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Dissertations / Theses on the topic 'Arteries'
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1
Bass, David Hyman. "Infra-inguinal arterial bypass procedures at Groote Schuur Hospital, 1977-1983 : analysis and evaluation of results." Master's thesis, University of Cape Town, 1987. http://hdl.handle.net/11427/26248.
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Infra-inguinal arterial bypass is becoming increasingly popular as a means of alleviating incapacitating symptoms of atherosclerosis and other progressive diseases affecting the arteries of the lower limb. The role of this procedure in limb salvage is controversial but an aggressive attitude is emerging from many centres. It is accepted that the majority of atherosclerotic patients have a short life expectancy but reconstructive vascular surgery has an important role to play in improving their quality of life. Progress in infra-inguinal bypass surgery has centred mainly on the development of synthetic grafts but the perfonnance of autologous saphenous vein has not been bettered in terms of longterm results and cost-effectivity. The initial experience of infra-inguinal bypass at Groote Schuur Hospital, Cape Town, is examined retrospectively with the objective of demonstrating the possible influence of patient factors and specific surgical practices on the outcome of results.
2
Peng, Siwei. "Medin Amyloid in Human Arteries and its Association with Arterial Diseases." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis (AUU) : Universitetsbiblioteket [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6700.
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Daly, Chris D. "Artificial arteries and bioreactors /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19028.pdf.
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Evans, Richard James. "Neuronal control mesenteric arteries." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279879.
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Fan, Jinwu. "Dynamic Strength of Porcine Arteries." Thesis, Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/19853.
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The failure behavior of collagenous soft tissues is important for clinical problems of plaque rupture and trauma. Cyclic tests require high frequencies that may affect the strength properties of the soft tissues. Experimental results of mechanical response of blood vessels to physiologic loads can be used to model and predict plaque rupture and direct medical therapy or surgical intervention. The goal of the study is to measure the mechanical failure properties of arteries to determine if they are strain rate and cycle dependant and to measure the progressive damage of arteries with time dependent loading.
Ring specimens of porcine carotid arteries were preconditioned and then pulled to failure. In all cases, the intima broke first. Ultimate stress increased as a weak function of increasing strain rates. The ultimate stress at 100 mm/s was 4.54 MPa, greater than the 3.26 MPa at 0.1 mm/s. Strain rates between 1 and 100 mm/s correspond to a cyclic frequency of 0.5 Hz to 5 Hz for fatigue testing. In contrast, ultimate strain in arteries was independent of strain rate over the range tested. The creep tests showed a logarithmic relationship between stress magnitude and stress duration for this soft tissue. The creep testing indicates that damage is accumulating above certain threshold stress levels. The values of ultimate strength showed a 35% increase after 10,000 cycling loading. In contrast, the ultimate strain had a 13% decrease after cycling and the difference was statistically significant with p=0.018. The testing results showed that there were no significant differences on strength among fresh arteries and arteries stored at 5¡ã C for up to two weeks.
The test results may be useful for developing a mathematical model to predict the behavior of arterial soft tissues and may be extended to estimate fracture and fatigue in the atherosclerotic plaque cap.
6
Chen, Changyi. "Intimal hyperplasia in endarterectomized arteries." Diss., Georgia Institute of Technology, 1996. http://hdl.handle.net/1853/25393.
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Priest, Rachel Michelle. "Vasorelaxant mechanism in pulmonary arteries." Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243439.
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Gammack, D. "Blood flow in twisted arteries." Thesis, University of Surrey, 1998. http://epubs.surrey.ac.uk/844008/.
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The motivation for this research into flow in pipes with non-uniform geometry comes from physiological flows. It is now widely believed that haemodynamics plays an important role in the initiation and development of atherosclerosis. Experiments have shown that the preferred sites for atherogenesis are regions of low wall shear stress. The build-up of atherosclerotic plaques in the coronary arteries can lead to arterial blockage and coronary failure. Previous studies have examined uniformly curved pipes and, more recently, uniformly curved and twisted pipes. However, it is well known that the arterial system displays non-uniform, time-dependent geometry. The main objective of this thesis is to describe flow in various pipes with weakly non-uniform curvature and torsion, with a view to understanding the resulting wall shear stress distribution and velocity profiles. The work herein models the flow of an incompressible Newtonian fluid through a pipe whose curvature and torsion vary along the pipe. The governing equations are first derived, then solved for both steady and oscillatory pressure gradients. The solution of these equations involves asymptotic and numerical techniques. The effects due to the non-uniform geometry and possible applications to physiology are discussed. Finally, the effects of torsion upon fluid motion are studied from the Lagrangian viewpoint, using numerical particle tracking.
