SEARCH · PubMed Health

Results for “VASA VASORUM”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources

PubMed1995

An ultrastructural and immunocytochemical study of thoracic aortic endothelium in aged Sprague-Dawley rats.

The distribution of various vasoactive agents [nitric oxide synthase (NOS)- type I, endothelin-1 (ET-1), arginine-vasopressin (AVP), serotonin (5-HT), histamine and substance P (SP)] in the thoracic aortic endothelium of aged Sprague-Dawley rats was investigated using electron microscopic immunocytochemical methods. The aged thoracic aortic intima was characterized by a large number of leukocytes that adhered to the endothelium, an accumulation of a flake-like precipitate and clusters of leukocytes and smooth muscle cells (SMC) in the subendothelium. Age-associated alterations were also seen in the medial and adventitial layers of the vascular wall. An extensive vasa-vasorum was present in the adventitia from which leukocytes penetrated into perivascular tissue. Some vasa-vasorum showed mast cells adhered to perivascular pericytes. Immunocytochemistry showed about 70% endothelial cells (EC) with positive immunostaining for the brain isoform NOS-type I, compared to 10% in adult mature rats. About 10% of cells showed a positive immunoreaction for ET-1, which is about the same as for the mature adult thoracic aorta (8-9%). Subendothelial macrophages often showed positive immunostaining for antibodies against ET-1. The percentage of EC immunopositive to AVP, 5-HT, and histamine was 16-18, 15 and 12%, respectively compared to 5-8, 7-8 and 6% in mature adult rats. A few cells showed an immunopositive reaction for SP. In summary, the ageing vessel was characterized by a large number of leukocytes adhering to the endothelium and also by the presence of many macrophages and SMC in the subendothelial layer. The percentage of EC in rat thoracic aorta showing NOS immunostaining increased substantially from 10% in mature rats to 70% in aged rats. The percentage of EC immunopositive for AVP, 5-HT and histamine also increased about twofold compared to mature adult rats, while no changes were seen for ET-1.

Aging↗

PubMed1991

Vascular response to basic fibroblast growth factor when infused onto the normal adventitia or into the injured media of the rat carotid artery.

Immunohistochemical techniques localize basic fibroblast growth factor (FGF) in endothelial and smooth muscle cells of the common carotid artery. Thus, we studied the effect in rats of basic FGF infused for 14 days onto the adventitia or into the media in vivo. In untreated rats, the adventitial layer is uniform, and few vessels are observed in cross sections (mean +/- SEM is 0.351 +/- 0.16 capillaries/field at a magnification of x 480). Whereas saline infusion increases the mean number of vasa vasorum to 2.73 +/- 0.011 capillaries/field (p less than 0.01), basic FGF (1 ng/microliter/hr) increases the capillary number to 13.4 +/- 0.67 capillaries/field. The effects are local and restricted to the site of delivery; no cell proliferation is observed even 2 mm from the site of infusion. There is also no evidence of the infiltration of macrophages and monocytes. In an effort to determine the effect of basic FGF in the media, a small longitudinal (1-mm) incision was made in the adventitia, and saline or basic FGF (1 ng/microliter/hr) was infused for 14 days into the arterial wall. Under these conditions, basic FGF is a potent inducer of smooth muscle cell proliferation in the vascular wall as well as of new capillaries. In these instances, however, the capillaries formed are thick-walled. The results support the hypothesis that basic FGF may be contributing to the growth and maintenance of the vasa vasorum and of vascular smooth muscle cells.

Animals↗

PubMed1986

Does the in situ technique for autologous vein femoropopliteal bypass offer any hemodynamic advantage?

