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PubMed1980

Hypoxia-induced structural changes in the media and adventitia of the rat hilar pulmonary artery and their regression.

Chronic hypobaric hypoxia induces structural features characteristic of pulmonary hypertension, but little is known of their reversal. In the present study, rats have been exposed to hypobaric hypoxia for 10 days and subsequently allowed to recover in room air for 3, 14, 28, or 70 days. With the use of 1-mu sections and electron-microscopic and point-counting techniques, the regression of the medial and adventitial changes in the rat hilar intrapulmonary artery has been followed. In the media, 10-day hypoxia causes more than a doubling in thickness due to 1) hypertrophy of smooth muscle cells, particularly of rough sarcoplasmic reticulum and Golgi apparatus; 2) an increase in extracellular connective tissue, microfibrils, collagen fibers, and elastin, and 3) edemalike fluid. In addition, the elestic laminas are doubled in thickness, and myofilamentous processes of the hypertrophied smooth muscle cells contact them. After just 3 days' recovery, some cells have already returned to normal diameter, although medial thickening is unchanged. By Day 14 and at Days 28 and 70 of recovery, medial thickness and cell diameter are within the normal range, and by recovery Day 70, there is a significant increase in the relative areal proportion of extracellular collagen fibers and a decrease in elastin (P less than 0.001). Hypoxia also produces a more than twofold increase in adventitial thickness. Hypertrophy of fibroblasts and an increase in their number contribute to the thickening, as does as increase in collagen fibers. During 3-70 days of recovery, thickness is gradually reduced to normal levels, although it is still significantly above normal at Days 3, 14, and 28. The increases in thickness at these times are due mainly to the accumulation of collagen fibers, which are still apparent after 70 days of recovery. Thus, hypoxia causes a doubling in thickness of the medial and adventitial coats of the hilar muscular pulmonary artery, which with recovery regain near normal thickness but whose structure is altered. The increase in collagen fibers contributes to contracture and reduced distensibility in these vessels, which is apparent in arteriograms as narrowed lumen diameter.

Animals↗
PubMed1995

[Cystic degeneration of the adventitia of the popliteal artery as a possible sequela of entrapment syndrome].

We report two cases of cystic adventitial degeneration of the popliteal artery in young sportsmen. The pathogenetic role of microtrauma is suggested by the localisation of the adventitial cysts, the clinical symptoms, as well as the immunohistochemical demonstration of foamy macrophages instead of endothelial cells in the wall of the cysts. In one case the cause of the intermittent claudication could be verified by duplex sonography and comparison of the arterial pressure of both legs with a Doppler method only after physical exercise. As expected, an angiodilatation has only a temporary effect. Therefore a surgical resection of the cyst or of the involved arterial segment had be performed.

Adult↗
PubMed1996

[Cystic degeneration of the adventitia of the popliteal artery after PTA of the superficial femoral artery].

Cystic adventitial degeneration is rare. Most frequently it occurs in the popliteal artery, occasionally it may be found in other arteries and even in veins. It is always localized in joint-adjacent vessel areas and appears to originate in ectopic synovial tissue occasionally with a stemlike connection with the adjacent joint. The diagnosis of a cystic adventitial degeneration should be considered in cases of isolated stenosis or occlusion of the popliteal artery. Realtime ultrasound or computerized tomography may help to establish the diagnosis. The treatment of choice is surgival removal of the cysts or reconstruction with an autologous vein interponate. A rare case of simultaneous occurrence of cystic adventitial degeneration and arteriosclerotic occlusive disease is described.

Angioplasty, Balloon↗
PubMed1996

Adventitial remodeling after coronary arterial injury.