9
Andreeva, V. S. "Arteries of the barrelled part." Thesis, Sumy State University, 2017. http://essuir.sumdu.edu.ua/handle/123456789/53936.
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Introduction. As well as all the mammals investigated earlier, in some sites of a trunk of a brain of the person have a combination rectilinear and a setevidny form in distribution of arterial vessels. Work purpose. To investigate a structure of internal arteries of a barreled part of a brain of the person.
10
Shubat, Pamela Jane. "Monocrotaline toxicity and pulmonary arteries." Diss., The University of Arizona, 1988. http://hdl.handle.net/10150/184533.
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Monocrotaline is a pyrrolizidine alkaloid found in plants implicated in livestock and human poisoning. Laboratory rats given monocrotaline develop pulmonary hypertension and right heart hypertrophy in the weeks following administration of the chemical. Lung weight increases and right heart hypertrophy correlate with increased pulmonary artery pressure. Rats which consumed monocrotaline drinking water (20 mg/l) for only 4 days developed significant increases in lung and heart weights 14 days after exposure began. This exposure was equivalent to a dose of 15 mg/kg. Other treatment combinations of time (0-10 days exposure) and monocrotaline concentration (5-60 mg/l in drinking water) were tested. The accumulative dose calculated for each of the treatment combinations which produced toxicity was in the range of 15 to 20 mg/kg. Monocrotaline injury appears to be cumulative, but organ weight increases reverse once exposure is stopped. As pulmonary hypertension develops and pulmonary arteries hypertrophy, the force with which isolated pulmonary artery segments contract decreases. This is a loss of efficacy rather than potency to the contracting agents KCl, norepinephrine, and 5-hydroxytryptamine. Relaxation of arteries under conditions of potassium-return (a measure of Na⁺/K⁺ ATPase activity) was also altered by monocrotaline treatment. In vivo monocrotaline treatment had little effect on the force of K⁺-return relaxation. However, the rate at which arteries relaxed was significantly decreased following 4 days ingestion of monocrotaline drinking water (20 mg/l). In vitro ouabain treatment and endothelial injury also decreased the rate of K⁺-return relaxation. Another Na⁺/K⁺ ATPase activity, ⁸⁶Rb⁺ uptake, was decreased following monocrotaline treatment only when 5-hydroxytryptamine was present and only uptake associated with the endothelium was affected. These studies utilized a very low exposure to monocrotaline (4 days ingestion of 20 mg/l monocrotaline drinking water or 15 mg/kg) to produce toxicity in rats. Monocrotaline-induced toxicity measured 20 days after treatment included right heart and lung hypertrophy and decreased contractions of isolated pulmonary arteries. Monocrotaline treatment decreased the rate of Na⁺/K⁺ ATPase-dependent relaxation of isolated pulmonary arteries 4 days after treatment began.
11
Gilpin, Crystal Marie. "Cyclic Loading of Porcine Coronary Arteries." Thesis, Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/6912.
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Atherosclerotic plaque caps are composed of a composite soft tissue material
that becomes subjected to cyclic loading under stenotic flow conditions.
The cyclic loading causes the plaque cap to fatigue and eventually fail. The
hypothesis of this work is that arteries and plaque caps may fatigue which may
be predicted by a stress vs. number of cycles (S-N) curve. The S-N curve has not
been determined for almost any biological soft tissue. The Specific Aim of the
thesis is to quantify an S-N curve for normal arterial soft tissue collected from
cyclic tension testing. Coronary arteries from porcine hearts will be tested as a
material that closely models the plaque cap in non-linear elastic behavior. The
S-N curve will be developed through failure testing with multiple cycles at
stresses between 0.5 and 5 MPa.
12
Donnelly, Patrick Martin. "Computed tomography of the coronary arteries." Thesis, Queen's University Belfast, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446135.
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Cartwright, Virginia Lucille, and n/a. "Biomechanical properties of arteries and veins." University of Otago. Department of Physics, 2005. http://adt.otago.ac.nz./public/adt-NZDU20060908.145011.
