Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VESSELS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 901 records · Page 50Linked to original sources

Light paths in retinal vessel oxymetry.

The oxygen utilization and, therefore, the metabolic state, of a distinctive area of the retina may be calculated from the diameter of the supplying artery and vein, the haemoglobin oxygenation, and the velocity of the blood. The first two parameters can be determined by imaging spectrometry at the patients ocular fundus. However, the reflected light emerging from a vessel followed different pathways through the ocular fundus layers and the vessel embedded in the retina. The contribution of the single pathways to the vessel reflection profile is investigated by a Monte Carlo simulation. Considering retinal vessels with diameters of 25-200 microm we found the reflection from a thin vessel to be determined by the single and double transmission of light at 560 nm. The backscattering from the blood column determines the reflectance in the case of a thick vessel. However, both components are in the same order of magnitude. This has to be considered in the calculation of the oxygen saturation of blood in retinal vessels from their reflection spectra.

Light↗

Adaptive approach to accurate analysis of small-diameter vessels in cineangiograms.

In coronary vessels smaller than 1 mm in diameter, it is difficult to accurately identify lumen borders using existing border detection techniques. Computer-detected diameters of small coronary vessels are often severely overestimated due to the influence of the imaging system point spread function and the use of an edge operator designed for a broad range of vessel sizes, Computer-detected diameters may be corrected if a calibration curve for the X-ray system is available. Unfortunately, the performance of this postprocessing diameter correction approach is severely limited by the presence of image noise. We report here a new approach that uses a two-stage adaption of edge operator parameters to optimally match the edge operator to the local lumen diameter. In the first stage, approximate lumen diameters are detected using a single edge operator in a half-resolution image. Depending on the approximate lumen size, one of three edge operators is selected for the second full-resolution stage in which left and right coronary borders are simultaneously identified. The method was tested in a set of 72 segments of nine angiographic phantom vessels with diameters ranging from 0.46 to 4.14 mm and in 82 clinical coronary angiograms. Performance of the adaptive simultaneous border detection method was compared to that of a conventional border detection method and to that of a postprocessing diameter correction border detection method. Adaptive border detection yielded significantly improved accuracy in small phantom vessels and across all vessel sizes in comparison to the conventional and postprocessing diameter correction methods (p < 0.001 in all cases). Adaptive simultaneous coronary border detection provides both accurate and robust quantitative analysis of coronary vessels of all sizes.

Algorithms↗

Automatic grading of retinal vessel caliber.

New clinical studies suggest that narrowing of the retinal blood vessels may be an early indicator of cardiovascular diseases. One measure to quantify the severity of retinal arteriolar narrowing is the arteriolar-to-venular diameter ratio (AVR). The manual computation of AVR is a tedious process involving repeated measurements of the diameters of all arterioles and venules in the retinal images by human graders. Consistency and reproducibility are concerns. To facilitate large-scale clinical use in the general population, it is essential to have a precise, efficient and automatic system to compute this AVR. This paper describes a new approach to obtain AVR. The starting points of vessels are detected using a matched Gaussian filter. The detected vessels are traced with the help of a combined Kalman filter and Gaussian filter. A modified Gaussian model that takes into account the central light reflection of arterioles is proposed to describe the vessel profile. The width of a vessel is obtained by data fitting. Experimental results indicate a 97.1% success rate in the identification of vessel starting points, and a 99.2% success rate in the tracking of retinal vessels. The accuracy of the AVR computation is well within the acceptable range of deviation among the human graders, with a mean relative AVR error of 4.4%. The system has interested clinical research groups worldwide and will be tested in clinical studies.

Algorithms↗

Matrix metalloproteinases in blood vessel development in human fetal skin and in cutaneous tumors.

