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PubMed1980

[Involvement of the large vessels supplying the brain in sickle cell disease: a possible cause of Moya-moya (author's transl)].

In two children (1 girl and 1 boy aged 6 years) with an SS haemoglobinopathy, a neurological deficit affecting one half of the body led to arteriograms being performed. These revealed stenoses of the major vessels (above all anterior and middle cerebral with development of a collateral circulation giving an appearance suggestive of Moya-moya syndrome). Various aetiologies have been suggested for this syndrome: congenital disease, oral contraceptives, atheroma. Sickle cell disease is a new cause. The mechanism would appear to be fibrosis proliferating secondary to sub-endothelial anoxia caused by sludging in the vasa vasorum.

Anemia, Sickle Cell↗
PubMed1980

Pneumatic tourniquet as a substitute for vascular clamps in distal bypass surgery.

The pneumatic tourniquet is an effective substitute for vascular clamps in tibial and popliteal artery surgery. Intimal trauma due to clamping is avoided. Because circumferential dissection of the vessel is not necessary, the vasa vasorum are preserved minimizing ischemic injury to the vessel wall. The technique has been employed in 40 distal popliteal and tibial reconsteal and tibial reconstructions during the past year with only one complication that may possibly be related to its use. Early patency was 92% at the patient's time of discharge from the hospital. In all four patients requiring below-knee amputation, primary wound healing and successful prosthetic rehabilitation were achieved. This technique appears to be safe and simplifies distal reconstructions for lower extremity ischemia.

Arteries↗
PubMed1995

Apolipoprotein(a) deposition in atherosclerotic plaques of cerebral vessels. A potential role for endothelial cells in lesion formation.

Atherosclerosis is the leading cause of death and serious morbidity in economically developed societies through its sequelae of coronary artery and cerebrovascular disease. The causes and mechanisms of atherosclerosis are still largely unknown. Serum levels of a lipoprotein, Lp(a), have been shown, in retrospective and some prospective clinical studies, to be associated with increased risk of myocardial and cerebral infarction. The active part of Lp(a), apo(a), has > 80% homology with plasminogen; thus it may competitively inhibit the thrombolytic action of plasminogen and enhance thrombogenesis. Lp(a) has been shown to be deposited in the vascular wall of the aorta and coronary vessels, but its presence in the cerebral vessels has not yet been shown. Autopsy specimens of vessels of the circle of Willis from 23 patients were examined for degree of atherosclerosis and deposition of apo(a) by immunohistochemistry with apo(a)-specific monoclonal antibodies. The amount of apo(a) deposition in cerebral vessels correlated well with the degree of cerebral atherosclerosis. Arterial deposition of apo(a) was found entirely within the endothelial cell and subendothelial cell layers. There was no staining within the media and adventitia, with the exception of staining within the endothelial cells of the vasa vasorum. Correlation between the morphology of apo(a) deposition and plaque stage was found suggesting that detection of apo(a) in endothelial cells is an early event in the development of the atherosclerotic plaque of cerebral vessels.

Adult↗
PubMedDate not supplied

[Structural and morphometric analysis of the internal mammary artery used in coronary bypass surgery].

The internal mammary artery is currently regarded as the optimal canal in coronary bypass surgery. Even if the motives for the excellent behaviour of this artery are still not fully clarified, the morphological and morphofunctional study of its wall can contribute to explain the clinical results obtained using this canal. In order to complete existing studies on this topic and to increase our knowledge of the structure of this artery, segments of internal mammary artery taken from patients undergoing coronary bypass surgery were analysed. Histological, immunohistochemical, histochemical and morphometrical tests were performed in these samples. The results of the tests underline the considerable complexity of the internal mammary artery whose walls appear to be rich in elastic fibres, divided into numerous lamellar structures concentric to the vasal lumen and without vasa vasorum in the tunica media given that this is adjacent to the tunica adventitia. Moreover, the marked presence of the NO-synthase enzyme, responsible for nitrogen monoxide synthesis, was observed in the endothelial layer and tunica media, as suggested by histochemical analysis. These data argue in favour of a structure able to resist the considerable hemodynamic stress to which the artery is subjected after bypass, a structure which is functionally well adapted to receive the majority of nutrition through its own lumen, and, lastly, a structure capable of self-regulation in response to the requirements made from time to time. These findings may further our understanding of the morphofunctional aspects of the internal mammary artery and may contribute to explaining the latter's relative immunity to atherosclerosis and, thus, its success in coronary bypass.