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Saphenous veins are widely used as graft material in coronary artery bypass surgery. Biomechanical testing may help identify veins with the optimum chance of longevity. In this thesis, the author has constructed an experimental apparatus to measure circumferential and axial stress-strain data for such arteries and veins. Three different experimental techniques were used to obtain the dimensions of the vessels during pressure-diameter tests; the traditional method of photographic and direct measurement of the external dimensions along with the assumption of incompressibility to approximate inner dimensions; second the use of intravascular ultrasound to obtain the inner and outer dimensions of the vessels; and third the use of intravascular ultrasound for internal dimensions and photography for the outer dimensions.
Three forms of mathematical expression were fitted to the circumferential and axial stress-strain data. The sensitivity of the resulting material parameters was investigated with regard to conversion and reference data variations, and data from repeated experiments, experiments fitting more than one axial strain, and experiments testing the variation in elastic properties were compared.
The combination of the ultrasound experimental technique and exponential form of mathematical expression was found to be the most robust. Using this combination, a significant difference between material parameters of pig arteries and human saphenous veins was found . While the data indicate that material parameters of healthy and diseased veins may also differ significantly, the number of healthy veins in this study was not sufficient to be conclusive.
14
Song, Ying Ching. "Cryopreservation of arteries with dimethyl sulphoxide." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315284.
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Juan, Alba de [Verfasser], and Christoph [Akademischer Betreuer] Scheiermann. "Sympathetic innervation of arteries drives rhythmic leukocyte adhesion to arteries and veins / Alba de Juan ; Betreuer: Christoph Scheiermann." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1192215338/34.
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Zhang, Rui. "Vasoactive effects of lysophosphatidylcholine in small arteries." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/7702.
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Lysophosphatidylcholine (1-acyl-sn-glycero-3-phosphocholine, LPC) is the most abundant glycerol-based lysophospholipid present in cell membranes and oxidized lipoproteins. It has been proposed that LPC contributes to the altered vaso-reactivity associated with various cardiovascular diseases in which elevated LPC levels were identified. However, the contribution of LPC in regulating vascular resistance has not been completely elucidated, as the majority of previous studies have used either large blood vessels or isolated cells. Therefore, our study aimed to investigate the vasoactive effects and the underlying mechanisms of LPC in small arteries/arterioles that are crucial in the determination of vascular resistance and the maintenance of organ function.
The unique finding of our investigation is that LPC possesses biphasic effects on both peripheral arterial resistance and coronary circulation, and even ventricular function. Specifically, in the isolated perfused rat mesenteric arterial bed, both endothelium-derived relaxing factors and thromboxane A₂ (TxA₂, a vasoconstricor) are diminished by LPC perfusion. However, LPC washout stimulates a rebound overproduction of TxA₂, which results in an enhanced contractile response to alpha1-adrenoceptor stimulation.
Our study next found that sustained perfusion of hearts with LPC augmented coronary perfusion pressure and reduced left ventricular developed pressure. These effects were exaggerated when LPC was removed from the perfusate. Furthermore, LPC selectively potentiated the receptor-coupled vasoconstrictor response of isolated rat septal coronary artery to U-46619, a TxA₂ mimetic. Interestingly, when LPC was washed out, the potentiation to U-46619 was even more pronounced. Both the immediate and residual effects of LPC were endothelium-dependent. Endothelium-derived hyperpolarizing factor was likely the sole mediator responsible for the direct effects of LPC on U-46619-vasoconstriction, whereas the augmented vasoconstrictor responses following LPC washout may in part be related to an increase in endothelin-1, and a striking reduction in the bioavailability of nitric oxide.
Our data suggest that simply reducing LPC levels to normal may not be sufficient to reverse the adverse consequences of this lysolipid accumulation in vasculature. Further understanding of the residual effects of LPC will enable the identification of more effective treatment targets for LPC-related diseases.
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Ingrassia, Chris. "Segmentation and tracking of the coronary arteries." Honors in the Major Thesis, University of Central Florida, 1998. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/35.
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This item is only available in print in the UCF Libraries. If this is your Honors Thesis, you can help us make it available online for use by researchers around the world by following the instructions on the distribution consent form at http://library.ucf.edu/Systems/DigitalInitiatives/DigitalCollections/InternetDistributionConsentAgreementForm.pdf You may also contact the project coordinator, Kerri Bottorff, at kerri.bottorff@ucf.edu for more information.Bachelors
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18
Khabbaza, Elias Joseph. "Regulation of contraction in porcine coronary arteries /." The Ohio State University, 1987. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487325740717536.
