and induction of endothelial nitric oxide synthase in peri-CV capillaries indicate expansion of CV. It was concluded that adventitial activation is associated with the development of CV through cell proliferation, production of growth factors, and induction of extracellular proteolysis thereby contributing to remodeling during adaptive arteriogenesis.

Animals↗
PubMed2005

Biaxial elastic material properties of porcine coronary media and adventitia.

The importance of mechanical stresses and strains has become well recognized in vascular physiology and pathology. To compute the stress and strain on the various components of the vessel wall, we must know the constitutive equations for the different layers of the vessel wall. The objective of the present study is to determine the constitutive equation of the coronary artery treated as a two-layer composite: intima-media and adventitial layers. Twelve hearts were obtained from a local slaughterhouse, and the right coronary artery and left anterior descending artery were dissected free from the myocardium. The vessel wall was initially mechanically tested biaxially (inflation and axial extension) as a whole (intact wall) and subsequently as intima-media or adventitial layer. A Fung-type exponential strain energy function was used to curve fit the experimental data for the intact wall and individual layers for the right coronary artery and left anterior descending artery. Two methods were used for the determination of material constants, including the Marquardt-Levenberg nonlinear least squares method and the genetic algorithm method. Our results show that there were no statistically significant differences in the material constants obtained from the two methods and that either set of elastic constants results in good fit of the data. Furthermore, at an in vivo value of axial stretch ratio, we find that the stiffness is as follows: intima-media > intact > adventitia. These results underscore the composite nature of coronary arteries with different material properties in each layer. The present results are necessary for analysis of coronary artery mechanics and to provide a fundamental understanding of vessel physiology.

Animals↗
PubMed2006

Role of the adventitia in pulmonary vascular remodeling.

An increasing volume of experimental data indicates that the adventitial fibroblast, in both the pulmonary and systemic circulations, is a critical regulator of vascular wall function in health and disease. A rapidly emerging concept is that the vascular adventitia acts as biological processing center for the retrieval, integration, storage, and release of key regulators of vessel wall function. In response to stress or injury, resident adventitial cells can be activated and reprogrammed to exhibit different functional and structural behaviors. In fact, under certain conditions, the adventitial compartment may be considered the principal injury-sensing tissue of the vessel wall. In response to vascular stresses such as overdistension and hypoxia, the adventitial fibroblast is activated and undergoes phenotypic changes, which include proliferation, differentiation, upregulation of contractile and extracellular matrix proteins, and release of factors that directly affect medial smooth muscle cell tone and growth and that stimulate recruitment of inflammatory and progenitor cells to the vessel wall. Each of these changes in fibroblast phenotype modulates either directly or indirectly changes in overall vascular function and structure. The purpose of this review is to present the current evidence demonstrating that the adventitial fibroblast acts as a key regulator of pulmonary vascular function and structure from the "outside-in."

Animals↗
PubMed1999

Potential functional significance of brain-type and muscle-type nitric oxide synthase I expressed in adventitia and media of rat aorta.

Skeletal muscle and myocardium express microNOS I, an elongated splice variant of neuronal-type nitric oxide (NO) synthase (NOS I), and NOS III, endothelial-type NO synthase, respectively. This study was designed to elucidate whether vascular smooth muscle also contains a constitutively expressed NO synthase isoform. In the rat, microNOS I contains an insert of 102 nucleotides after nucleotide 2865 of the cDNA, yielding a protein of 164 kd. Reverse transcription-polymerase chain reaction with primers flanking this insert and with insert-specific primers indicated that endothelium-denuded rat aorta expresses both brain-type NOS I and microNOS I. RNase protection analyses with an antisense RNA probe overlapping the microNOS I insert detected significant amounts of NOS I mRNA and lesser amounts of microNOS I mRNA in endothelium-denuded aorta. Western blots using a specific polyclonal antibody recognizing NOS I and microNOS I showed a major band of the 160-kd NOS I and a lesser band of a slightly larger protein in endothelium-denuded aorta. Immunohistochemistry demonstrated low levels of NOS I/microNOS I immunoreactivity in the medial layer of rat aorta, whereas the endothelium expressed only NOS III immunoreactivity. When the adventitia also was removed, NOS I and microNOS I mRNA decreased markedly but remained detectable in the medial layer. In functional experiments with endothelium-denuded rat aortic rings (that contained no NOS III), contractions induced by KCl were markedly increased in the presence of the NOS inhibitor N(G)-nitro-L-arginine. These data demonstrate that 2 subforms of NOS I are expressed in nonendothelial components of rat aorta: NOS I and lesser amounts of microNOS I. Under certain conditions, this NOS I/microNOS I expression could serve as a backup system to the functionally predominant NOS III.

Animals↗
PubMed1996

Identification of a potential role for the adventitia in vascular lesion formation after balloon overstretch injury of porcine coronary arteries.

BACKGROUND: In the present series of experiments, we examined the onset of cell proliferation and growth factor expression after balloon overstretch injury to porcine coronary arteries. METHODS AND RESULTS: Domestic juvenile swine underwent balloon overstretch injury to the left anterior descending and circumflex coronary arteries with standard percutaneous transluminal coronary angioplasty balloon catheters. To identify proliferating cells, 5-bromo-2-deoxyuridine (BrDU) was administered over a period of 24 hours before the animals were killed at either 1, 3, 7, or 14 days after injury. Immunohistochemistry was performed with monoclonal antibodies to BrDU and smooth muscle cell markers. Three days after injury, a large number of proliferating cells were located in the adventitia, with significantly fewer positive cells found in the media and lumen. Seven days after injury, proliferating cells were found primarily in the neointima, extending along the luminal surface. In situ hybridization for PDGF A-chain and beta-receptor mRNAs revealed that the expression of these two genes was closely correlated with the sites of proliferation at each time point. Studies in which BrDU was injected between days 2 and 3 and the animals were killed on day 14 suggested that the proliferating adventitial cells may migrate into the neointima. CONCLUSIONS: These data suggest that adventitial myofibroblasts contribute to the process of vascular lesion formation by proliferating, synthesizing growth factors, and possibly migrating into the neointima. Increased synthesis of alpha-smooth muscle actin observed in the adventitial cells after arterial injury may constrict the injured vessel and contribute to the process of arterial remodeling and late lumen loss after angioplasty.

Animals↗