In vitro angiogenesis models suggest that new blood vessel formation requires the induction and secretion by endothelial cells of matrix metalloproteinases. These enzymes assist in the controlled proteolytic degradation of the surrounding extracellular matrix during blood vessel formation. The results of in vitro studies cannot be extrapolated directly to the process of in vivo angiogenesis because the type of matrix employed and the repertoire of enzymes secreted by cells in vivo differ dramatically from in vivo conditions. To investigate the in vivo role of matrix metalloproteinases in blood vessel development, we looked for the presence of these proteinases in endothelial cells involved in fetal angiogenesis and in neovascularization of certain invasive skin tumors using immunofluorescent staining. In fetal tissue, interstitial collagenase was present in both early microvessels developing from undifferentiated mesoderm and in microvessels involved in elongation and sprout formation from preexisting blood vessels. In aggressive skin tumors, i.e., morpheaform and recurrent basal cell carcinomas and squamous cell carcinomas, there was a marked increase in the number of collagenase-containing blood vessels, often extending into the tumor nests. Immunofluorescent staining failed to detect stromelysin, matrilysin, or gelatinase A and B (72- and 92-kDa type IV collagenases, respectively) in fetal or tumor blood vessels. These findings are consistent with the hypothesis that proteolytic degradation of the extracellular matrix is required for the formation of new blood vessels. Interstitial collagenase appears to play an important role in this process.

Adult↗

Role of hematopoietic lineage cells as accessory components in blood vessel formation.

In adults, the vasculature is normally quiescent, due to the dominant influence of endogenous angiogenesis inhibitors over angiogenic stimuli. However, blood vessels in adults retain the capacity for brisk initiation of angiogenesis, the growth of new vessels from pre-existing vessels, during tissue repair and in numerous diseases, including inflammation and cancer. Because of the role of angiogenesis in tumor growth, many new cancer therapies are being conducted against tumor angiogenesis. It is thought that these anti-angiogenic therapies destroy the tumor vessels, thereby depriving the tumor of oxygen and nutrients. Therefore, a better understanding of the molecular mechanisms in the process of sprouting angiogenesis may lead to more effective therapies not only for cancer but also for diseases involving abnormal vasculature. It is widely believed that after birth, endothelial cells (EC) in new blood vessels are derived from resident EC of pre-existing vessels. However, evidence is now emerging that cells derived from the bone marrow may also contribute to postnatal angiogenesis. Most studies have focused initially on the contribution of endothelial progenitor cells in this process. However, we have proposed a concept in which cells of the hematopoietic lineage are mobilized and then entrapped in peripheral tissues, where they function as accessory cells that promote the sprouting of resident EC by releasing angiogenic signals. Most recently we found that hematopoietic cells play major roles in tumor angiogenesis by initiating sprouting angiogenesis and also in maturation of blood vessels in the fibrous cap of tumors. Therefore, manipulating these entrapment signals may offer therapeutic opportunities to stimulate or inhibit angiogenesis.

Angiotensin I↗

Endothelium modulation of the effects of nitroglycerin on blood vessels from dogs with pacing-induced heart failure.

1. The relaxant actions of nitroglycerin (previously considered to be an endothelium-independent relaxing agent) and acetylcholine (an endothelium-dependent relaxing agent) were compared on 4 vascular preparations (dorsal pedal artery, saphenous vein, left anterior descending coronary artery and circumflex coronary artery) from dogs with and without pacing-induced congestive heart failure (CHF). 2. Responses of the coronary arteries to acetylcholine were unaltered in endothelium-intact rings from dogs with and without heart failure. Similarly no such changes were observed in the peripheral vessels. The maximum relaxation produced by acetylcholine was always greater in the coronary vessels compared to the peripheral vessels. 3. Before heart failure, the coronary vessels were more sensitive and reactive to nitroglycerin compared to the peripheral vessels. 4. Removal of the endothelium in both the control (dogs without CHF) and experimental (dogs with CHF) rings enhanced the relaxant effects of nitroglycerin, such that the EC50 for nitroglycerin became significantly lower in all denuded rings, with the exception of the saphenous vein and the left anterior descending coronary artery, before the development of CHF. 5. When CHF was maximally developed, vascular sensitivity to nitroglycerin was increased in peripheral vessels with an intact endothelium, but not in the coronary vessels. 6. These findings indicate that relaxation produced by nitroglycerin cannot be considered as entirely endothelium-independent but should be considered endothelium-modulated.

Acetylcholine↗

Origins and assembly of avian embryonic blood vessels.