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Pugliese, Francesca. "Multi-slice computed tomography of coronary arteries." [S.l. : Rotterdam : The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/13655.
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Saur, Stefan. "Quantitative assessment of atherosclerosis in coronary arteries." Konstanz Hartung-Gorre, 2009. http://d-nb.info/997605278/04.
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Alberding, Jonathan Paul. "Nonsteady pressure affects large arteries and endothelium." Diss., The University of Arizona, 2004. http://hdl.handle.net/10150/280582.
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Convective fluid motion through artery walls aids in transvascular transport of macromolecules. Although measurements of convective filtration have been reported, they were all obtained under constant transmural pressure. However, arterial pressure in vivo is pulsatile. Therefore experiments were designed to compare filtration under steady and pulsatile pressure conditions. Hydraulic conductance was measured in cannulated excised rabbit carotid arteries at steady pressure. Next, pulsatile pressure trains were applied within the same vessels, and simultaneously, arterial distension was monitored using Optical Coherence Tomography (OCT). For each pulse train, the volume of fluid lost through filtration was measured (subtracting volume change due to residual distension), and compared to that predicted from steady pressure measurements. In order to determine the role of the endothelium in this response, and the effect of increasing pulsatile frequency from an initial value, one of each pair was de-endothelialized in some cases, and in other experiments a pulsatile pressure of 1 Hz was initially applied, followed by a pulsatile frequency of 2 Hz. In all cases the experimental filtration volumes were significantly increased compared to those predicted for steady pressure, but over time, the magnitude of the excess fluid loss was reduced. For de-endothelialized vessels, this reduction was not so marked. These studies suggest that changes in arterial pulsatility may transiently increase convective flux of macromolecules into the artery wall and that this is regulated by the endothelium. In a parallel study, Bovine Aortic Endothelial Cells (BAEC) were exposed to a transient pressure gradient and then held at 20 mmHg for ten or thirty minutes. After staining for actin fibers and/or catenin, the cells were examined using a deconvolution microscope. The location of actin fibers changed from the body of the cell (central fibers) to the edges of the cell (peripheral fibers), and beta-catenin increased around the periphery. This result indicates that cultured endothelial cells can sense a change in transcellular pressures and respond so as to maintain cell-to-cell adhesion. Overall, the observed responses of arteries and endothelial cells to transient pressure gradients in these studies suggest a dynamic role for the endothelium in regulating transvascular transport in vivo.
22
Gade, Jan-Lucas. "Mechanical Properties of Arteries : Identification and Application." Licentiate thesis, Linköpings universitet, Mekanik och hållfasthetslära, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-159942.
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In this Licentiate of Engineering thesis, a method is proposed that identifies the mechanical properties of arteries in vivo. The mechanical properties of an artery are linked to the development of cardiovascular diseases. The possibility to identify the mechanical properties of an artery inside the human body could, thus, facilitate disease diagnostization, treatment and monitoring. Supplied with information obtainable in the clinic, typically limited to time- resolved pressure-radius measurement pairs, the proposed in vivo parameter identi- fication method calculates six representative parameters by solving a minimization problem. The artery is treated as a homogeneous, incompressible, residual stress- free, thin-walled tube consisting of an elastin dominated matrix with embedded collagen fibers referred to as the constitutive membrane model. To validate the in vivo parameter identification method, in silico arteries in the form of finite element models are created using published data for the human abdominal aorta. With these in silico arteries which serve as mock experiments with pre-defined material parameters and boundary conditions, in vivo-like pressure-radius data sets are generated. The mechanical properties of the in