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At least 19 recordsLinked to original sources

PubMed2006

Adventitia contribution in vascular tone: insights from adventitia-derived cells in a tissue-engineered human blood vessel.

Whether the adventitia component of blood vessels directly participates in the regulation of vascular tone remains to be demonstrated. We have recently developed a human tissue-engineered blood vessel comprising the three tunicae of a native blood vessel using the self-assembly approach. To investigate the role of the adventitia in the modulation of vascular tone, this tissue-engineering method was used to produce three vascular constructs from cells explanted and proliferated from donor vessel tunicae 1) an adventitia + a media, or only 2) an adventitia, or 3) a media. The vasoconstriction responses of these 3 constructs to endothelin, the most potent vasopressor known up-to-date, as well as to nonselective and selective agonists and antagonists, were compared. The adventitia contracted to endothelin-1, -2, whereas the media and the media+adventitia contracted to all three endothelins. Endothelin-induced contraction of the adventitia was dependent on ET(A) receptors, whereas that of the media and the adventitia+media was ET(A) and ET(B) receptor-dependent. RT-PCR studies corroborated these results. SNP induced a dose-dependent relaxation of the three tissue constructs. We also demonstrated that the endothelin-converting enzyme, responsible for the formation of the active endothelin peptides, was present and functional in the adventitia. In conclusion, this is the first direct demonstration that the adventitia has the capacity to contract and relax in response to vasoactive factors. The present study suggests that the adventitia of a blood vessel could play a greater role than expected in the modulation of blood vessel tone.

Aspartic Acid Endopeptidases↗

PubMed2006

Adventitia-dependent mechanical properties of brachiocephalic ovine arteries in in vivo and in vitro studies.

AIM: An adventitia dependent regulation of the vascular smooth muscle tone has been described. However, if the adventitia plays an active role on arterial wall biomechanical behaviour and functions remains to be established. Our aim was to characterize the influence of adventitia on arterial wall mechanical properties and the arterial conduit and buffer functions. METHODS: Ovine brachiocephalic arteries were studied in vivo (n = 8) and in vitro (with null tone) in a circulation mock (n = 8). Isobaric, isoflow and isofrequency studies were performed. In each segment, pressure and diameter waves were assessed before and after adventitia removal. From the arterial stress-strain relationship, we derived the elastic and the viscous modulus. The buffering and conduit functions were calculated using the Kelvin-Voigt's time constant and the inverse of the characteristic impedance, respectively. RESULTS: In in vivo studies arterial diameter decreased after adventitia removal (P < 0.05). Elastic and viscous modulus in in vivo studies were significantly higher in adventitia-removed arteries, compared with values in intact vessels (P < 0.05). This behaviour was not observed in in vitro experiments. An impairment of buffer and conduit functions was observed in vivo after adventitia removal (P < 0.05), while both functions remain unchanged in in vitro studies (P > 0.05). CONCLUSIONS: Arterial wall viscosity and elasticity were influenced by adventitia removal in in vivo studies, possibly by a smooth muscle-dependent mechanism, since it was not present in in vitro experiments. Adventitia would be involved in a physiological mechanism of arterial wall viscous and elastic properties regulation, that could influence arterial buffering and conduit functions.

Animals↗

PubMed2001

The adventitia of atherosclerotic coronary arteries frequently contains Chlamydia pneumoniae.

The presence of Chlamydia pneumoniae in the human arterial system has mainly been determined in atherosclerotic plaque, whereas the adventitia has remained relatively unexplored. We assessed the presence of C. pneumoniae in all three vessel wall layers of coronary (n=72) and brachial (n=48) arteries in relation to local atherosclerosis. Immunohistochemical staining of C. pneumoniae was observed in plaque and adventitia. Cells stained for C. pneumoniae were detected in the same areas as cells stained for macrophages in adjacent sections. C. pneumoniae staining in the adventitia was associated with the extent and severity of atherosclerosis. Coronary sections with C. pneumoniae staining in both adventitia and plaque more often contained advanced atherosclerosis than sections with staining only in the adventitia. Staining was observed more often in the coronary artery than in the brachial artery (24/72 vs. 5/48 and 51/72 vs. 8/48 for plaque and adventitia, respectively, P=0.004 and P<0.001). PCR confirmed the presence of C. pneumoniae DNA in the adventitia. In summary, the adventitia of atherosclerotic coronary arteries frequently contains C. pneumoniae that seems to be located within macrophages. These results might indicate a possible route for infected circulating macrophages to home into atherosclerotic lesions in the artery via vasa vasorum.

