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At least 145 records · Page 8Linked to original sources
PubMed1986

The effect of maternal smoke exposure on the ultrastructure of fetal peripheral blood vessels in the mouse.

Ultrastructural changes have been found in umbilical blood vessels, placental blood vessels, and peripheral blood vessels of human fetuses whose mothers smoked during pregnancy. This study was undertaken to determine if similar changes could be found in peripheral blood vessels of mice fetuses whose mothers were exposed to cigarette smoke during pregnancy. Breeding mice of the C57BL/KsJ strain were placed in a smoking box similar to that described by Younoszai and exposed to cigarette smoke intermittently. This produces carbon monoxide levels in the adult mice similar to that found in human adults smoking one pack of cigarettes per day. Similarly caged mice of the same strain were used as controls. The female mice were not removed from their cage from pre-conception time until after delivery. Upon delivery each pup was sacrificed via neck fracture and the entire pup was immersed in a solution of 2.5% glutaraldehyde in 0.1 M cacodylate buffer at pH 7.3. While still under solution, the rear leg muscles were dissected free, sliced, and immersed in the same preservative for four to five hours. They were then placed in fresh 2.5% glutaraldehyde mixture overnight. The tissues were post-fixed in osmium ferrocyanide and en-block stained with uranyl acetate in a graded series of alcohol. The tissues were infiltrated with and embedded in Spurr. Sections were taken via an ultramicrotome and post-stained with uranyl acetate and lead citrate. The sections were examined in a Philips 201 electron microscope at 60 KV. In the peripheral vessels of the fetuses from smoke-exposed mothers, endothelial blebbing (both surface-type and vacuole-type) was seen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Contributions of donor and host blood vessels in CNS allografts.

The contributions of blood vessels in various transplantation paradigms of solid CNS tissue or cell suspension allografts placed into adult host brains were investigated immunohistochemically using the PVG-RT1C and PVG-RT1U inbred rat strains and a panel of highly specific monoclonal antibodies. The monoclonal antibodies included OX-27 and U9F4 against major histocompatibility complex (MHC) class I antigens of the PVG-RT1C and PVG-RT1U rats, respectively; OX-26 against the rat transferrin receptor located on blood-brain barrier (BBB) endothelia; and OX-7 against rat neuronal Thy 1.1 for evaluating graft survival. Our study is the first to address the immunogenicity of blood vessels in surviving CNS allografts. Solid fetal or neonatal PVG-RT1C cortex was grafted into the third or lateral cerebral ventricle or caudate/putamen of PVG-RT1U adult hosts for 30 days to 7 months. All allografts expressed demonstrable Thy 1.1 immunoreactivity with OX-7 antibody and appeared well-vascularized with blood vessels that immunostained with the OX-26 antibody against the transferrin receptor. For the most part, the allografts were supplied sparsely with donor (PVG-RT1C) MHC class I-positive (OX-27) blood vessels clustered in pockets. Donor MHC class I-positive vessels entered the host brain only from allografts in the third ventricle; these vessels were restricted to the host median eminence and no longer immunostained with OX-26 for the transferrin receptor (normally the median eminence is supplied with non-BBB vessels that do not possess the transferrin receptor and do not stain with OX-26). In host brains harboring a third ventricle allograft, host MHC class I-positive vessels immunostained with the U9F4 antibody were evident throughout the host CNS, including the median eminence, and throughout the allografts excluding sites inhabited by donor PVG-RT1C vessels. Cell suspension neural allografts (donor PVG-RT1C) placed within the brain parenchyma of PVG-RT1U hosts revealed no significant differences in vascular contributions between donor and host when compared to results obtained from solid CNS allografts. A unique immunohistochemical approach of introducing ascites fluid OX-27 as the primary antibody intravenously to the PVG-RT1U host demonstrated that in donor PVG-RT1C posterior pituitary allografts, donor and not host vessels predominate and are restricted to the graft. Finally, blood vessels isolated from adult PVG-RT1C brains were mixed with solid fetal PVG-RT1U cortical tissue and grafted into the brain parenchyma of adult PVG-RT1U hosts. Immunostaining with OX-27 antibody against MHC class I of the PVG-RT1C rat strain disclosed that the PVG-RT1C blood vessels survived and were confined to the PVG-RT1U syngeneic graft. The results suggest that blood vessels supplying CNS allografts placed within the host brain are predominantly of host origin; surviving donor vessels are restricted to the allograft with rare exceptions, which may be dictated by the type of neural allograft and the host CNS site receiving the allograft. The survival of isolated allogeneic CNS blood vessels grafted into the host brain suggests that such blood vessels can present an endothelial genotype and phenotype different from those of host vessels indigenous to the CNS site receiving the allogeneic vessel graft. This finding may have implications in the circumvention of the blood-brain fluid barriers for the CNS delivery of blood-borne therapeutics.