Aged↗
PubMed1994

Chondroid metaplasia in the tunica media of the aorta in dogs submitted to saphenous vein aorto-cava by-pass.

We submitted twelve dogs to aorto-superior vena cava by-pass with saphenous vein. Six months later, all dogs had developed areas of chondroid metaplasia in the tunica media of the aorta, near the area of anastomosis. Three dogs also had bony metaplasia. The Foci of metaplasia had no relation to sutures. This lesion begins with a build-up store of glycosaminoglycans in the tunica media. Later, elastic fibers show a fenestration and dissolution, while chondrocytes replace smooth muscle fibres. We suggest that the rupture of the vasa vasorum during operation and the traction and pulsation of the by-pass over the area of suture could be the cause of this direct metaplasia.

Anastomosis, Surgical↗
PubMed1976

[Hypertensive arteriopathy: aortic histo-metabolic changes during postnatal ontogenesis in spontaneous hypertensive rats (Okamoto-Aoki strain) (author's transl)].

27 aortic histoenzymatic activities and 6 aortic macromolecular substances were comparatively studied in spontaneous hypertensive rats (SHR) and normotensive Wistar rats (3, 5, 13 and 16 month-old). The earlier aortic changes (3rd month) were only histoenzymatic: 5 Nase and LDH were increased in the entire aorta: some oxido-reductases increase near the intima. These early minor changes might represent some of the factors of the functional disturbance of the arterial smooth muscle cell. At the stage of stable hypertension (5th-13th month) two lesion patterns were seen: 1) metabolic: increase of the histoenzymatic activities involved in lipolysis, GAG anabolism, glycolysis, cell respiration, energizing metabolism and nucleotides-esterolysis. 2) Structural: cell hypertrophy and hyperplasia, interstitial fibrosis. The stimulus of the metabolic changes seems to be dual: 1) the hypertensive factor acting upon smooth muscle cells and/or vasa vasorum. 2) The intraarterial pressure increasing endothelial crossing and stimulating myocyte contraction. The structural change is more probably the reaction to elevated pressure; it has led to diffuse medial thickening providing a balance between hypertension and arterial wall stress. On the 16th month, the cell reaction developed in two ways: 1) increase of metabolic and morphogenetic activation of some cells. 2) irreversible degeneration in some other cell groups (media necrosis, cicatricial fibrosis, decrease of oxidoreductases and lipolytic activities, increase of lysosomal enzymes). Aortic lesions during spontaneous hypertension were less dramatic and occurred later than after experimental hypertension. Some of the observed histometabolic changes might lead to maintenance and worsening of hypertension.

Animals↗
PubMed1994

Plasminogen activator inhibitor-1 expression in human liver and healthy or atherosclerotic vessel walls.

Individuals with elevated levels of plasminogen activator inhibitor type 1 are at risk of developing atherosclerosis. The mechanisms leading to increased plasma PAI-1 concentrations are not well understood. The link observed between increased PAI-1 levels and insulin resistance has lead workers to investigate the effects of insulin or triglyceride rich lipoproteins on PAI-1 production by cultured hepatocytes or endothelial cells. However, little is known about the contribution of these cells to PAI-1 production in vivo. We have studied the expression of PAI-1 in human liver sections as well as in vessel walls from different territories, by immunocytochemistry and in situ hybridization. We have observed that normal liver endothelial cells expressed PAI-1 while parenchymal cells did not. However, this fact does not refute the role of parenchymal liver cells in pathological states. In healthy vessels, PAI-1 mRNA and protein were detected primarily at the endothelium from the lumen as well as from the vasa vasorum. In normal arteries, smooth muscle cells were able to produce PAI-1 depending on the territory tested. In deeply altered vessels, PAI-1 expression was observed in neovessels scattering the lesions, in some intimal cells and in smooth muscle cells. Local increase PAI-1 mRNA described in atherosclerotic lesions could be due to the abundant neovascularization present in the lesion as well as a raised expression in smooth muscle cells. The increased PAI-1 in atherosclerosis could lead to fibrin deposit during plaque rupture contributing further to the development and progression of the lesion.

Arteriosclerosis↗
PubMed1994

[Morphological comparison between arterial grafts and venous grafts].