BACKGROUND: Intraluminal thrombus formation and medial smooth muscle (SM) cell proliferation are recognized responses of the arterial system to injury. In contrast to these well-characterized processes during vascular repair, changes involving the adventitia have been largely neglected in previous studies. Hence, the goal of this investigation was to assess the response of the adventitia to coronary arterial injury. METHODS AND RESULTS: Adventitial changes in porcine coronary arteries subjected to medial injury were characterized by immunohistochemistry, histochemistry, and microscopic morphometry. The rapid development of a hypercellular response in the adventitia was evident 3 days after balloon-induced medial injury. Cell proliferation, as assessed by proliferating cell nuclear antigen immunostaining, reached the maximum level in the adventitia at 3 days, whereas at 14 and 28 days, the number of replicating cells reverted toward the baseline. The proliferating activity in the adventitia exceeded that seen in the media at all times after injury. To further define the changes in the phenotype of adventitial cells, the expression of three cytoskeletal proteins (vimentin, alpha-SM actin, and desmin) was characterized. Fibroblasts in normal adventitia expressed vimentin but no alpha-SM actin or desmin. After injury, these cells acquired characteristics of myofibroblasts expressing alpha-SM actin, which peaked at 7 and 14 days. Desmin expression was patchy in the adventitia, as opposed to its homogeneous distribution in medial SM cells. The modulation of fibroblast phenotype was transient, inasmuch as alpha-SM actin immunostaining declined at 28 days after injury, when dense, collagen-rich scar was evident within the adventitia. The above-described changes involving hypercellularity of the adventitia, myofibroblast formation, and fibrosis were associated with a significant focal adventitial thickening at 3, 7, 14, and 28 days after injury (P < .01 versus uninjured coronary arteries). CONCLUSIONS: This study demonstrates the involvement of the adventitia in the vascular repair process after medial injury. The hypercellularity of the adventitial layer, proliferation of fibroblasts, and modulation of their phenotype to myofibroblasts are associated with the development of the thickened adventitia. It is postulated that these phenomena affect vascular remodeling and may provide an important insight into the mechanisms of vascular disorders.

Actins↗
PubMed1999

Adventitial delivery minimizes the proinflammatory effects of adenoviral vectors.

PURPOSE: Adenovirus-mediated arterial gene transfer is a promising tool in the study of vascular biology and the development of vascular gene therapy. However, intraluminal delivery of adenoviral vectors causes vascular inflammation and neointimal formation. Whether these complications could be avoided and gene transfer efficiency maintained by means of delivering adenoviral vectors via the adventitia was studied. METHODS: Replication-defective adenoviral vectors encoding a beta-galactosidase (beta-gal) gene (AdRSVnLacZ) or without a recombinant gene (AdNull) were infused into the lumen or the adventitia of rabbit carotid arteries. Two days after infusion of either AdRSVnLacZ (n = 8 adventitial, n = 8 luminal) or AdNull (n = 4 luminal), recombinant gene expression was quantitated by histochemistry (performed on tissue sections) and with a beta-gal activity assay (performed on vessel extracts). Inflammation caused by adenovirus infusion was assessed 14 days after infusion of either AdNull (n = 6) or vehicle (n = 6) into the carotid adventitia. Inflammation was assessed by means of examination of histologic sections for the presence of neointimal formation and infiltrating T cells and for the expression of markers of vascular cell activation (ICAM-1 and VCAM-1). To measure the systemic immune response to adventitial infusion of adenovirus, plasma samples (n = 3) were drawn 14 days after infusion of AdNull and assayed for neutralizing antibodies. RESULTS: Two days after luminal infusion of AdRSVnLacZ, approximately 30% of luminal endothelial cells expressed beta-gal. Similarly, 2 days after infusion of AdRSVnLacZ to the adventitia, approximately 30% of adventitial cells expressed beta-gal. beta-gal expression was present in the carotid adventitia, the internal jugular vein adventitia, and the vagus nerve perineurium. Elevated beta-gal activity (50- to 80-fold more than background; P <.05) was detected in extracts made from all AdRSVnLacZ-transduced arteries. The amount of recombinant protein expression per vessel did not differ significantly between vessels transduced via the adventitia (17.1 mU/mg total protein [range, 8.1 to 71.5]) and those transduced via a luminal approach (10.0 mU/mg total protein [range, 3.9 to 42.6]). Notably, adventitial delivery of AdNull did not cause neointimal formation. In addition, vascular inflammation in arteries transduced via the adventitia (ie, T-cell infiltrates and ICAM-1 expression) was confined to the adventitia, sparing both the intima and media. Antiadenoviral neutralizing antibodies were present in all rabbits after adventitial delivery of AdNull. CONCLUSION: Infusion of adenoviral vectors into the carotid artery adventitia achieves recombinant gene expression at a level equivalent to that achieved by means of intraluminal vector infusion. Because adventitial gene transfer can be performed by means of direct application during open surgical procedures, this technically simple procedure may be more clinically applicable than intraluminal delivery. Moreover, despite the generation of a systemic immune response, adventitial infusion had no detectable pathologic effects on the vascular intima or media. For these reasons, adventitial gene delivery may be a particularly useful experimental and clinical tool.