Age Factors↗
PubMed1987

Possible prorenin activating mechanisms in the blood vessel wall.

The blood-vessel wall has the potential for activating circulating prorenin by several mechanisms. Prorenin may be taken up by the blood vessel and activated by enzyme(s) localized on the vascular cells. We do not know whether this mechanism is usually operative or is only activated under certain conditions. This local activation system can increase the vascular-wall renin concentration and may be involved with the regulation of local vascular tone and regional blood flow. Circulating blood cells may release enzymes which can activate prorenin. At the inflammatory site, a neutrophil-dependent prorenin activating mechanism may be important for the increased production of angiotensin II which modulates vascular permeability and tone. In addition, at sites of vascular injury where platelets aggregate, prorenin may be activated locally and may play a role in the genesis of vasospasm.

Blood Platelets↗
PubMed1977

Electrophoretic patterns of serum albumins collected from different blood vessels.

Rabbit sera collected from different blood vessels, e.g. vena renales, vena mesenterica, vena portae, vena hepatica and aorta, were electrophoresed in an urea-containing polyacrylamide gel. The albumin fraction was separated into 5-6 sub-bands. The profile of these sub-bands (electrophoretic pattern) of the sample from one blood vessel differed from that of another blood vessel. Especially, the electrophoretic pattern of serum collected from the renal vein 2h after deprivation of food differed from that of other blood vessels. Free fatty acid concentrations of each sample were also measured, and differences in these levels were observed in sera collected from different blood vessels. However, the fatty acid concentrations in serum from the renal vein were not low enough to permit detection of any abnormality in electrophoretic pattern in the albumin. This suggests the possibility of decreased concentration of lysolecithin in the renal vein which binds to albumin and changes the electrophoretic mobility of albumin, as do the free fatty acids.

Animals↗
PubMed1986

[Behavior of the blood vessels of the lung on the roentgen image in children with bronchial asthma--determination of the width of the blood vessels].

On x-ray films of 51 children with asthma bronchiale the authors determined the vascular diameter of the right ascending pulmonary artery, the right vein of the upper lobe, and the peripheral vessels in the upper and lower pulmonary fields at an exactly defined distance from the hilus point, and compared these data with those of a control group of 143 healthy children. During the asthma attack the width of the right descending pulmonary artery and of the vein of the upper lobe corresponded to the values of the control group, whereas the vascular diameters in the upper and lower fields were clearly narrowed. Moreover, in most of the asthmatic children the authors found arc-shaped vessels and irregularly occluded vessels in the periphery of the lungs.

Adolescent↗
PubMed1982

Adrenergic and peptidergic innervation of cochlear blood vessels.

Guinea pig cochlear blood vessels were investigated with regard to their supply of adrenergic and peptidergic nerve fibers. Using the glyoxylic acid histofluorescence technique, numerous adrenergic fibers were seen around the labyrinthine artery, whereas the spiral modiolar artery contained only few such fibers. Immunocytochemistry revealed nerve fibers containing immunoreactive avian pancreatic polypeptide, vasoactive intestinal peptide, substance P, or gastrin-releasing peptide around the labyrinthine and spiral modiolar arteries. Adrenergic or peptidergic nerve fibers were not seen around the blood vessels of the stria vascularis. Upon removal of the superior cervical ganglion, adrenergic fibers disappeared and fibers displaying avian pancreatic polypeptide immunoreactivity were reduced in number. These data suggest co-occurrence of catecholamines and immunoreactive avian pancreatic polypeptide in a population of adrenergic nerves.

Adrenergic Fibers↗
PubMed1998

Gene transfer into normal and atherosclerotic human blood vessels.