We have extendedly used arterial grafts in coronary bypass surgery because of their better patency rate. We have operated 134 cases of coronary bypass during recent 27 months. Postoperative angiography showed high patency rate in arterial grafts, such as 97% (59/61) of right internal thoracic artery (RITA), 98% (107/109) of left internal thoracic artery (LITA), 96% (83/86) of right gastroepiploic artery (RGEA), comparing with 86% (26/30) of saphenous vein graft (SVG). Pathological examination was done by specimens of grafts obtained during operation. Vasa vasorum was poorly developed in ITA and RGEA. ITA had several layers of elastic fiber in media and RGEA had smooth muscular media. Both arterial grafts showed low atherosclerotic scores (intima/media), 7.1% in RITA, 7.3% in LITA and 6.8% in RGEA. But some cases with hyperlipidemia and/or diabetes showed high score of atherosclerosis in arterial grafts. Endothelial cells were well preserved in both arterial grafts after harvesting, in contrast with poor endothelial preservation in SVG. Endothelial appearance of RGEA was similar to that of the coronary artery and different from that of ITA. RGEA is superior grafts for CABG as coronary bypass because of their structural superiority.

Abdominal Muscles↗
PubMed1993

Management of patients with intramural hematoma of the thoracic aorta.

BACKGROUND: Intramural hematoma of the thoracic aorta (IMH) is a diagnosis of exclusion and represents spontaneous, localized hemorrhage into the wall of the thoracic aorta in the absence of bona fide aortic dissection, intimal tear, or penetrating atherosclerotic ulcer. This process may arise from primary vasa vasorum hemorrhage within the aortic media or rupture of an atherosclerotic plaque. The clinical presentation of patients with IMH mimics that of acute aortic dissection; moreover, considerable diagnostic confusion exists despite the use of many different imaging modalities. The optimal mode of management of patients with IMH (medical versus medical plus surgical) remains problematic because of the paucity of information available. METHODS AND RESULTS: Thirteen patients with IMH were managed at two medical centers between 1983 and 1992. Patients with IMH caused by giant penetrating atherosclerotic ulcers were specifically excluded. There were 8 women and 5 men (mean age, 70 years [range, 54 to 82 years]). The admitting clinical diagnosis was acute aortic dissection, and all patients had a history of hypertension. There was no evidence of aortic dissection or intimal disruption as assessed by computed tomographic (CT) scan (n = 11), aortography (n = 10), magnetic resonance imaging (MRI) scan (n = 9), transesophageal echocardiography (TEE) (n = 6), or intravascular ultrasound (n = 1). The diagnosis of IMH was established by exclusion. The descending thoracic aorta was involved in 10 cases and the ascending/arch in 3. Conservative medical management was attempted initially. All 3 patients with IMH involving the ascending aorta ultimately required operative intervention, and 2 individuals died; 2 of 10 patients with descending aortic involvement eventually underwent surgery. Average hospital stay was 11 days; the mean follow-up interval for discharged patients was 29 months. CONCLUSIONS: IMH is a distinct pathological entity, should not be confused with aortic dissection, and probably will be identified more frequently in the future. All patients with IMH should be monitored carefully and treated with aggressive antihypertensive therapy. Frequent serial assessment is necessary using TEE or MRI/CT scans. Based on this small experience, patients with ascending/arch IMH, ongoing pain, or IMH expansion should probably undergo early graft replacement. Patients with IMH involving the descending thoracic aorta who have no evidence of progression and become pain free can probably be treated conservatively but require antihypertensive therapy and serial aortic imaging surveillance indefinitely.

Aged↗
PubMed1993

Disseminated giant cell arteritis.

A 76-yr-old woman with widespread giant cell arteritis and polymyalgia rheumatica is described. The patient had an unusual simultaneous involvement of the cranial (temporal) arteries demonstrated by biopsy, and of large elastic arteries (aorta and its major branches), medium-sized and small muscular arteries, arterioles and vasa vasorum found at autopsy. Coronary arteritis was responsible for the fatal myocardial infarction.

Aged↗
PubMedDate not supplied

[Calcitonin gene-related peptide in diabetes mellitus type 2: a possible etiopathogenetic role].

The Calcitonin Gene-Related Peptide (CGRP) is a 37 aminoacid peptide displaying about 50% homology with amylin which is secreted from the pancreatic islets of Langerhans. The main form, the beta-CGRP, is produced by the enteric nervous system and perivascular nerves of the vasa vasorum. It represents the most powerful vasodilator yet discovered but its role is not yet completely clarified. Recently it has been implicated in the control of regional blood flow and some authors have hypothesized its role in the development of Non Insulin Dependent Diabetes Mellitus (NIDDM). CGRP and amylin seem to inhibit the release of insulin from beta-cells and to play a role in local paracrine control of insulin secretion. In addition it is also shown to decrease the uptake of glucose by striated muscle. This has led to the suggestion that CGRP might be a circulating hormone implicated in the regulation of peripheral insulin sensitivity. In this review we examine the possible role of CGRP in the development of peripheral insulin resistance and altered insulin secretion which is characteristic of NIDDM.