Adenoviridae↗
PubMed1991

Proliferation of smooth muscle cells in the inner and outer layers of the tunica media of arteries: an in vitro study.

During the development of atherosclerotic and fibromuscular proliferates/lesions, smooth muscle cells (SMC) in the media, particularly near the lumen, are activated to migrate into the intima, where they continue to proliferate to form an intimal thickening. It is to date unclear whether SMCs situated adjacent to the adventitia possess a lower capacity to proliferate because they are a special subpopulation of medial SMCs or because the adventitia excerts an inhibitory effect. We have, therefore, developed an in vitro system whereby we have attempted to clear up this uncertainty. The following observations were made from the in vitro experiments: Media-explants from rabbit aorta were laid on a polycarbonate filter with pores 5 microns in diameter. The SMCs migrated through the pores and formed a fibromuscular proliferate on the other side of the filter. Endothelial cells were seeded on one side of the filter before media-explants were laid on the other side of the filter. The confluent endothelium inhibited migration of SMCs through the filter pores. Media-explants were placed between two polycarbonate filters (pores 5 microns diameter). In this "sandwich" arrangement SMCs migrated through both filters, i.e., in both directions. The quantity of migrating and proliferating cells through both filters was almost identical. This suggests that there is no difference in the migratory and proliferative capacity of SMCs in the inner and outer layers in the media of arteries. To investigate the influence of the adventitia on medial SMCs, media-explants were placed between a lower (5 microns) and an upper (0.2 micron) filter. On the 0.2 micron filter adventitia-explants were laid above the media-explants. The 0.2 micron filter prevented migration of SMCs from the media-explant into the adventitia and migration of fibroblasts from the adventitia into the media. Interestingly, the adventitial tissue inhibited proliferation of SMCs at the abluminal and migration and proliferation at the luminal side of the media-explant; the number of cells migrating through the 5 microns pores at the luminal side was diminished, suggesting that the adventitial tissue has an antiproliferative influence on SMCs. Moreover, it was found that in media-explants near the filter with adventitia, the medial SMCs were in a better preserved condition than at the de-endothelialised luminal side. As a control, cultures consisting of media-explants were incubated without filters (i.e., explant organ cultures). The proliferates in the concavity (luminal side) exhibited a pattern of proliferating SMCs different from that of the cells at the abluminal convexity.(ABSTRACT TRUNCATED AT 400 WORDS)

Actins↗
PubMed1998

Role of adventitial nitric oxide in vascular hyporeactivity induced by lipopolysaccharide in rat aorta.

This study was designed to elucidate the role of the adventitia in NO-mediated vascular effects of lipopolysaccharide (LPS). After incubation of rat aorta with LPS, the adventitia generated 3.5 times more nitrite plus nitrate than a corresponding segment of media. Control media covered by adventitia from LPS-treated aortic rings exhibited a 4 fold elevated level of cyclic GMP. Medial layers from LPS-treated aortic rings (like LPS-treated adventitia-intact rings) exhibited a decrease in sensitivity to noradrenaline (NA) that was reversed by 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one (1 microM) or N omega-nitro-L-arginine methylester (0.3 mM). However, in contrast to LPS-treated adventitia-intact rings, medial layers showed no reduction in maximal contraction to NA and virtually no relaxation to L-arginine. These data indicate that in blood vessels exposed to LPS, the adventitia is a more powerful source of NO than the media. The adventitia-derived NO can reach soluble guanylyl cyclase in the medial layer and contribute greatly to vascular hyporeactivity and L-arginine-induced relaxation observed in blood vessels exposed to LPS.