Aged↗

PubMed1996

The role of the adventitia in the arterial response to angioplasty: the effect of intravascular radiation.

PURPOSE: In the current series of experiments we have characterized cell proliferation leading to vascular lesion formation in a porcine model for post-angioplasty restenosis and examined the mechanism of action of intravascular beta irradiation in the prevention of lesion formation in this model. METHODS AND MATERIALS: Juvenile male pigs were subjected to balloon overstretch injury of the left anterior descending and circumflex coronary arteries using clinical angioplasty catheters. Proliferating cells were labelled by injections of 50 mg/kg of bromo-deoxyuridine (BrDU) 24, 16 and 8 hrs prior to sacrifice and were detected by immunohistochemistry using a specific antibody to BrDU. In some cases, BrDU was given as a pulse 3 days after angioplasty and the animals sacrificed on day 14 to follow the migration of the cells which had proliferated earlier. Characterization of the proliferating cells was performed by immunohistochemistry using antibodies to specific cytoskeletal proteins specific for smooth muscle cells and myofibroblasts. Some vessels were treated at the time of angioplasty with 14 or 28 Gy (to a depth of 2 mm) intravascular irradiation using a flexible catheter with a pure beta emitter 90 SR/Y and the effect on cell proliferation and terminal transferase-mediated UTP nick-end labelling (TUNEL) examined 3 or 7 days later. RESULTS: The first major site of cell proliferation between 2-3 days after angioplasty is the adventitia and not the medial wall. Seven days after angioplasty cell proliferation is predominant in the neointima and is reduced in the media and adventitia. Differential staining with antibodies directed against smooth muscle alpha actin and other cytoskeletal proteins indicates that the proliferating adventitial cells are myofibroblasts. Pulse label studies with BrDU indicates that the proliferating adventitial myofibroblasts migrate into the neointima and contribute to the mass of the restenosis lesion. Fourteen days after angioplasty the myofibroblasts in the neointima and the adventitia express alpha smooth muscle actin and form a fibrotic scar in the adventitia surrounding the injury site. Endovascular irradiation appears to inhibit development of the restenosis lesion by significantly reducing cell proliferation in the media and adventitia at early time points after injury. There were no significant differences in the percent of TUNEL labelled cells in the irradiated vessels compared to controls. Alpha actin staining of myofibroblasts in the adventitia was reduced in the irradiated vessels suggesting a positive effect of intravascular irradiation on vascular remodeling. CONCLUSIONS: These studies have shown that adventitial myofibroblasts contribute to the problem of post-angioplasty restenosis by proliferating, forming a fibrotic scar surrounding the injury site, and migrating into the neointima. We hypothesize that the adventitial fibrosis which develops at the injury site contributes to negative vascular remodeling associated with clinical restenosis. Experiments in which vessels were exposed to intravascular irradiation at the time of angioplasty indicate that this treatment reduces post-angioplasty restenosis by inhibiting early cell proliferation in the media and adventitia and by preventing the fibrotic changes in the adventitia without a corresponding increase in cellular death or apoptosis in these tissues.

Angioplasty, Balloon, Coronary↗

PubMed2002

Perigraft adventitia and intima remodeling after synthetic patch implantation in sheep carotid artery: role of apoptosis and proliferation.