Calcitonin Gene-Related Peptide↗
PubMed1995

Non-giant cell arteritis of the temporal artery presenting as the polymyalgia rheumatica-temporal arteritis syndrome.

We describe a heterogeneous group of 4 elderly patients with atypical vasculitis of the temporal artery who presented clinically with the polymyalgia rheumatica-temporal arteritis syndrome. The first had apparently isolated eosinophilic necrotizing vasculitis without peripheral blood eosinophilia, history of asthma, or pulmonary vasculitis (so called limited form of Churg-Strauss syndrome). Temporal artery biopsy in the 2nd patient revealed small vessel necrotizing vasculitis in the fragment of skeletal muscle surrounding a normal temporal artery (i.e., negative for giant cell arteritis, GCA). This patient subsequently developed rheumatoid polysynovitis. The temporal artery biopsies in the remaining 2 patients showed vasa vasorum vasculitis, without GCA, associated with malignancy in Patient 3 and as an unexpected and apparently isolated finding in Patient 4. All 4 patients responded to the standard corticosteroid therapy for giant cell temporal arteritis. Unusual temporal artery biopsies such as these should be interpreted in relation to clinical findings.

Adrenal Cortex Hormones↗
PubMed1996

A study of the ultrastructure of developing human umbilical vessels.

Electron microscopic techniques were used to examine the ultrastructure of developing human umbilical arteries and vein (8-12, 13-17 and 37-40 wk gestational age). These showed that with increasing age there is (1) an increase in the size of the lumen and the thickness of the media; (2) an increase in the ratio of contractile smooth muscle phenotypic cells; (3) an increase in the myofilament content of the smooth muscle cells and the number of Weibel-Palade bodies; (4) a decrease in the glycogen content; (5) an appearance of microvilli on the luminal surface of the endothelium. Lipid vesicles, nerves and vasa vasorum were not observed in any region of the umbilical vein or arteries.

Endothelium, Vascular↗
PubMed1996

Expression of the adhesion molecules ICAM, VCAM, and ELAM in the arteriosclerotic plaque.

Subject of investigation was the demonstration of the different expression of ICAM-1, and VCAM in 13 complete cross sections of the Aorta abdominalis and the Arteria iliaca immediately available post operationem during the process of arteriosclerosis. With increasing severity of the arteriosclerosis, ELAM showed a decreasing expression of the endothelium of the main vessel and a moderate one of the cells in the adventitia. On the endothelium of the main vessel and the vasa vasorum, we detected ELAM-1, showing a decreasing tendency when the arteriosclerosis was aggravating. In case of severe arteriosclerosis, a focal expression was also found on cells in the intima and media. In the adventitia, the expression was relatively constant during the process of arteriosclerosis. The more serious the disease, the more provable was VCAM on endothelial cells. In cases of severe arteriosclerosis, we also detected a focal staining in deeper layers of the wall. This study supports the concept of the active role of endothelial cells in the recruitment of leucocytes during the early steps of the arteriosclerotic process. In this process, with the disease aggravating, the endothelium seems to be less significant than the smooth muscle cells, which obviously play an important role in the course of arteriosclerosis.

Aorta, Abdominal↗
PubMed1996

Localization of fibrinolytic activators and inhibitors in normal and atherosclerotic vessels.

UNLABELLED: Local fibrinolytic changes in atherosclerotic arteries have been suggested to influence plaque growth and promote mural thrombosis on ruptured or ulcerated plaques. Increased levels of plasminogen activator inhibitor (PAI-1) have been found in atherosclerotic arteries. In this study tissue plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA) and PAI-1 were localized in arterial biopsies of healthy and atherosclerotic vessels by immunohistochemistry. The expression of fibrinolytic regulators was related to the distribution of endothelial cells (EC) and macrophages. RESULTS: t-PA was expressed in vasa vasorum. PAI-1 was positive in endothelial cells, in the media and in the adventitia. Increased expression of t-PA, u-PA and PAI-1 was found in atherosclerotic vessels. t-PA, u-PA, PAI-1 and macrophages were co-localized in plaques. These results support the concept that macrophages can be important in the local regulation of fibrinolysis in atherosclerotic vessels.