The improved patency rates that have been claimed for in situ femoropopliteal vein bypass have been attributed to improved hemodynamics because of the natural taper of the vein and maintenance of wall compliance because of preservation of the nutrient vasa vasorum. Blood flow in 31 in situ and 21 reversed vein grafts was measured noninvasively with a duplex ultrasound scanner at a median of 6 months after operation. There was no significant difference in the resting or hyperemic flows between the two groups (p much greater than 0.1). The compliance of 15 undisturbed and 15 fully mobilized in situ vein grafts was measured noninvasively by Doppler ultrasonography immediately after operation and at 3 months. There was a significant fall in compliance in both groups (p less than 0.001) but no significant difference between them (p much greater than 0.1). We have been unable to demonstrate any significant hemodynamic advantage with the in situ technique but believe that its use is still justified because of technically easier anastomoses and an improved utilization rate. Preservation of the vasa vasorum does not maintain wall compliance and complete mobilization of the vein relieves any uneven tension and ensures that all venous tributaries are ligated, removing the risk of arteriovenous fistulas.

Compliance↗

PubMed1998

Human vascular to cardiac tissue selectivity of L- and T-type calcium channel antagonists.

1. Voltage-operated calcium channel (VOCC) antagonists are effective antihypertensive and antianginal agents but they also depress myocardial contractility. 2. We compared four L-type calcium channel antagonists, felodipine, nifedipine, amlodipine and verapamil and a relatively T-type selective calcium channel antagonist, mibefradil, on human and rat isolated tissue assays to determine their functional vascular to cardiac tissue selectivity (V/C) ratio. 3. The V/C ratio was calculated as the ratio of the IC50 value of the antagonist that reduced (by 50%) submaximally contracted (K+ 62 mM) human small arteries from the aortic vasa vasorum (vascular, V) mounted in a myograph and the IC50 value of the antagonist that reduced (-)-isoprenaline (6 nM) submaximally stimulated human right atrial trabeculae muscle (cardiac, C) mounted in organ chambers. 4. The average pIC50 values (-log IC50 M) for the human vascular preparations were felodipine 8.30, nifedipine 7.78, amlodipine 6.64, verapamil 6.26 and mibefradil 6.22. The average pIC50 values for the cardiac muscle were felodipine 7.21, nifedipine 6.95, verapamil 6.91, amlodipine 5.94, and mibefradil 4.61. 5. The V/C ratio calculated as antilog [pIC50V-pIC50C] is thus mibefradil 41, felodipine 12, nifedipine 7, amlodipine 5 and verapamil 0.2. 6. In rat small mesenteric arteries the pIC50 values for the five drugs were similar to the values for human vasa vasorum arteries contracted by K+ 62 mM. However for methoxamine (10 microM) contraction in the rat arteries the pIC50 values were lower for felodipine 7.24 and nifedipine 6.23, but similar for verapamil 6.13, amlodipine 6.28 and mibefradil 5.91. 7. In conclusion. in the human tissue assays, the putative T-channel antagonist mibefradil shows the highest vascular to cardiac selectivity ratio; some 3 fold higher than the dihydropyridine, felodipine, and some 200 fold more vascular selective than the phenylalkylamine, verapamil. This favourable vascular to cardiac selectivity for mibefradil, from a new chemical class of VOCC antagonist, may be explained by its putative T-channel selectivity.

Animals↗

PubMed1996

Arterial fatty lesions have increased uptake of chylomicron remnants but not low-density lipoproteins.