Gene transfer to blood vessels is a promising new approach to the treatment of the vascular diseases, but the feasibility of gene transfer to adult human vessels has not been explored. We introduced an adenovirus vector encoding a marker gene human placental alkaline phosphatase into normal and atherosclerotic human vessels in organ culture. In the normal vessels, recombinant gene was expressed preferentially in the endothelial cells (approximately 100%), intimal smooth muscle cells (1.3+/-0.4%, 1.4+/-1.0%, and 3.8+/-0.8% in the internal mammary arteries, saphenous veins, and normal coronary arteries, respectively), and various adventitial cells. Advanced, complicated atherosclerotic plaques demonstrated a similar efficiency of recombinant gene expression (3.1+/-0.5% and 3.8+/-0.3% of nonendothelial intimal cells in the coronary artery and carotid artery plaques, respectively). Of these intimal cells, macrophages and smooth muscle cells expressed a transgene, identifying them as targets for gene transfer. Areas of plaque rupture and thrombus are sites of predilection for expression of recombinant genes. Collagenase and elastase treatment increased the percentage of transgenic alkaline phosphatase-positive cells 7 times (P<0.001), suggesting that the pattern of gene expression was affected by the amount of surrounding extracellular matrix. These studies demonstrate the feasibility of gene transfer to human blood vessels. However, these studies also highlight important barriers to adenoviral gene delivery to the actual normal and atherosclerotic human vessels of clinical interest.

Adenoviridae↗
PubMed1997

Molecular analysis of blood vessel formation and disease.

Blood vessels affect the quality of life in many ways. They provide an essential nutritive function during growth and repair of tissues but, on the other hand, can become affected by disorders or trauma, resulting in bleeding, thrombosis, arterial stenosis, and atherosclerosis. Three molecular systems, the vascular endothelial growth factor (VEGF) system, the plasminogen system, and the coagulation system, have been implicated in the formation and pathobiology of blood vessels. This review focuses on the role of these systems in these processes. Recent gene-targeting studies have identified VEGF as a potent modulator of the formation of endothelial cell-lined channels. Somewhat unanticipated, the initiator of coagulation is not only involved in the control of hemostasis but also in the maturation of a muscular wall around the endothelium. With different murine models of cardiovascular disease, a pleiotropic role of the plasminogen system was elucidated in thrombosis, in arterial neointima formation after vascular wound healing and allograft transplantation, in atherosclerosis, and in the formation of atherosclerotic aneurysms. Surprisingly, tissue-type plasminogen activator is also involved in brain damage after ischemic or neurotoxic insults. The insights from these gene-targeting studies have formed the basis for designing gene therapy strategies for restenosis and thrombosis, which have been successfully tested in these knockout models.

Animals↗
PubMed2006

Ephrin-B2 controls cell motility and adhesion during blood-vessel-wall assembly.

New blood vessels are initially formed through the assembly or sprouting of endothelial cells, but the recruitment of supporting pericytes and vascular smooth muscle cells (mural cells) ensures the formation of a mature and stable vascular network. Defective mural-cell coverage is associated with the poorly organized and leaky vasculature seen in tumors or other human diseases. Here we report that mural cells require ephrin-B2, a ligand for Eph receptor tyrosine kinases, for normal association with small-diameter blood vessels (microvessels). Tissue-specific mutant mice display perinatal lethality; vascular defects in skin, lung, gastrointestinal tract, and kidney glomeruli; and abnormal migration of smooth muscle cells to lymphatic capillaries. Cultured ephrin-B2-deficient smooth muscle cells are defective in spreading, focal-adhesion formation, and polarized migration and show increased motility. Our results indicate that the role of ephrin-B2 and EphB receptors in these processes involves Crk-p130(CAS) signaling and suggest that ephrin-B2 has some cell-cell-contact-independent functions.

Animals↗
PubMed1985

Adrenergic nervous control of resistance and capacitance vessels. Studies on isolated blood vessels from the rat.