Adult↗
PubMed1997

Prenatal diagnosis, pathology, and genetic study of fetus in fetu.

We report the prenatal diagnosis, pathology, cytogenetics, and molecular studies of a retroperitoneal fetus in fetu. Prenatal ultrasonography of the host fetus in the third trimester showed an anencephalic, acardiac mass with identifiable extremities and spine within an intra-abdominal cystic mass. Pathological examination revealed a fetiform mass weighing 20 g with four extremities, digits, vertebral bodies, an oral cavity with developing teeth, primitive male external genitalia, a urinary bladder, a cloaca with an external opening, large intestines, a membranous capsule, and an umbilical cord with one artery, one vein, and Wharton's jelly. Histological examination demonstrated nerve bundles in the fibrocollagenous tissue below the cuboidal surface epithelium of the membranous capsule, and absence of lamina elastica interna and vasa vasorum in the single artery of the umbilical cord. Both the host infant and the fetus in fetu had a normal 46,XY karyotype. Molecular analysis using informative genetic markers showed no genetic difference between the host infant and the fetiform mass. We report this case as an unusual example of fetus in fetu in co-existence with an amnion-like membrane containing nerve bundles and with a well-formed umbilical cord. We demonstrate that fetus in fetu can be diagnosed prenatally if the fetiform mass has well-developed limbs and spine. We emphasize the necessity for suspicion of fetus in fetu when a well-defined encapsulated cystic mass with calcified solid components is detected prenatally in a fetus by ultrasonography.

Adult↗
PubMed1997

Light and scanning electron microscopy of the porcine mesometrial and paraovarian lymphatic networks.

Uterine lymphatics were examined in 38 pigs using light microscopy, stereomicroscopy, and scanning electron microscopy. Uterine lymphatics were initially filled with plastic materials: Microfil for stereomicroscopy, Mercox-corrosion cast for scanning electron microscopy (SEM), and Micropaque for x-ray photographs. Lymph precollectors of the uterine horns formed two superficial layers, ventral and dorsal. At the level of the ovary, precollectors joined to become collector lymph vessels, which entered nearby lymph nodes. Among the lymph vessels emanating from the uterus, there was a characteristics band of lymphatics that bordered on the isthmus of the oviduct. These passed toward the ovary to form the paraovarian lymphatic plexus. Segments of collector lymphatics were longer than precollectors, had thicker walls consisting of endothelial cells, smooth muscle (uniformly forming a continuous band around lymphatics) and fibroblasts. Both precollector and collector lymphatics were covered and surrounded by a fine network of blood microvessels (vasa-vasorum) especially well seen in corrosion casts (SEM).

Animals↗
PubMed1997

Adeno-associated virus vectors for vascular gene delivery.

A variety of delivery systems have been used to genetically modify vascular endothelial cells and smooth muscle cells (SMCs), but currently available systems suffer from either inefficient in vivo gene transfer, transient episomal vector expression, or significant immune responses and inflammation. In the present study, we evaluated an alternate vector system, recombinant adeno-associated virus (rAAV) for transduction of vascular cells in culture and in vivo. Primary cultures of rabbit, monkey, and human SMCs; macaque and human microvascular endothelial cells; and human umbilical vein endothelial cells were efficiently transduced at a dose of 100 to 1000 DNase-resistant particles per cell. rAAV-mediated transduction of the vasculature in vivo was observed after intraluminal gene delivery or after intra-adventitial injection in carotid arteries of atherosclerotic cynomolgus monkeys. Whether vector delivery was intraluminal or adventitial, transduction was observed in the adventitia, particularly within microvessels (vasa vasorum) but not in cells of the intima or media. Transduction of adventitial microvessels was enhanced by balloon injury 4 days before gene transfer. This was particularly true for adventitial delivery. We have previously shown that adventitial cell proliferation increases significantly 4 days after balloon injury (45%) in this animal model. Together, these data suggest that cell proliferation may enhance AAV transduction in vivo in the vasculature. AAV vectors exhibited a tropism in vivo for the microvascular endothelium at the doses used in the present study, which may provide the opportunity for targeting gene delivery. In summary, we have demonstrated the utility of rAAV vectors for ex vivo vascular cell gene delivery and present an initial experience with rAAV for in vivo vascular gene delivery. This alternate vector system may overcome some of the limitations hampering the development of gene therapy for vascular disorders.

Animals↗