BACKGROUND: This study compares the accumulation of pre-formed chylomicron-remnants, chylomicrons and low-density lipoproteins (LDL) in rabbit thoracic aorta. To determine whether lipoproteins are delivered via the vasa vasorum, the aortic uptake of lipoproteins was compared to that of the common carotid artery. The uptake of chylomicron remnants and LDL were compared in lesioned and non-lesioned aortic tissue from Watanabe heritable hyperlipidaemic (WHHL) rabbits. METHODS: Chylomicrons, chylomicron-remnants and LDL were radio-labelled with tyramine-cellobiose and injected into rabbits. Arterial uptake was determined after 2 h as the percentage of injected lipoproteins associated with arterial tissue and also expressed as a fraction of mean arterial exposure. RESULTS: Aortic accumulation of radio-labelled chylomicron-remnants was substantially greater than for chylomicrons, and both were significantly greater than LDL. The data suggests that chylomicrons must first be hydrolysed to smaller particles before uptake. In normal rabbits, there was no difference in uptake of the lipoproteins between the aorta and carotid vessels, suggesting that the vasa vasorum is not significantly involved in lipoprotein delivery. However, in WHHL rabbits there was significantly greater aortic uptake of chylomicrons and LDL compared to the carotid vessel and, in cholesterol-fed rabbits, significantly greater aortic uptake of chylomicrons, suggesting that in hypercholesterolaemia the lipoprotein retention properties of some arterial beds change. In arterial fatty lesions from WHHL and cholesterol-fed rabbits there was an exclusive increase in chylomicron remnant uptake, whereas LDL uptake was similar to non-lesioned tissue. CONCLUSIONS: Chylomicron remnants and not their precursors might be primary atherogenic lipoprotein because they penetrate arterial tissue efficiently and are selectively retained in sites of lesion formation.

Animals↗

PubMed2000

A potential role for endothelin-1 in peripheral vascular disease.

The distribution of endothelin-1 (ET-1) and its receptors (ET(A)/ET(B)) has been studied in segments of femoral artery obtained from patients undergoing operation for peripheral vascular disease (PVD) using a combination of immunohistochemistry and autoradiography. Both receptor subtypes were located on the tunica media of vessel segments, with ET(A)-receptors predominating. Densitometric analysis showed that there was no difference in receptor binding to proximal/distal arterial segments from PVD patients. High-resolution autoradiography identified ET(B) binding to vascular nerves and vasa vasorum, mainly in distal portions of femoral arteries. Immunoreactive ET-1 was also identified that was associated with the vasa vasorum.

Autoradiography↗

PubMed1996

Receptors for advance glycation end-products (AGE) - expression by endothelial cells in non-diabetic uraemic patients.

BACKGROUND: Cellular actions of advanced glycation end-products (AGE) are mediated by a receptor for AGE (RAGE), a novel integral membrane protein. Immunohistochemical studies show only low-level RAGE antigen expression in endothelial cells. Design. It was the purposes of the study to compare expression of RAGE antigen by endothelial cells in non-diabetic uraemic patients (n=8) with non-uraemic controls (n=11). Samples of arterial tissue were obtained at the time of renal transplantation (in uraemic patients) and abdominal surgery (in controls). RAGE antigen was visualized using guinea-pig anti-RAGE IgG and PAP technique. RESULTS: Marked staining for RAGE was noted in endothelial cells, both arterial endothelium and endothelium of vasa vasorum of normoglycaemic uraemic patients, but was not demonstrable in endothelial cells of large arteries and only faintly expressed in vasa vasorum of non-uraemic individuals. CONCLUSION: Normal endothelial cells do not constitually express RAGE antigen; in contrast it is expressed by arterial and capillary endothelial cells of uraemic patients. The observation is of note in view of the putative role of AGE of causing atherosclerotic and non-atherosclerotic vascular lesions.

Adult↗

PubMed2006

Inhibition of cyclooxygenase isoforms in late- but not midgestation decreases contractility of the ductus arteriosus and prevents postnatal closure in mice.