Two processes by which embryonic blood vessels develop are well-known: angiogenesis (growth by budding and branching of existing vessels) and local formation of endothelial vesicles that coalesce with elongating vessels. The former process appears to be more prevalent, with the latter restricted to vessels that form near the endoderm-mesoderm interface. The contributions of endothelial cells formed by each of these processes to specific blood vessels has not been defined, however, nor have the origins of precursors (angioblasts) of intraembryonic endothelial populations been established. To identify the origins of endothelial cells, precursor populations from quail embryos were transplanted into chick embryos. Antibodies that recognize quail endothelial cells were applied to sections from chimeric embryos fixed 2-5 days after surgery. These experiments reveal that all intraembryonic mesodermal tissues, except the notochord and prechordal plate, contain angiogenic precursors. Many angioblasts emigrate from the grafted tissue, invading surrounding mesenchyme and contributing to the formation of arteries, veins, and capillaries in a wide area. The invasive behavior of these angioblasts is unlike that of any other embryonic mesenchymal cell type and represents a third process operating during embryonic blood vessel formation. Transplanted angioblasts, even those excised from quail trunk regions, form normal craniofacial vascular channels, including the cardiac outflow tract. These results demonstrate that the control over blood vessel assembly resides within the connective tissue-forming mesenchyme of the embryo, not within endothelial precursors.

Animals↗

Proteinase-activated receptor 2 activation modulates guinea-pig mesenteric lymphatic vessel pacemaker potential and contractile activity.

Lymphatic vessels rhythmically constrict to avoid fluid and protein accumulation in the interstitial space. This activity is critical during inflammation to prevent excessive oedema. Lymphatic pumping is intrinsic to the smooth muscle in the vessel wall and is due to the spontaneous occurrence of action potentials, the pacemaker of which is proposed to be spontaneous transient depolarizations (STDs). This function is highly susceptible to the fluid load and modulated by chemical agents, amongst which inflammatory mediators are important players. Activation of proteinase-activated receptors (PARs) has been involved in inflammation and affects vascular smooth muscle tone. The present study aims to investigate the role of PAR2, a member of the PAR family, in lymphatic vessel pumping. RT-PCR experiments revealed that PAR2 message is present in lymphatic vessels of the guinea-pig mesentery. Agonists of PAR2 such as trypsin and the activating peptide, SLIGRL-NH2, caused a decrease in the contractile activity of intraluminally perfused lymphatic vessels. Moreover, intracellular microelectrode recordings from isolated vessels revealed that PAR2 activation hyperpolarized the lymphatic smooth muscle membrane potential and altered STD amplitude and frequency. The decreases in constriction frequency and STD activity as well as the hyperpolarization were dependent on a functional endothelium, not affected by NO synthase or guanylyl-cyclase inhibition, but mimicked by PGE2 and iloprost and blocked by indomethacin (10 microM) and glibenclamide (1 microM). These results show that PAR2 activation alters guinea-pig lymphatic vessel contractile and electrical activity via the production of endothelium-derived cyclo-oxygenase metabolites.

Animals↗

Remodeling of the constitutive equation while a blood vessel remodels itself under stress.

Changes in the mechanical properties of a blood vessel when it remodels itself under stress are reviewed. One of the recent findings about blood vessels is the rapidity of tissue remodeling when the blood pressure is changed. When the tissue structure and material composition remodel, the zero-stress state of the vessel changes. The mechanical properties change also in the remodeling process. If the elastic behavior is expressed in terms of a pseudo-elastic strain-energy function, then the constants in the function will change in the course of the remodeling. With all these changes taking place, the scope of constitutive equations broadens: it should now include a mass-and-structure growth-stress relationship as well as a stress-strain-relationship. To obtain the mass-and-structure growth-stress relationship, one must be able to determine the mechanical properties of the different layers of the vessel wall, as well as the chemical composition and morphology. For the blood vessels, new methods of mechanical testing must be introduced. A key thought is to use bending of the blood vessel wall. By bending, different layers of the vessel wall are subjected to different stresses, leading to equations that can be used to solve the inverse problem of determining the stress-strain law from measured stress and strain. In vitro and in vivo experiments and theoretical prospectives are presented.

Adaptation, Physiological↗

Heat transfer to blood vessels.