Animals↗
PubMed2006

Balloon injury alters alpha-adrenoceptor expression across rat carotid artery wall.

alpha(1)-Adrenoceptors (AR) mediate growth factor-like activity of catecholamines on vascular smooth muscle cells (SMC) and adventitial fibroblasts. This trophic activity is strongly augmented by balloon injury, contributes significantly to subsequent proliferation, wall hypertrophy and lumen loss and is mediated by alpha(1A)- and alpha(1B)-AR. However, it is not known how injury augments adrenergic trophic activity. The aim of the present study was to examine alpha-AR expression in rat carotid artery and to test the hypothesis that balloon injury augments a(1)-AR expression. 2. Neointima, media and adventitia were isolated at various days after balloon injury of rat carotid artery and subjected to quantitative reverse transcription-polymerase chain reaction and radioligand binding. Cultured SMC were also studied. 3. Transcripts for alpha(1A)-, alpha(1B)-, alpha(1D)- and alpha(2D)-AR were expressed in different proportions in media and adventitia from uninjured carotid artery. Injury caused a reduction by as much as 85% at day 4 in all alpha-AR mRNA (but not cyclophilin) in both the media and adventitia. In both layers, expression returned to control by day 21 for alpha(2D)-AR and by day 42 for alpha(1A)-AR, but remained reduced by 25-50% for alpha(1B)- and alpha(1D)-AR at 42 days. alpha(1)-Adrenoceptor transcripts in the neointima at 21 and 42 days after injury were expressed at levels more than 80% lower than in the media or adventitia of uninjured carotid; alpha(2D)-AR mRNA was undetectable. The density of total alpha(1)-AR binding sites was similar in the media and adventitia of uninjured carotid. Density was reduced by approximately 60% in the intima-media and adventitia 21 days after injury. To examine possible mechanisms, early passaged cultured SMC were studied that express alpha(1D)- and alpha(1B)-AR at levels similar to in vivo but that do not express other alpha-AR. Basic fibroblast growth factor caused downregulation of alpha(1D)-AR mRNA and alpha(1)-AR density, without affecting mRNA half-life, whereas transforming growth factor-beta1 had no effect. Neither growth factor altered alpha(1B)-AR message expression. 4. These data demonstrate that: (i) carotid artery expresses the same four alpha-AR genes and similar total alpha(1)-AR density in the SMC media and fibroblast-rich adventitia; and (ii) injury induced enhancement of adrenergic trophic activity is not caused by upregulation of alpha(1)-AR, but, instead, is associated with a generalized reduction in alpha-AR expression.

Animals↗
PubMed2001

Expression of alpha-adrenoceptor subtypes by smooth muscle cells and adventitial fibroblasts in rat aorta and in cell culture.

Previous radioligand binding reports of vascular alpha-adrenoceptor (AR) density have been limited to total alpha1- or alpha2-ARs. Studies using whole blood vessel homogenates have not differentiated among receptor or mRNA expression by medial smooth muscle cells (SMCs) versus adventitial fibroblasts (AFBs). Therefore, we used quantitative reverse transcription-polymerase chain reaction and radioligand binding to measure alpha-AR subtypes in media, adventitia, and cultured SMCs and AFBs from rat aorta. Both media and adventitia expressed alpha1A-, alpha1B-, alpha1D-, and alpha2D-AR mRNAs, but in markedly different abundances. Total alpha1-AR density was the same for media and adventitia (Bmax = 101 +/- 10 versus 96 +/- 16 fmol/mg of protein). However, densities for alpha1A-, alpha1B-, and alpha1D-AR subtypes in media were 19 +/- 2, 26 +/- 4, and 55 +/- 2%, and in adventitia were 44 +/- 3, 37 +/- 5, and 19 +/- 2%. No alpha2B- or alpha2C-AR transcripts were detected in either layer or in cultured SMCs or AFBs. Total alpha1-AR densities in cultured SMCs and AFBs (Bmax = 111 +/- 4 and 48 +/- 6 fmol/mg of protein, respectively) were similar to media and adventitia, with alpha1B- and alpha1D-AR transcript levels and receptors largely sustained. However, alpha1A- and alpha2D-AR expression in cultured SMCs and AFBs was strongly reduced, compared with media and adventitia, an effect not prevented by 30 different culture conditions. Like SMCs, exposure of AFBs to norepinephrine induced protein synthesis and proliferation of AFBs. This is the first study to quantitate alpha-AR subtype expression in media and adventitia and in cultured SMCs and AFBs. In addition, we report the intriguing finding that AFBs express alpha1-ARs in similar abundance as medial SMCs and that norepinephrine induced them to proliferate.

Adrenergic alpha-Agonists↗