Use of cyclooxygenase (COX) inhibitors to delay preterm birth is complicated by in utero constriction of the ductus arteriosus and delayed postnatal closure. Delayed postnatal closure has been attributed to loss of vasa vasorum flow and ductus wall ischemia resulting from constriction in utero. We used the murine ductus (which does not depend on vasa vasorum flow) to determine whether delayed postnatal closure may be because of mechanisms independent of in utero constriction. Acute inhibition of both COX isoforms constricted the fetal ductus on days 18 and 19 (term) but not earlier in gestation; COX-2 inhibition constricted the fetal ductus more than COX-1 inhibition. In contrast, mice exposed to prolonged inhibition of COX-1, COX-2, or both COX isoforms (starting on day 15, when the ductus does not respond to the inhibitors) had no contractile response to the inhibitors on days 18 or 19. Newborn mice closed their ductus within 4 h of birth. Prolonged COX inhibition on days 11-14 of gestation had no effect on newborn ductal closure; however, prolonged COX inhibition on days 15-19 resulted in delayed ductus closure despite exposure to 80% oxygen after birth. Similarly, targeted deletion of COX-2 alone, or COX-1/COX-2 together, impaired postnatal ductus closure. Nitric oxide inhibition did not prevent the delay in ductus closure. These data show that impaired postnatal ductus closure is not the result of in utero ductus constriction or upregulation of nitric oxide synthesis. They are consistent with a novel role for prostaglandins in ductus arteriosus contractile development.

Animals↗

PubMed1998

A solitary iliac artery aneurysm caused by Candida infection. Report of a case.

We report a very rare case of an infected aneurysm of solitary common iliac artery by Candida albicans. The patient, a 70 year-old male, had a history of systemic Candidemia infected through intravenous hyperlimentation (i.v.H) catheter 2 years ago. By physical examinations and laboratory data, infectious disease was suspected. Computed tomography showed right hydronephrosis and right solitary common iliac artery aneurysm, and operation was performed with diagnosis of infected aneurysm. The aneurysm was removed with the end of the abdominal aorta, and the arterial blood flow was restored by axillo-bifemoral bypass. Histopathological findings revealed abscess formation around the aneurysm with phlogocytes infiltration in both outer media of aneurysmal wall and vasa vasorum. Candida albicans was found as causative pathogen from resected specimens. This aneurysm is considered to be resulted from surviving candida in vasa vasorum after previous candidemia.

Aged↗

PubMed1996

Transforming growth factor-beta protein and messenger RNA expression is increased in the closing ductus arteriosus.

In full-term newborns, permanent closure of the ductus arteriosus is associated with the formation of a neointima that is characterized by extracellular matrix deposition and smooth muscle cell migration. Transforming growth factor-beta (TGF-beta), a potent modulator of extracellular matrix deposition and smooth muscle cell migration, has been found to play a role in the remodeling associated with several forms of vascular disease. We examined the protein and mRNA expression of the three mammalian isoforms of TGF-beta (TGF-beta1, TGF-beta2, and TGF-beta3) during ductus arteriosus closure in full-term lambs. We found that the temporal changes and cellular localization of the proteins and mRNAs of all three TGF-beta isoforms were similar. TGF-beta proteins and mRNAs were present in very low levels in the late-gestation fetal ductus. Within 24 h of delivery, there was enhanced expression of TGF-beta in the newly forming neointima and outer muscle media; this continued to increase over the next 10 d. Increased expression of TGF-beta in the inner muscle media and adventitia lagged behind that of the neointima and outer muscle media. TGF-beta was not found in the luminal endothelial cells at any time. In contrast to the pattern described above, the appearance of TGF-beta protein differed from that of mRNA in the vasa vasorum of the ductus wall. After delivery, there was an increase in TGF-beta immunoreactivity in the smooth muscle cell layers of the vasa vasorum without any concurrent mRNA expression. The appearance of TGF-beta at the time of ductus closure suggests an important role for this growth factor in the reorganization of the ductus wall after birth.

Animals↗

PubMed2005

[A case of spontaneous dissection of the cervical carotid artery with pseudoaneurysm].