BACKGROUND: The mechanisms of neointima formation after synthetic vascular grafting are not clear. The aim of this study was to investigate the intima and perigraft adventitia remodeling process in terms of cell apoptosis versus proliferation after synthetic patch implantation. METHODS: Female Merino sheep were randomized equally into two groups and underwent implantion with a patch of gelatin sealed Dacron graft into the left common carotid artery. At 1 and 6 months, grafted vessels were harvested, processed, and assessed. Intimal area and lumen sizes were measured with histologic assessment of eight segments from each animal assisted with image analysis. Immunohistochemical labeling of alpha-actin and D33 desmin was performed on tissue sections of perigraft adventitia, graft matrix, and intima. Cell proliferation and cell phenotype were determined with double immunohistochemical staining with anti-proliferating cell nuclear antigen and anti-alpha-actin or antimacrophage antibodies (HAM 56) in perigraft adventitia, graft matrix, and intima. Apoptosis was detected with in situ terminal deoxynucleiotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-fluorescence nick end labeling (TUNEL) in perigraft adventitia, graft matrix, and intima. RESULTS: The carotid artery lumen size at 6 months was significantly larger than at 1 month (P <or=.05). The intimal area was significantly reduced at 6 months compared with 1 month (P <.05). At 1 month and 6 months, perigraft adventitia, graft matrix, and intima showed positive alpha-actin expression but negative desmin staining. In the anastomotic area, a small number of intimal cells suggested their muscle origin (expression alpha-actin and desmin). The number of proliferating cells in the intima was significantly greater at 1 month than at 6 months (P =.01). TUNEL-positive cells were significantly greater in the intima at 1 month than at 6 months (P <.05), whereas TUNEL-positive cells were significantly greater at 6 months in the perigraft adventitia (P <.05). HAM 56-positive cells in the intima at 1 month were significantly greater compared with 6 months (P <.05), whereas in graft and perigraft regions, no significant difference was seen between 1 month and 6 months. CONCLUSION: The cell proliferation and cell phenotype change in intima and perigraft adventitia are associated with thickening of perigraft adventitia and intima at 1 month. The balance between cell proliferation and apoptosis could account in part for the reduction in intima area and perigraft adventitial cellularity at 6 months.

Actins↗

PubMed2001

Effect of removal of adventitia on vascular smooth muscle contraction and relaxation.

The aim of the present study was to determine whether the adventitia of large arteries modulates vascular function. We developed a method to obtain functional vascular rings devoid of adventitia. Carotid and iliac arteries from 3-mo-old Sprague-Dawley rats were denuded from adventitia after treatment with collagenase followed by gentle peeling. Adventitia removal and integrity of the media was demonstrated by optical and confocal microscopy. Arterial rings with or without adventitia and with or without endothelium were mounted in an organ bath for isometric tension recording. Responses to 75 mM KCl or norepinephrine (0.1 nM-1 microM) were significantly reduced in segments without adventitia. Acetylcholine-induced relaxation (0.1 microM-0.1 mM) was enhanced in arteries without adventitia, whereas sodium nitroprusside-induced responses were not modified. These results demonstrate that the combination of stripping with a previous collagenase treatment allows us to obtain functional rings devoid of adventitia and that this layer plays a role in contractile capacity and in endothelium-modulated responses.

Acetylcholine↗

PubMed2006

Urokinase plasminogen activator in injured adventitia increases the number of myofibroblasts and augments early proliferation.

Myofibroblasts are involved in vessel remodeling during the development of hypertension as well as after angioplasty and aortocoronary grafting, but the mechanisms of myofibroblastic phenotypic modulation are not fully elucidated. We assessed the role of urokinase plasminogen activator (uPA) and its proteolytic activity in myofibroblast differentiation and the early proliferation following mechanical injury of the rat carotid adventitia. The effects of perivascular application of recombinant uPA (r-uPA), proteolytically inactive r-uPA(H/Q) and uPA neutralizing antibody were evaluated 4 days after surgical injury to the adventitia. The phenotype of adventitial cells was assessed using anti-alpha-smooth muscle actin (alpha-SM actin) antibody, anti-SM heavy chain myosin, anti-high-molecular-weight caldesmon, anti-smoothelin and anti-ED-1 antibodies, proliferation by the expression of proliferating cell nuclear antigen, and the size of the adventitia by quantitative morphometry. Four days after injury, the intensive immunostaining for urokinase appeared in the rat carotid artery adventitia. At the same time, the frequency of alpha-SM actin-positive adventitial cells was 1.8+/-1.1% in uninjured arteries and 25.2+/-5.4% in injured arteries (p<0.05), and the respective frequency of ED-1-positive cells 1.5+/-1.1 and 25.0+/-5.2%. The application of exogenous r-uPA doubled the numbers of alpha-SM actin-positive adventitial cells to 55.7+/-6.8% (p<0.05). ED-1-positive cells and proliferating cell nuclear antigen-positive cells as well as the size of the adventitia were also significantly increased after r-uPA compared with injury alone. In contrast, the proteolytically inactive r-uPA(H/Q) did not affect any parameters. The application of uPA neutralizing antibody attenuated the frequency of alpha-SM actin-positive cells to 12.6+/-3.5% (p<0.05), the frequency of ED-1-positive cells, and the numbers of adventitial cells. r-uPA stimulation of cultured human skin fibroblasts significantly increased the alpha-SM actin content in a concentration-dependent manner. In contrast, r-uPAH/Q did not induce changes in alpha-SM actin content. We conclude that uPA, which is upregulated in the injured adventitia, can augment adventitial cell accumulation, including myofibroblasts, and adventitia growth early after injury of the rat carotid artery adventitia by mechanisms involving proteolysis.