Heat transfer to individual blood vessels has been investigated in three configurations: a single vessel, two vessels in counterflow, and a single vessel near the skin surface. For a single vessel the Graetz number is the controlling parameter. The arterioles, capillaries, and venules have very low Graetz numbers, Gz < 0.4, and act as perfect heat exchangers in which the blood quickly reaches the tissue temperature. The large arteries and veins with Graetz numbers over 10(3) have virtually no heat exchange with the tissue, and blood leaves them at near the entering temperature. Heat transfer between parallel vessels in counterflow is influenced most strongly by the relative distance of separation anad by the mass transferred from the artery to the vein along the length. These two effects are of the same order of magnitude, whereas the film coefficients in the blood flow are of significant but lesser importance. The effect of a blood vessel on the temperature distribution of the skin directly above it and on the heat transfer to the environment increases with decreasing depth-to-radius ratio and decreasing Biot number based on radius. The absolute magnitude of these effects is independent of other linear effects, such as internal heat generation or a superimposed one-dimensional heat flux.

Arteries↗

Distribution of lymphatic vessels in normal and arthritic human synovial tissues.

OBJECTIVES: To investigate the distribution of lymphatic vessels in normal, rheumatoid arthritis (RA) and osteoarthritis (OA) synovium. METHODS: Synovial tissues from 5 normal controls, 14 patients with RA, and 16 patients with OA were studied. Lymphatic vessels were identified by immunohistochemistry using antibodies directed against the lymphatic endothelial hyaluronan receptor (LYVE-1) and recognised blood vessel endothelial markers (factor VIII, CD34, CD31). RESULTS: Lymphatic vessels were found in all zones of the normal, OA, and RA synovial membrane. Few lymphatic vessels were seen in the sublining zone in normal and OA synovium which did not show villous hypertrophy. However, in both RA synovium and OA synovium showing villous hypertrophy and a chronic inflammatory cell infiltrate, numerous lymphatic vessels were seen in all zones of the synovial membrane, including the sublining zone of the superficial subintima. CONCLUSIONS: Lymphatic vessels are present in normal and arthritic synovial tissues and are more numerous and prominent where there is oedema and an increase in inflammatory cells in the subintima, particularly in RA. This may reflect increased transport of hyaluronan and leucocyte trafficking in inflamed synovial tissues.

Arthritis, Rheumatoid↗

Flow and pressure distributions in vascular networks consisting of distensible vessels.

We examine the influence of vessel distensibility on the fraction of the total network flow passing through each vessel of a model vascular network. An exact computational methodology is developed yielding an analytic proof. For a class of structurally heterogeneous asymmetric vascular networks, if all the individual vessels share a common distensibility relation when the total network flow is changed, this methodology proves that each vessel will continue to receive the same fraction of the total network flow. This constant flow partitioning occurs despite a redistribution of pressures, which may result in a decrease in the diameter of one and an increase in the diameter of the other of two vessels having a common diameter at a common pressure. This theoretical observation, taken along with published experimental observations on pulmonary vessel distensibilities, suggests that vessel diameter-independent distensibility in the pulmonary vasculature may be an evolutionary adaptation for preserving the spatial distribution of pulmonary blood flow in the face of large variations in cardiac output.

Algorithms↗

Significance of vessel size and type in vascular heat transfer.

This study was undertaken to gain a better understanding of the fundamental mechanisms of micro- and macrovascular heat transfer by experimentally identifying those vessels most important in the process. Tissue temperature fields around thermally nonequilibrated vessels were determined using a small temperature sensor that was guided through the rabbit thigh to generate a detailed temperature map. The measurements revealed that the lower limit of vessel size for thermal nonequilibration was 100 microns for arteries and 400 microns for veins. Local temperature fields were found around four of the five (80%) arteries that were greater than 300 microns in diameter but in only 3 of the 12 (25%) veins greater than 400 microns. These experimental results are in good agreement with previously published theoretical studies (5) in which it was concluded that thermal equilibration in the branching countercurrent vascular network of the rabbit limb occurs in vessels an order of magnitude larger than the capillaries. In those studies the smallest vessels capable of carrying heat were predicted to be 50 microns ID with the major blood tissue heat exchange occurring in vessels greater than 100 micron ID. These findings contrast with the view that most heat transfer occurs in the capillaries and suggest that vascular heat transfer analysis must take into account the vascular architecture of the 50- to 1,000-micron vessels where most heat transfer occurs.