We experienced the case of a dissecting carotid artery presenting with a pulsatile neck mass. This 60-year-old man was admitted to our department due to a progressive, painful left neck mass. The lesion was diagnosed as a dissecting left internal carotid artery with the subsequent formation of a giant pseudoaneurysm. First, the patient underwent an endovascular treatment using self-expandable stent and Guglielmi detachable coils (GDCs). However, four months after the treatment, recurrence of the pseudoaneurysm happened to him, and he was readmitted to our department. Angiographies revealed an enlargement of the pseudoaneurysm. Then, proximal occlusion of the left internal carotid artery was performed using a balloon and GDCs. Ten months after the second endovascular treatment, since symptoms of the central retinal artery embolism and progression of the mass effect occurred, surgical treatment with trapping and resection of the pseudoaneurysm was performed. We investigated pathologically the surgical specimen and could observe a partial thrombosed wall of the pseudoaneurysm. The multiple neovascular channels in the intima and media layers of the aneurysmal wall could be found, and the vasa vasorum in the adventitia was also noted. We thus suggest that mechanism of the enlargement of the pseudoaneurysm may be due to the retrograde neovascular supplies from the vasa vasorum. As a consequence, repeated bleeding and thrombosis in the dissecting arterial wall may result in the formation of partial thrombosed giant aneurysms.

Aneurysm, False↗

PubMed1990

Comparative anatomic studies of various arterial conduits for myocardial revascularization.

Comparison was made between the morphologic condition of the left anterior descending artery and four arterial conduits: the internal mammary, right gastroepiploic, inferior epigastric, and radial arteries, harvested from 17 patients (aged 15 to 85 years, mean 64 years) who had died of nonvascular diseases. Proximal, mid, and distal segments were examined microscopically. The internal mammary artery was elastic, but the others were muscular. In all four conduits, atherosclerosis was absent to mild, the internal elastic lamina showed only minimal defects, and the vasa vasorum were confined to the adventitia. In all cases the left anterior descending artery showed mild to severe atherosclerosis and substantial defects in the internal elastic lamina with penetration of the vasa vasorum into the media and intima. Comparison of the mean distance (+/- standard deviation) from the lumen to the outermost portion of the media for the left anterior descending artery (320 +/- 63 microns) with the four conduits gave comparable values for the internal mammary artery (350 +/- 92 microns); p = not significant) and the right gastroepiploic artery (291 +/- 109 microns; p = not significant), versus 529 +/- 52 microns; p less than 0.002) for the radial artery and 249 microns (+/- 87 microns) (p less than 0.04) for the inferior epigastric artery (Kruskal-Wallis and Mann-Whitney U tests). The relatively scanty presence of smooth muscle cells in the thin-walled media of the internal mammary artery combined with a well-formed internal elastic lamina, even at advanced age, may be an important cause for its low susceptibility to atherosclerosis and a major determinant in its superior long-term patency as a coronary artery bypass graft. This finding emphasizes the justification of continued use of the ideally matching internal mammary artery, either as in situ or free graft, in coronary artery bypass grafting. In contrast to the thick-walled radial artery, which may be relatively prone to ischemia, an acceptable long-term patency of the inferior epigastric artery and right gastroepiploic artery, if harvested as pedicled grafts, is anticipated.

Adolescent↗

PubMedDate not supplied

[Diminished vascular density in the aortic wall. Morphological and functional characteristics of atherosclerosis].

PURPOSE: To determine disproportion in thicknesses of the vascular wall and vasa vasorum in eight fragments of human aorta because of the irregular distribution of atherosclerosis in arterial walls. METHOD: The length and thickness of the wall and its layers were measured and the vasa vasorum were conted. Vascular density, considered as the number of vessels per square millimeter in healthy and diseased areas, was calculated along with mean value, variance, standard deviation and the confidence interval for values and null hypotesis. Variances were analyzed, and the comparative and paired "t" test was applied. RESULTS: There were differences in thicknesses of the healthy (27 :m) and diseased (120.5 :m) intima (p < 0.001) and between the healthy (125.2 :m) and diseased (102.3 :m) media (P < 0.001). Vascular density was higher in healthy fragments (mean +/- Cl 99% = 4.40 +/- 1.4 vs 2.20 +/- 0.8, = < 0.001 for Ha; 0 +/- 1.0775 for Ho; paired "t" 2.1 +/- 1.1, P < 0.01), and higher compared to the healthy intima area (31.6 vs 5.1, P < 0.01). There were no differences compared to the media layer area. The relation between the number of vessels and the length of the vascular segments was greater in the healthy fragments (mean +/- Cl 95% = 4.9 +/- 1.02 vs 3.5 +/- 0.68; 1.4 difference, P < 0.05). CONCLUSION: Vascular density is lower in the atherosclerotic aortic wall than in the healthy aorta and this could initiate the pathologic process.