Animals↗

PubMed1998

Superoxide anion from the adventitia of the rat thoracic aorta inactivates nitric oxide.

The purpose of this study was to determine whether superoxide anion is produced endogenously in the rat aortic adventitia and whether sufficient superoxide anion is produced to interfere with the response of the rat aorta to nitric oxide. Relaxation was measured in rings of the rat thoracic aorta, which were oriented so that the adventitial or luminal surface could be preferentially exposed to nitric oxide or sodium nitroprusside. To accomplish this, the rings were mounted (1) with the adventitia facing outward, (2) with the adventitia facing inward after inverting, or (3) with the adventitia facing outward after inverting twice (to control for the inverting procedure). The relaxation to nitric oxide, but not to sodium nitroprusside, was less in rings with the adventitia facing outward compared with those in which it faced inward. In contrast, the response to nitric oxide via either surface was similar when extracellular superoxide anion was scavenged with superoxide dismutase. Incubation of rings with nitro blue tetrazolium (NBT) resulted in blue formazan staining of the adventitia, and lucigenin chemiluminescence was significantly greater when detected from the adventitial compared with the intimal aspect of the artery. The reduction of NBT in intact aortic rings was 30+/-2 pmol x min(-1) x mg(-1) and was significantly decreased by superoxide dismutase to 19+/-2 pmol x min(-1) x mg(-1) and by a synthetic superoxide dismutase mimic, Euk-8, to 11+/-2 pmol x min(-1) x mg(-1). The NADPH oxidase inhibitor, diphenyleneiodonium, decreased NBT reduction to 9+/-1 pmol x min(-1) x mg(-1), whereas inhibitors of xanthine oxidase, mitochondrial oxidases, and nitric oxide synthase were ineffective. Immunohistochemical staining indicated the localization of NADPH oxidase proteins gp91phox, p22phox, p47phox, and p67phox almost exclusively in the adventitia of the rat aorta with no substantial staining in the media. These results indicate that NADPH oxidase located in the adventitia of rat thoracic aorta generates sufficient extracellular superoxide anion to constitute a barrier capable of inactivating nitric oxide. This study suggests that adventitial superoxide anion can play a role in the pathophysiology of the arterial wall.

Acridines↗

PubMed2003

[Effect of removal of the adventitia on vascular remodeling and vasoconstriction in rabbits].

The aim of the present study was to investigate the effect of removal of the adventitia on vascular remodeling and vasoconstriction of the carotid artery in New Zealand rabbit. Adventitia of carotid artery was removed mechanically. The histology, morphology and reactivity of the carotid artery was observed by immunohistochemistry and measurement of carotid ring tension immediately, 1 week and 2 weeks after removal of the adventitia. No damage of intima and media was observed after removing the adventitia. Removal of the adventitia caused a remarkable proliferation of the vascular media and formed the neointima. Compared with the control ring, norepinephrine (NE)-induced vasocontraction in adventitia-denuded carotid artery was significantly reduced immediately and 1 week after the operation (P<0.05). Adventitia removal promoted the neointima formation and decreased vasoconstriction of the carotid artery, indicating that the adventitia is involved in the regulation of vascular remodeling and vasoconstriction.

Animals↗

PubMedDate not supplied

Distribution of acidic glycosaminoglycans in the intima, media and adventitia of bovine aorta and their anticoagulant properties.