Animals↗

A distensible vessel model applied to hypoxic pulmonary vasoconstriction in the neonatal pig.

Recently, we presented a simple two-parameter distensible vessel model as a potential tool for characterizing pulmonary vascular pressure vs. flow curves under zone 3 conditions (Linehan et al. J. Appl. Physiol. 73: 987-994, 1992). One parameter, alpha, represents the distensibility of the resistance vessels as the fractional change in vessel diameter per Torr change in pressure, and the other parameter, R0, represents the vascular resistance that would exist if the resistance vessels were at their respective diameters obtained if the vascular pressure were zero. The objective of the present study was to determine whether this distensible vessel model was capable of describing the pressure vs. flow data obtained during hypoxia vasoconstriction and under control conditions in isolated lungs from neonatal pigs. The piglet lungs were perfused with autologous blood, and the pulmonary arterial pressure was measured over a range of flow rates from 15 to 250 ml.min-1 x kg-1 at constant left atrial (3 Torr) pressure. The model provided a reasonable fit to the data under both conditions. Hypoxia resulted in a significant increase in R0, from 0.39 +/- 0.10 Torr.ml-1 x min.kg during control conditions to 1.41 +/- 0.46 Torr.ml-1 x min.kg during hypoxia. alpha was 2.4 +/- 0.4%/Torr under control conditions and 2.0 +/- 0.4%/Torr during hypoxia, but this difference was not statistically significant. The results suggest that the distensible vessel model may be useful for interpreting pressure-flow data in terms of changes in geometry and distensibility of the resistance vessels in response to a vasoconstrictor stimulus such as hypoxia.

Animals↗

Enhanced susceptibility of irradiated tumor vessels to vascular endothelial growth factor receptor tyrosine kinase inhibition.

Previous experiments with PTK787/ZK222584, a specific inhibitor of vascular endothelial growth factor receptor (VEGFR) tyrosine kinases, using irradiated human FaDu squamous cell carcinoma in nude mice, suggested that radiation-damaged tumor vessels are more sensitive to VEGFR inhibition. To test this hypothesis, the tumor transplantation site (i.e., the right hind leg of nude mice) was irradiated 10 days before transplantation of FaDu to induce radiation damage in the host tissue. FaDu tumors vascularized by radiation-damaged blood vessels appeared later, grew at a slower rate, and showed more necrosis and a smaller vessel area per central tumor section than controls. PTK787/ZK222584 at a daily dose of 50 mg/kg body weight had no impact on growth of control tumors. In contrast, tumors vascularized by radiation-damaged vessels responded to PTK787/ZK222584 with longer latency and slower growth rate than controls, and a trend toward further increase in necrosis, indicating that irradiated tumor vessels are more susceptible to VEGFR inhibition than unirradiated vessels. Although not proving causality, expression analysis of VEGF and VEGFR2 shows that enhanced sensitivity of irradiated vessels to a specific inhibitor of VEGFR tyrosine kinases correlates with increased expression of the molecular target.

Animals↗

Does the source of laser energy influence the coagulation of chorionic plate vessels? Comparison of Nd:YAG and diode laser on an ex vivo placental model.

OBJECTIVES: To compare the histological effects of diode and Neodymium-Yttrium Aluminium Garnet (Nd:YAG) laser coagulation of chorionic plate vessels. METHODS: In selected chorionic plate vessels in an ex vivo term placenta perfused with warm saline solution, diode (wavelength 940 nm) and Nd:YAG (wave length 1,064 nm) laser were used with an output of 30, 40, and 50 W, and 55 and 70 W respectively using preset energy and duration of impact. All vessels were examined histologically blindly to the procedures' characteristics. RESULTS: A total of 23 vessels were coagulated. Similar histological lesions were observed using diode and Nd:YAG lasers. The lesions were compatible with an acceptable clinical effect at all power outputs tested. The results were not related to the diameter or type of vessels. Lesions of the endothelium and reduction of the vessel lumen were best achieved with a diode laser at 40 W. CONCLUSION: Nd:YAG and Diode laser induce significant and comparable changes in chorionic plate vessels compatible with an efficient coagulation process under the experimental condition used.