A systematic comparison of neurogenic responses from consecutive sections of the cardiovascular system has not yet been performed under the well-defined conditions that an in-vitro system can offer. The present investigation aimed at analysing the neuroeffector properties of different isolated vessels, mounted in a myograph, where isotonic and isometric responses to transmural nerve stimulation could be determined. The vessels investigated were the abdominal aorta and caval vein, the superior mesenteric artery and vein, and 200-micron arteries and corresponding veins from the mesenteric arcades, the latter representing true resistance and capacitance vessels, respectively. Further, the vascular adrenergic innervation was visualized by Hillarp-Falck's formaldehyde fluorescence technique as well as immunohistochemical methods. In all vessels the innervation was confined to the adventitio-medial border. The responses to single neurogenic impulses differed markedly between the vessels, being distinct and rapid in the small, slow in the intermediate vessels, and absent in the aorta and the caval vein. This was in contrast to the responses to direct electrical activation of the muscle, which were quite rapid in all vessels. The organisation of the neuromuscular transmission thus has a marked influence on the effector response. The maximal neurogenic responses parallelled the innervation density, being greatest in the small arteries and least in the abdominal aorta. The frequency for half-maximal response appeared to depend also on other factors, such as velocity of contraction and relaxation of the smooth muscle. Of the small vessels, the veins were relatively more activated by low frequencies. Stimulation with an irregular impulse pattern, derived from human sympathetic nerve discharge, had greater effects than the corresponding constant-frequency stimulation on the resistance arteries; the small veins responded equally to either pattern. This difference could be related to the observed frequency-response relations around the average frequency used. The effects of inhibition of neuronal amine uptake on neurogenic responses and on responses to exogenous noradrenaline differed considerably, particularly in the resistance arteries. Here the magnitude of the neurogenic responses were hardly affected by this inhibition, whereas responses to exogenous noradrenaline were strongly enhanced. On its own, blockade of prejunctional adrenergic alpha 2-receptors had little effect on either response, but blocking both alpha 2-receptors and reuptake clearly potentiated the neurogenic responses.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic Fibers↗
PubMed2001

Changes in gastrointestinal lymph and blood vessels in patients with cirrhotic portal hypertension.

BACKGROUND: The aim of this study was to characterize the lymph vessels in different parts of the gastrointestinal tract and also to evaluate morphometric changes in these vessels during cirrhotic portal hypertension. METHODS: Sixteen patients with cirrhotic portal hypertension and 18 control subjects without portal hypertension were enrolled in the study. Tissue specimens were collected at autopsy or surgery, and were stained enzyme histochemically, using 5'-nucleotidase and alkaline phosphatase to distinguish lymph vessels and blood vessels, respectively. The numbers of vessels and their luminal areas were estimated using computer graphics software (National Institutes of Health [NIH] image program). RESULTS: The numbers and luminal areas of the lymph vessels varied considerably among the different organs of the gastrointestinal tract, both in controls and in the patients with cirrhotic portal hypertension. There was no significant difference in the numbers of lymph vessels between controls and patients with cirrhotic portal hypertension. However, the luminal area of the lymph vessels in the esophagus and stomach was significantly greater in the patients with cirrhotic portal hypertension than in the controls. These differences in lymph vessels were not seen in the small intestine and colon. CONCLUSIONS: These data indicate that dilatation of lymph vessels may be related to the absorption of excess interstitial fluid, resulting from congestion, in cirrhotic portal hypertension.

5'-Nucleotidase↗
PubMed1995

Adenovirus-mediated gene transfer in vivo to cerebral blood vessels and perivascular tissue.

Gene transfer to blood vessels in vivo generally requires interruption of blood flow. Thus, gene transduction to cerebral blood vessels in vivo has not yet been achieved. In this study, we injected replication-deficient adenovirus into cerebrospinal fluid in an attempt to transduce genes to cerebral blood vessels. Recombinant adenovirus (1 x 10(9) infectious units) expressing nuclear-targeted bacterial beta-galactosidase driven by the cytomegalovirus promoter was injected into the cisterna magna of Sprague-Dawley rats. The brains were examined histochemically after staining with 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside 1 to 7 days after injection of adenovirus. Leptomeningeal cells overlying the major arteries were efficiently transduced, and adventitial cells of large vessels and smooth muscle cells of small vessels were occasionally stained. beta-Galactosidase was expressed on days 1 and 3 after injection but was undetectable by day 7. Expression of the gene was 'targeted' by altering the position of the head. When viral suspension was injected while the rat was in a nose-down position, the reporter gene was expressed extensively on the ventral surface of the brain, especially along the circle of Willis. When the position was changed to the nose-up or lateral position, the inferior or lateral region of the brain was stained primarily. Administration of the virus into the lateral ventricle provided extensive expression in ependymal cells and leptomeninges with some transduction to cerebral blood vessels. Thus, adenovirus injected into cerebrospinal fluid provides gene transfer in vivo to cerebral blood vessels and, with greater efficiency, to perivascular tissue. Furthermore, cisternal delivery may target specific brain regions by positioning of the head.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoviridae↗