SUMMARY: 1. The constituents of acidic glycosaminoglycans in the tunica intima, media and adventitia were studied by means of an enzymatic assay with chondroitinases and by electrophoretic characterization. 2. The content of the acidic glycosaminoglycans was higher in the intima than in the adventitia based on defatted dry tissue weight. The gel filtration pattern showed that, with chondroitinase-AC, the proportion of the intact glycosaminoglycans is greater in the adventitia than in the intima. 3. Electrophoresis before and after digestion with chondroitinases indicated that the three layers contain chondroitin-4- and -6-sulfates, dermatan sulfate, heparan sulfates and hyaluronic acid. In the case of the adventitia, bands migrating like the heparin standard were also detected. 4. Paper chromatographic separation of the unsaturated disaccharides after digestion with chondroitinases revealed that the proportion of chondroitin-6-sulfate is predominant in the intima, whereas the proportion of heparan sulfates, hyaluronic acid and dermatan sulfate is one and one-half-2 times higher in the adventitia than in the intima. 5. Anticoagulant activity, measured by thrombelastography, of the acidic glycosaminoglycans in the three layers clearly indicated that the glycosaminoglycans in the adventitia possess the highest potency among the three layers. It was considered that the higher activity of the glycosaminoglycans in the adventitia is due to the relatively greater proportion of heparan sulfates and dermatan sulfate.

Animals↗

PubMed2006

Altered L-arginine/nitric oxide synthase/nitric oxide pathway in the vascular adventitia of rats with sepsis.

1. In recent studies, the vascular adventitia has been established as an important source of inducible nitric oxide synthase (iNOS) and subsequent nitric oxide (NO) production, even more powerful than the media in response to certain inflammatory factors, such as lipopolysaccharide (LPS). The adventitia has an independent L-arginine (L-Arg)/NOS/NO pathway and is involved in the regulation of vascular function. In the present study, we explored the changes in and the pathophysiological significance of the L-Arg/NOS/NO pathway in the adventitia of rats with sepsis. 2. Sepsis was induced by caecal ligation and puncture in order to observe changes in L-Arg transport, NOS gene expression and activity and NO generation in the vascular adventitia to determine the mechanism of activation of the L-Arg/NOS/NO pathway. 3. Severe sepsis resulted in severe disturbance of haemodynamic features, with decreased mean arterial blood pressure, brachycardia and inhibited cardiac function (decreased left ventricular +/-dP/dt(max)). Left ventricular end-diastolic pressure was elevated threefold (P < 0.01) under anaesthesia. Rats with sepsis showed severe glucopenia and lacticaemia. Plasma levels of the inflammatory factors macrophage chemoattractant protein-1 and interleukin-8 were increased five- and 29-fold, respectively (P < 0.01). 4. In the adventitia of the thoracic and abdominal aortas, the L-Arg/NO pathway was similarly characterized: the uptake of [(3)H]-L-Arg was Na(+) independent, with the peak occurring at approximately 40 min incubation. Total NOS activity was largely calcium independent (> 90%). The V(max) of L-Arg transport in the sepsis group was increased by 83.5% (P < 0.01), but the K(m) value was not significantly different compared with controls. 5. The mRNA levels of cationic amino acid transporter (CAT)-1 and CAT-2B in the sepsis group were increased by 86 and 62%, respectively (both P < 0.01). Inducible NOS activity was increased 2.8-fold compared with controls (P < 0.01) and iNOS mRNA levels were elevated approximately sixfold (P < 0.01). The NO levels in the plasma and incubation media (incubation for 40 min) in the sepsis group were increased by 144 and 273%, respectively (both P < 0.01). 6. The Arg/NOS/NO pathway was activated in the vascular adventitia of rats with sepsis shock. The L-Arg/NOS/NO pathway in the aortic adventitia may play an important role in the pathogenesis of sepsis and septic shock.

Animals↗

PubMed1996

[Development and clinical anatomy of the rectal adventitia. significance for radical operation of rectal carcinoma].

The development, topography and clinical anatomy of the adventitia recti were studied in 300- to 600-microns-thick sections through the pelves of human fetuses and newborn children and 5-mm sections through the pelves of adults. The adventitia recti constitutes a continuous compartment bordered laterally by the fascia recti. In the adult the adventitia recti consists mainly of adipose tissue. The extent of the adventitia recti differs in different parts of the rectal wall. The branches of the vasa rectalia superiora and the visceral lymph nodes of the rectum are situated within the adventitia recti. Our findings suggest that it is necessary to remove the adipose tissue of the adventitia recti and the adjoining lymph nodes individually during resection of the rectum in order to minimize the risk of tumor recurrence.