Aluminum↗

Three-dimensional black-blood cardiac magnetic resonance coronary vessel wall imaging detects positive arterial remodeling in patients with nonsignificant coronary artery disease.

BACKGROUND: Direct noninvasive visualization of the coronary vessel wall may enhance risk stratification by quantifying subclinical coronary atherosclerotic plaque burden. We sought to evaluate high-resolution black-blood 3D cardiovascular magnetic resonance (CMR) imaging for in vivo visualization of the proximal coronary artery vessel wall. METHODS AND RESULTS: Twelve adult subjects, including 6 clinically healthy subjects and 6 patients with nonsignificant coronary artery disease (10% to 50% x-ray angiographic diameter reduction) were studied with the use of a commercial 1.5 Tesla CMR scanner. Free-breathing 3D coronary vessel wall imaging was performed along the major axis of the right coronary artery with isotropic spatial resolution (1.0x1.0x1.0 mm(3)) with the use of a black-blood spiral image acquisition. The proximal vessel wall thickness and luminal diameter were objectively determined with an automated edge detection tool. The 3D CMR vessel wall scans allowed for visualization of the contiguous proximal right coronary artery in all subjects. Both mean vessel wall thickness (1.7+/-0.3 versus 1.0+/-0.2 mm) and wall area (25.4+/-6.9 versus 11.5+/-5.2 mm(2)) were significantly increased in the patients compared with the healthy subjects (both P<0.01). The lumen diameter (3.6+/-0.7 versus 3.4+/-0.5 mm, P=0.47) and lumen area (8.9+/-3.4 versus 7.9+/-3.5 mm(2), P=0.47) were similar in both groups. CONCLUSIONS: Free-breathing 3D black-blood coronary CMR with isotropic resolution identified an increased coronary vessel wall thickness with preservation of lumen size in patients with nonsignificant coronary artery disease, consistent with a "Glagov-type" outward arterial remodeling. This novel approach has the potential to quantify subclinical disease.

Adult↗

Investigation of coronary vessels in microscopic dimensions by two- and three-dimensional NMR microscopic imaging in the isolated rat heart. Visualization of vasoactive effects of endothelin 1.

BACKGROUND: Nuclear magnetic resonance (NMR) imaging of macroscopic coronary vessels is rapidly advancing, whereas little attention has focused on development of NMR techniques for investigation of coronary microvessels. Such techniques would be of particular importance, since conventional methods to visualize coronary microvessels have specific limitations. The aim of our study was to develop two- and three-dimensional (2D and 3D) high-resolution imaging of coronary microvessels. Quantitative analysis of vessel size was performed in tomograms and applied to evaluate the vasoconstrictor effect of endothelin 1. METHODS AND RESULTS: Angiographic imaging was performed on an 11.75-T magnet by 2D and 3D gradient-echo pulse sequences. In tomograms, the validity of this method in providing correct vessel size was tested by phantom experiments. Experiments were carried out in the isolated constant-pressure-perfused rat heart with continuous registration of coronary flow and left ventricular pressure. NMR pulse sequences were pressure-triggered in mid diastole. Four groups of hearts were studied. In group 1 (n = 20), 2D imaging perpendicular and parallel to the long axis of the heart was performed. Cross sections of vessels with diameter > 140 microns were clearly detectable. In group 2 (control, n = 5) and group 3 (n = 13), tomograms perpendicular to the long axis were obtained before and after administration of vehicle (group 2) and 200 pmol endothelin 1 bolus (group 3). Vehicle had no effect on vessel cross section. Endothelin 1, which decreased global coronary flow by 47%, reduced vessel cross section by 38 +/- 19%. A weak but, on average, significant inverse correlation between area of cross section and vessel size was found. In group 4 (n = 10), 3D imaging was performed in 7 normal hearts and 3 hearts with anterior myocardial infarction. A 3D image of the entire coronary artery tree was obtained, revealing excellent agreement with anatomic studies. In infarcted rat hearts, occlusion of the left coronary artery was demonstrated. CONCLUSIONS: Visualization and quantification of coronary microvessels are feasible by NMR microscopy. NMR microscopy bears the potential of becoming a powerful tool for the investigation of the coronary microcirculation.

Animals↗