silico arteries are then determined using the proposed parameter identification method. By comparing the identified and the pre-defined parameters, the identification method is quantitatively validated. The parameters for the radius of the stress-free state and the material constant associated with elastin show high agreement in case of healthy arteries. Larger differences are obtained for the material constants associated with collagen, and the largest discrepancy occurs for the in situ axial prestretch. For arteries with a pathologically small elastin content, incorrect parameters are identified but the presence of a diseased artery is revealed by the parameter identification method. Furthermore, the identified parameters are used in the constitutive membrane model to predict the stress state of the artery in question. The stress state is thereby decomposed into an isotropic and an anisotropic component which are primarily associated with the elastin dominated matrix and the collagen fibers, respectively. In order to assess the accuracy of the predicted stress, it is compared to the known stress state of the in silico arteries. The comparison of the predicted and the in silico decomposed stress states show a close agreement for arteries exhibiting a low transmural stress gradient. With increasing transmural stress gradient the agreement deteriorates. The proposed in vivo parameter identification method is capable of identifying adequate parameters and predicting the decomposed stress state reasonably well for healthy human abdominal aortas from in vivo-like data.In diesem Lizentiat der Ingenieurwissenschaften wird eine Methode zur Identifikation der mechanischen Eigenschaften von Arterien in vivo vorgestellt. Die mechanischen Eigenschaften einer Arterie sind mit der Ausbildung kardiovaskulärer Krankheiten verknüpft und deren Identifikation hat daher das Potenzial die Diagnose, die Behandlung und die Überwachung dieser Krankheiten zu verbessern. Basierend auf klinisch möglichen Messungen, die üblicherweise auf ein zeitaufgelöstes Druck-Radiussignal limitiert sind, werden sechs repräsentative Parameter durch Lösen eines Minimierungsproblems berechnet. Die sechs Parameter sind dabei die Eingangsparameter des zur Hilfe gezogenen konstitutiven Schalenmodells welches eine Arterie als eine homogene, inkompressible, restspannungsfreie und dünnwandige Röhre beschreibt. Weiterhin wird angenommen, dass die Arterienwand aus einer elastindominierten Matrix mit eingebetteten Kollagenfasern besteht. Um die in vivo Parameteridentifikationsmethode zu validieren, werden in silico Arterien in Form von Finite Elemente Modellen erstellt. Diese in silico Arterien beruhen auf publizierten Materialparametern der menschlichen Abdominalaorta und dienen als Pseudoexperimente mit vordefinierten mechanischen Eigenschaften und Randbedingungen. Mit diesen Arterien werden in vivo-ähnliche Druck-Radiussignale erstellt und anschliesend werden ihre mechanischen Eigenschaften mit Hilfe der Parameteridentifikationsmethode bestimmt. Der Vergleich der identifizierten und der vordefinierten Parameter ermöglicht die quantitative Validierung der Methode. Die Parameter des spannungsfreien Radius und der Materialkonstanten für Elastin weisen hohe Übereinstummung im Falle gesunder Arterien auf. Die Abweichung der Materialkonstanten für Kollagen sind etwas gröser und der gröste Unterschied tritt beim axialen in situ Stretch auf. Für Arterien mit einem pathologisch geringen Elastinbestandteil werden falsche Parameter identifiziert, wobei die Parameteridentifikationsmethode eine krankhafte Arterie offenlegt. Weiterhin werden mit Hilfe der identifizierten Parameter und des konstitutiven Schalenmodells der Spannungszustand in der Arterienwand berechnet. Dieser ist dabei aufgeteilt in einen isotropen und einen anisotropen Anteil. Der isotrope Anteil wird mit der elastindomierten Matrix und der anisotrope Anteil mit den Kollagenfasern verknüpft. Um die Genauigkeit des berechneten Spannungszustandes beurteilen zu können, wird dieser mit dem Zustand in den in silico Arterien verglichen. Im Fall von Arterien, die einen geringen transmuralen Spannungsgradienten aufweisen, entspricht der berechnete Spannungszustand dem in silico Zustand. Mit zunehmendem transmuralen Spannungsgradienten lässt die Übereinstimmung nach. Für die gesunde menschliche Abdominalaorta ist die entwickelte in vivo Parameteridentifikationsmethode in der Lage, basierend auf in vivo-ähnlichen Messsignalen, adäquate Parameter zu identifizieren und einen zufriedenstellenden Spannungszustand zu berechnen.