Adipose Tissue↗

PubMed2004

Urotensin-II activates L-arginine/nitric oxide pathway in isolated rat aortic adventitia.

Urotensin-II (U-II), a cyclic peptide widely expressed in blood vessels, has diverse vascular actions that range from potent vasoconstriction to vasodilation. Although, U-II-induced vasodilation has been shown to be partially dependent on nitric oxide (NO), the involvement of vascular adventitia-derived NO, remains unknown. The present study aimed to elucidate the activation of U-II on L-arginine/NO pathway in isolated rat aortic adventitia. In adventitia of thoracic and abdominal aortas, the l-arginine/NO pathway was similarly characterized: the uptake of l-[(3)H]arginine was Na(+)-independent, with the peak occurring over around 40 min incubation; the total NO synthase (NOS) activity was mostly calcium-independent (>90%), and significantly inhibited by a specific iNOS inhibitor AMT; the production of NO metabolites nitrate and nitrite (NO(x)) was stimulated by L-arginine but not by D-arginine. In aortic adventitia exposed to rat U-II (10(-9) and 10(-8)M) for 6 h, the V(max) of l-[(3)H]arginine uptake over 40 min incubation was significantly increased, while the K(m) of l-[(3)H]arginine uptake showed no significant change. Besides, the iNOS mRNA level was up-regulated, the total NOS activity, largely calcium-independent, was significantly induced, and the NO(x) production was significantly stimulated by U-II. According to the same protocol as U-II, the positive control lipopolysaccharide (LPS, 10 microg/ml), which had been established to activate adventitial L-arginine/NO pathway, increased l-[(3)H]arginine uptake, iNOS activity and NO(x) production to a greater extent than U-II. In addition, the total NOS activities induced by 3 and 6h incubation of U-II and LPS were significantly inhibited by a specific inhibitor of protein synthesis, actinomycin D. In conclusion, the results showed that rat U-II activated L-arginine/NOS/NO pathway in rat aortic adventitia, suggesting a potential contributive role of adventitia-derived NO in the vasodilator response of U-II.

Animals↗

PubMed2004

Effects of adrenomedullin on cell proliferation in rat adventitia induced by aldosterone.

OBJECTIVE: Aldosterone is involved in cardiovascular diseases such as hypertension and heart failure by inducing sodium retention and vascular remodeling, which is characterized by fibroblast proliferation and migration in adventitia. It is well known that aldosterone stimulates vascular smooth muscle cells and fibroblasts to produce and secrete adrenomedullin (ADM), a multiple functional peptide with an important cytoprotective effect against cardiovascular damage. We examined the effect of aldosterone on ADM production and secretion and its mRNA expression in rat aortic adventitia to study the paracrine/autocrine interaction between endogenous ADM and aldosterone. METHODS: ADM produced and secreted from adventitia stimulated by aldosterone in the absence or presence of spironolactone, RU486 or spironolactone together with RU486 were detected by radioimmunoassay, proliferation in adventitia cells was evaluated by the level of [H]-thymine incorporation, and preproADM gene expression was measured by semi-quantitative reverse transcriptase polymerase chain reaction. RESULTS: Adventitial ADM secretion and mRNA expression stimulated by aldosterone were concentration-dependent as was the inhibitive effect of ADM on aldosterone-induced proliferation. The induction of aldosterone in ADM secretion was mediated by mineralocorticoid receptor. Antagonists of specific receptors of calcitonin gene-related peptide (CGRP) receptor type 1 and ADM both potentiated the proliferation effect induced by aldosterone; and thiorphan, an inhibitor of the enzyme for ADM degradation, inhibited the adventitial [H]-thymine incorporation induced by aldosterone. ADM inhibited the activity of extracellular signal related kinase (ERK) stimulated by aldosterone. CONCLUSION: Aldosterone stimulates adventitia to produce and secrete ADM, which in turn, antagonizes the aldosterone-induced proliferation in adventitia.

Adrenomedullin↗

PubMed2005

Role of the adventitia in the cyclic GMP-mediated relaxant effect of N-hydroxy-L-arginine in rat aorta.