Aged↗

PubMed1998

Expression of vascular adhesion molecules in saphenous vein coronary bypass grafts.

BACKGROUND: Adhesion of blood elements to the endothelium is an important step in the development of vein graft disease. This study examines the expression of vascular adhesion molecules on explanted saphenous vein bypass grafts. METHODS: Immunocytochemical staining was performed using explanted saphenous vein grafts from 28 patients. Antibodies against the endothelial markers CD31, von Willebrand factor, intercellular adhesion molecule-1, vascular adhesion molecule-1, and E-selectin were used. RESULTS: Staining for CD31 and von Willebrand factor demonstrated the presence of endothelial cells in the lumen and the vasa vasorum. Expression of intercellular adhesion molecule-1 was variable between grafts, whereas vascular adhesion molecule-1 and E-selectin were almost always absent on the luminal endothelium. In contrast, the endothelium of the vasa vasorum stained positively for intercellular adhesion molecule-1 and vascular adhesion molecule-1, and was also seen on nonendothelial cells within the vessel wall. Expression of these adhesion molecules did not vary with the severity of vein graft disease. CONCLUSIONS: This study highlights the blood vessels in the adventitia as possible sites for the adhesion and migration of cells into the vessel wall.

Aged↗

PubMed1996

[Measurement of oxygen tension in normal and varicose vein walls].

Oxygen tension (PO2) was investigated in vivo in the long saphenous vein from 21 varicose patients (31 veins) during venous surgery and 7 patients with normal venous network undergoing popliteo-femoral by-pass. Measurement was achieved using computerized polarographic system Kimoc 6650 (Eppendorf, Hamburg) providing a microdriven stepwise progression of a needle probe. Oxygen tension profile was similar in both groups of patients. A slow PO2 decrease was observed from adventitia up to the union of the middle and inner thirds of the media where values were at the lowest then followed by a marked increased in the intima and the saphenous lumen. Oxygenation of the two external thirds of the venous wall was provided by vasa vasorum. The average minimum values in the media was significantly reduced in varicose veins compared to no-varicose veins (7,9 mmHg versus 13,4 mmHg; p < 0,05). These results indicated the key role of vasa vasorum flux in the long saphenous vein nutrition and suggest a primary or secondary deficiency in oxygen supply in varicose veins.

Adult↗

PubMed1990

Histologic, morphometric, and biochemical evolution of vein bypass grafts in a nonhuman primate model. I. Sequential changes within the first three months.