I denna licentiatavhandling föreslås en metod för att identifiera mekaniska egenskaper hos artärer in vivo. De mekaniska egenskaperna är kopplade till utvecklingen av hjärt-kärlsjukdomar, och möjligheten att identifiera dessa egenskaper skulle således kunna underlätta diagnostisering, behandling och uppföljning av dessa sjukdomar. Den förslagna metoden använder kliniskt mätbara tryck-radie-signaler och löser ett minimeringsproblem för att bestämma sex parametrar som beskriver kärlets mekaniska egenskaper. Artären modelleras som ett homogent, inkompressibelt och spänningsfritt tunnväggigt rör där kärlväggen utgörs av en elastindominerad matris armerad med inbäddade kollagenfibrer. För att validera parameteridentifieringen skapas en uppsättning representativa, virtuella artärer med hjälp av finita element. Dessa in silico-artärer baseras på publicerade data för mänsklig bukaorta och används för att generera fiktiva tryckradie-signaler vilka sedan matas in i den förslagna modellen. Genom att parametrar och randvillkor för in silico-artärerna är kända fungerar dessa som en kontroll mot vilka resultatet från parameteridentifieringen kan jämföras. Parametrarna som beskriver den icke trycksatta radien och den elastindominerade matrisen visar god överensstämmelse med de in silico-artärerna för friska kärl. Större diskrepans erhålls för de parametrar som associeras med kollagenet, och den största avvikelsen erhålls för den parameter som beskriver den axiella försträckningen. För artärer med patologiskt lågt elastininnehåll identifieras felaktiga parametrar, men resultatet avslöjar ändå tydligt en sjuk artär. De identifierade parametrarna har också använts för att jämföra spänningstillst åndet i membranmodellen och in silico-artäreren. Spänningstillståndet har delats upp i en isotrop och en anisotrop komponent svarande mot, i huvudsak, den elastindominerade matrisen samt kollagenfibrerna. Resultatet visar en mycket god överensstämmelse för bägge komponenterna hos in silico-artärer med låg spänningsgradient genom väggen. Med ökande spänningsgradient försämras dock överensstämmelsen. Resultatet visar att den förslagna metoden är kapabel att identifiera adekvata parametrar och att förutsäga spänningskomponenterna i en frisk aorta.
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Lewis, M. H. "Peripheral arterial disease from aetiology to surgical management." Thesis, University of South Wales, 2013. https://pure.southwales.ac.uk/en/studentthesis/peripheral-arterial-disease-from-aetiology-to-surgical-management(7defd31a-6995-4fc7-9302-2fced42b5982).html.
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The work presented includes over thirty peer reviewed published manuscripts based on studies undertaken during my surgical career. As Principal Investigator, I led the study conception/design/data acquisition/analysis/interpretation and was involved with writing the final drafts of all manuscripts prior to their formal submission to high impact factor peer-reviewed specialist journals. The thesis is divided into subsections reflecting my development and different interests within surgery. The subsections start with my learning basic research principles, moving onto clinical problem solving in general surgical dilemmas, followed by a collection of papers in my subspecialty of vascular surgery. The work culminates with a group of papers focused on aneurysmal disease, specifically, abdominal aortic aneurysms (AAA), the clinical impact of which has had a bearing on the introduction of a National AAA Screening Program in Wales in 2013. I conclude these sections with a collection of papers that reflect my long term commitment to surgical training both at regional level (as Secretary and Deputy Chairman to the Higher Surgical Training Committee and Chairman of the Basic Surgical Training Committee) and national level including my involvement with the Four Royal Colleges of Surgeons for the Intercollegiate Examinations in General Surgery. This examination is undertaken at completion of junior surgical training and used to confirm a doctor's competence for safe independent practice as a consultant. In conclusion, over forty years of academic research during my career as a vascular surgeon has provided unique insight into the pathophysiology, treatment and ultimately prevention of artherosclerotic disease. These findings have improved health policies in Wales and significantly reduced patient morbidity and mortality.
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Megens, Remco Theodorus Adrianus. "Vital imaging of large arteries using two-photon laser scanning microscopy focus on the arterial wall /." Maastricht : Maastricht : [Maastricht University] ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=10706.
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Ullberg, Ulla. "The human placenta : an angiographic study /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-499-2/.
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Lara-Montalvo, Ruben Angel. "Ultrasound determination of absolute backscatter from arterial wall structures." Link to electronic thesis, 2002. http://www.wpi.edu/Pubs/ETD/Available/etd-1203102-165958.
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Ögren, Mats. "Vascular morbidity and mortality in men with non-invasively detected peripheral arterial disease results from the prospective population study "Men born in 1914" /." Lund : Dept. of Community Health Sciences and the Dept. of Clinical Physiology, Malmö General Hospital, Lund University, 1994. http://catalog.hathitrust.org/api/volumes/oclc/39693808.html.
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Vedam, Hima. "Short-term hypoxia and arterial stiffness." Thesis, The University of Sydney, 2007. https://hdl.handle.net/2123/28093.