N(omega)-hydroxy-L-arginine (L-NOHA), the stable intermediate of the nitric oxide synthase (NOS)-catalyzed reaction, can induce NO/cyclic GMP-dependent relaxation in the rat aorta, in an endothelium- and NOS-independent manner. In this study, the role of the adventitia in the endothelium-independent effect of L-NOHA was investigated. Despite a decrease in norepinephrine (NE)-induced precontraction, adventitia removal in the rat aorta did not markedly alter the relaxant effect of forskolin, S-nitroso-N-acetylpenicillamine or glyceryl trinitrate. In contrast, both inhibition of NE-induced contraction and relaxation of NE-precontracted rings produced by L-NOHA were diminished in the absence of adventitia. Moreover, exposure to L-NOHA significantly enhanced the cyclic GMP level in the media of the aorta with, but not without adventitia. These findings demonstrate the role of the adventitia in the L-NOHA-induced decrease in tone and increase in cyclic GMP in the endothelium-denuded rat aorta. They suggest that NO or an NO-related compound formed from L-NOHA in the adventitia may produce paracrine effects.

Animals↗

PubMed1988

Increased DNA replication in the arterial adventitia after aortic ligation.

After microsurgical dissection of the thoracic aorta of normotensive rats, biochemical and morphological comparisons were performed between the intima-media and adventitia. The DNA content, wet weight, and dry defatted weight of the adventitia were half that of the intima-media. Collagen was the main component of the adventitia (collagen greater than nonfibrous protein greater than elastin) whereas elastin was the main protein in the intima-media (elastin greater than nonfibrous protein greater than collagen), and the results correlated with morphological observations. Hypertension induced by aortic ligation between the renal arteries resulted in rapid elevations in circulating humoral factors and blood pressure. A sixfold increase in DNA synthesis was observed in the adventitia (p less than 0.001), resulting in a significant increase in DNA content as early as 6 days after aortic ligation (75% increase; p less than 0.001). Increased DNA replication was accompanied by elevations in nonfibrous protein and elastin contents. Autoradiograms showed labeled adventitial fibroblasts throughout the thickness of the adventitia and along the entire length of the aorta and smaller vessels. DNA synthesis and content and labeled smooth muscle cells were increased in the intima-media. These studies indicate that the adventitia participates in the development of vascular hypertrophy and arterial disease produced by aortic ligation.

Animals↗

PubMed1991

[The adventitia wrapping technique in microvascular surgery].

The success of microvascular anastomosis on fine vessels is essential not only for expanding the possibility of surgical treatment in such cases as replanting severed fingers of children, and vascularized nerve and joint grafting, but also for diminishing the damage to donors as well. This report describes the details of our study on a adventitia wrapping technique in which the adventitia was utilized for wrapping anastomosis. This study demonstrates that the advantages of the adventitia wrapping technique are as follows; (1) Adventitia wrapping technique provides a higher patency rate in smaller microvascular anastomosis. (2) Adventitia wrapping technique aids in reducing operative time and stitches. (3) Adventitia wrapping technique increases tolerable pressure of the anastomosis site and prevents aneurysm. (4) Immediate postoperative hemorrhage at the anastomosis site is lesser than that of the standard suture technique. These results indicate that this technique utilizes the tissue in site, therefore, is simple and useful for microvascular anastomoses.

Anastomosis, Surgical↗

PubMed1997

Adventitial stripping does not strip the adventitia.

This study investigates the process of stripping the adventitia off a blood vessel, which is a normal procedure prior to performing a microvascular anastomosis. In five rats, the common carotid and the superficial femoral arteries of one side were stripped sharply, whereas the arteries of the other side were left unstripped to serve as controls. In a further set of five rats, the arteries were stripped bluntly. Immediately following stripping, experimental and control arterial segments were removed. Histology of cross sections of the segments was studied. In no case was there complete removal of the adventitia. When stripped and control arterial sections were compared, no significant difference between cross-sectional adventitial areas could be demonstrated. Morphologic study revealed that stripping mainly removes large collagen fibers from the adventitia. The small collagen fibrils that are still in place fan out in such a way that although considerable tissue is removed, the volume that the adventitia occupies remains the same. Stripping the adventitia does not cause complete removal of the adventitia, and in this study no significant reduction in the adventitial volume could be found. Stripping does, however, allow a better view of the cut edge of the vessel wall under an operating microscope. Since blunt stripping could cause damage to other vessel wall layers, sharp stripping is to be preferred.

Anastomosis, Surgical↗