The objective of this study was to define the histologic and morphometric evolution that accompanies the increase in cholesterol content of vein bypass grafts in a nonhuman primate model. Cephalic vein grafts were interposed bilaterally in the femoral arteries of 15 stump-tailed macaque monkeys (Macaca arctoides), which were fed a diet that sustains plasma cholesterol levels of approximately 225 mg/dl. Grafts were excised from five animals for analysis on each of postoperative days 3, 7, 14, 30, 60, and 90. Cholesterol content increased from 69 +/- 24 micrograms/100 mg (mean +/- standard deviation) in ungrafted vein to 473 +/- 122 micrograms/100 mg in grafts 90 days after implantation (p less than 0.05). By stepwise regression analysis, cholesterol content was best predicted by abundance of foam cells (r2 = 0.82). Intima comprised 13% +/- 5% of the total cross-sectional area of the wall in ungrafted vein and 59% +/- 11% at day 90 (p less than 0.001). With cholesterol content excluded from the stepwise regression, intimal area was best predicted by the presence of foam cells (r2 = 0.39). There was consistently an increase in the prevalence of polymorphonuclear leukocytes on the luminal surface and in both the intima and media during the first 14 days after grafting. Vasa vasorum, which were always present in ungrafted vein, were sparse at 3 days but reappeared by day 7. Medial fibrosis occurred in grafts, and in the 30- to 90-day interval it was directly correlated with the number of adventitial vasa vasorum present (r = 0.64, p less than 0.05). Immunohistochemistry revealed prominent staining for both platelet factor VIII and fibronectin during the first month, with a gradual decline in staining intensity thereafter. The evolution of changes in vein bypass grafts documented in this report are in general agreement with graft changes observed in humans and support the validity of our model in evaluating the histologic correlates of increased graft cholesterol content.

Animals↗

PubMed1994

Anatomic barriers influence the distribution of in vivo gene transfer into the arterial wall. Modeling with microscopic tracer particles and verification with a recombinant adenoviral vector.

We evaluated the extent to which anatomic barriers to vector penetration might influence the distribution of successful in vivo gene transfer into the normal arterial wall. A double-balloon catheter technique with infusion pressures of 100 to 400 mm Hg was used to infuse microscopic tracer particles of the size range of liposomes and viral vectors into normal elastic arteries of sheep. Localization of the tracer particles in tissue sections by light, fluorescence, and electron microscopy suggested that vector-sized particles were delivered to the intima by direct infusion and to the adventitia via the arterial vasa vasorum. Particles were virtually absent from the arterial media. To test the predictions made from the particle studies, we repeated the infusion protocol with high-titer adenoviral vectors. Gene transfer occurred at high levels in the intima and along the adventitial vasa vasorum but again was virtually absent within the media. The ability of medial smooth muscle cells to be transduced was established in separate experiments with a high-pressure (5 atm) porous balloon infusion catheter. We conclude that (1) the anatomy of the normal elastic arterial wall imposes significant limitations on the penetration of particles in the size range of most gene-transfer vectors and (2) the distribution of in vivo gene transfer with adenoviral vectors is correctly predicted by the distribution of inert tracer particles. These findings have important implications for the design of arterial gene-transfer and gene-therapy protocols.

Adenoviridae↗

PubMed2004

Early recruitment of phagocytes contributes to the vascular inflammation of giant cell arteritis.

Vascular inflammation in giant cell arteritis is generally described as a process involving dendritic cells, T-lymphocytes, and effector tissue macrophages. Less is known about the contribution of phagocytes that are recruited early, such as monocytes and neutrophils. These cells express and secrete pro-inflammatory S100 proteins which directly activate endothelial cells. In this study the expression of S100A8/S100A9 and S100A12, pro-inflammatory proteins specific for early recruited phagocytes, was studied in biopsies from 36 patients with giant cell arteritis. In addition, serum concentrations of these proteins were analysed in serum samples from 42 patients and 35 healthy controls. The S100A8/S100A9 complex was found to be abundant in the adventitia and media in affected arteries. Besides neutrophils, cells expressing these proteins belonged to a pro-inflammatory subtype of CD68-positive monocytes. In contrast, S100A12 expression was restricted to neutrophils that were found around the vasa vasorum within the adventitial layer. Both S100A8/S100A9 and S100A12 serum concentrations were significantly higher in patients with giant cell arteritis than in healthy controls. In conclusion, recently recruited phagocytes expressing pro-inflammatory S100 proteins take part in the vascular inflammation of giant cell arteritis. They may play important roles at the vasa vasorum of affected vessels, which represent sites of entry for recruited inflammatory cells. These data indicate that phagocytes within the adventitia and media contribute to the process of inflammation via release of the pro-inflammatory S100 proteins S100A8, S100A9, and S100A12.

Aged↗