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The studies in this thesis assess the ventilatory and vascular effects of short-term awake isocapnic hypoxia in healthy subjects and those with obstructive sleep apnoea (OSA). The particular focus of this thesis is the impact of the hypoxic stimulus on indices of arterial stiffness, in particular the augmentation index (AIx) and time to reflection (Tr). The role of nitric oxide in this response in healthy subjects is also examined.
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Samuilis, Artūras. "Anatomical variants of the hepatic arteries and their influence on superior mesenteric artery hemodynamics." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2011. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2011~D_20110502_093516-43858.
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Anatomical variants of hepatic arteries are frequent. One of the most common origins of aberrant (atypically branching) hepatic arteries is superior mesenteric artery. Many physiologic and pathologic features influence hemodynamics of the latter artery. There were some sporadic cases in literature about the influence of aberrant hepatic artery arising from superior mesenteric artery to the hemodynamics of the latter artery, but no evidence based large extent studies were performed. Therefore the aim of this study was to evaluate how significant the aberrant hepatic artery branching from the superior mesenteric artery influences the hemodynamics of superior mesenteric artery.
Anatomical variants of the hepatic arteries were evaluated by computed tomography angiography also the candidates for Doppler ultrasound were selected. Doppler ultrasound was used to evaluate the hemodynamics of the superior mesenteric artery in patients with aberrant hepatic artery arising from the superior mesenteric artery and in those with typical hepatic artery anatomy. The influence of the aberrant hepatic artery arising from superior mesenteric artery to the hemodynamics (resistance) of the superior mesenteric artery was assessed.
The results of the investigation show that anatomical variants of the hepatic arteries are frequent. The aberrant hepatic artery arising from superior mesenteric artery significantly lowers resistance of the superior mesenteric artery. Practical recommendations were set... [to full text]Kepenų arterijų anatominiai variantai yra dažni. Viena dažniausių aberantinių (netipiškai atsišakojančių) kepenų arterijų atsišakojimo vietų yra viršutinė pasaito arterija. Pastarosios arterijos kraujotaka yra įtakojama daugybės fiziologinių ir patologinių veiksnių. Literatūroje taip pat aprašyti pavieniai atvejai apie iš viršutinės pasaito arterijos atsišakojančios aberantinės kepenų arterijos įtaką viršutinės pasaito arterijos hemodinamikai, tačiau didesnės apimties įrodymais pagrįstų tyrimų šioje srityje iki šiol nebuvo atlikta. Todėl šio tyrimo tikslas buvo įvertinti, ar aberantinė kepenų arterija, atsišakojanti iš viršutinės pasaito arterijos, reikšmingai įtakoja pastarosios kraujagyslės hemodinamiką. Šiame tyrime kompiuterinės tomografijos angiografijos pagalba įvertinti kepenų arterijų anatominiai variantai, atrinkti pacientai doplerio ultragarso tyrimams. Pastaruoju metodu tirta viršutinės pasaito arterijos kraujotaka pacientams, kurių vieni turėjo aberantinę kepenų arteriją, atsišakojančią iš viršutinės pasaito arterijos, o kiti turėjo įprastą kepenų arterijų anatomiją. Vertinta aberantinės kepenų arterijos, atsišakojančios iš viršutinės pasaito arterijos, įtaka pastarosios arterijos hemodinamikai (rezistentiškumui). Remiantis tyrimo duomenimis nustatyta, kad kepenų arterijų anatominiai variantai yra dažni. Aberantinė kepenų arterija, atsišakojanti iš viršutinės pasaito arterijos, reikšmingai mažina pastarosios arterijos rezistentiškumą. Pateiktos praktinės... [toliau žr. visą tekstą]
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Wadsworth, R. M. "Regulation of contraction of arterial smooth muscle." Thesis, University of Strathclyde, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248764.
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Hu, Jie. "Non-invasive assessment of dynamic properties in human arteries : with special reference to gestation and diabetes /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980925hu.
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梁永雄 and Wing-hung Leung. "Quantitative coronary arteriography." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1991. http://hub.hku.hk/bib/B31981483.
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Wake, Amanda Kathleen. "Modeling Fluid Mechanics in Individual Human Carotid Arteries." Diss., Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/7562.
Full textAbstract:
In the interest of furthering the understanding of hemodynamics, this study has developed a method for modeling fluid mechanics behavior in individual human carotid arteries. A computational model was constructed from magnetic resonance (MR) data of a phantom carotid bifurcation model, and relevant flow conditions were simulated. Results were verified by comparison with previous in vitro experiments. The methodology was extended to create subject-specific carotid artery models from geometry data and fluid flow boundary conditions which were determined from MR and phase contrast MR (PCMR) scans of human subjects. The influence of subject-specific boundary conditions on the flow field was investigated by comparing a model based on measured velocity boundary conditions to a model based on the assumption of idealized velocity boundary conditions.
It is shown that subject-specific velocity boundary conditions in combination with a subject-specific geometry and flow waveform influence fluid flow phenomena associated with plaque development. Comparing a model with idealized Womersley flow boundary conditions to a model with subject-specific velocity boundary conditions demonstrated the importance of employing inlet and flow division data obtained from individual subjects in order to predict accurate, clinically relevant, fluid flow phenomena such as low wall shear stress areas and negative axial velocity regions. This study also illustrates the influence of the bifurcation geometry, especially the flow divider position, with respect to the velocity distribution of the common carotid artery on the development of flow characteristics. Overall it is concluded that accurate geometry and velocity measurements are essential for modeling fluid mechanics in individual human carotid arteries for the purpose of understanding atherosclerosis in the carotid artery bifurcation.
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Mokori, E. B. "The role of pannexin channels in small arteries." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/38019/.
Full textAbstract:
Pannexins (Panx) are membrane bound channels which allow the exchange of molecules, particularly ATP, between the cytoplasm and the extracellular space. Panx channels have been shown to be expressed in the vasculature, and there is evidence suggesting that they are involved in the regulation of vasoconstriction in small arteries. In mice thoracodorsal resistance arteries Panx1 channels are co localized with α1D-adrenoceptors on smooth muscle cells, and have been reported to open after α1D-adrenoceptor stimulation to release ATP which is then responsible for causing vasoconstriction by activating P2 purinoceptors (Billaud et al., 2011). This thesis examined the expression and the role of Panx channels in rat mesenteric and cerebral arteries. Western blotting was used to probe for the presence of pannexin proteins in rat mesenteric and cerebral arteries. The functional role of pannexin channels in the mesenteric and cerebral arterial vasoconstriction was studied using pressure myography. The effects of the pannexin channel inhibitors, mefloquine, probenecid, and carbenoxolone were tested against sympathetic nerve mediated vasoconstriction in 2nd order mesenteric arteries. The effects of purinoceptor antagonists, suramin, and NF449 as well as apyrase an ectonucleotidase that degrades ATP and αβ-MeATP which desensitises P2X1 purinoceptors and mefloquine, probenecid and carbenoxolone were examined against responses to noradrenaline (NA) and potassium chloride (KCl) in pressurized 2nd order mesenteric arteries. The effects of increasing concentrations of pannexin channel inhibitors, mefloquine, probenecid, and carbenoxolone, and purinoceptor antagonists, suramin, and NF449 were also examined against the myogenic tone of 3rd order mesenteric arteries and cerebral arteries. Panx1 siRNAs were used to try to knock down the Panx1 protein in isolated mesenteric arterial smooth muscle cells and mesenteric arteries. Panx1 and Panx2 proteins were detected in rat mesenteric and cerebral arteries, but no Panx3 protein was detected. The activation of the sympathetic nerves in the 2nd order mesenteric arteries resulted in a frequency-dependent vasoconstriction, which was reduced in the presence of all the pannexin channel inhibitors (mefloquine, probenecid and carbenoxolone). Mefloquine caused a significant difference in the vessel diameter, the vessel diameter was 91.00 ± 36.19 µm in the absence of mefloquine and 1.00 ± 0.70 µm in its presence (Student’s t test, p > 0.05). Probenecid caused a significant change in the vessel diameter, at 10Hz the vessel diameter was 60.75 ± 4.59 µm in the absence of probenecid and 26.25 ± 2.83 µm in the presence of probenecid (Student’s t test, p>0.05). Similarly NA and KCl caused a concentration dependent contraction of the 2nd order mesenteric arteries. All the agents tested against the NA mediated responses, pannexin channel inhibitors, purinoceptor antagonists (suramin, NF449), and αβ-MeATP except apyrase resulted in the reduction in the contraction. The concentration that caused a 20% reduction in the vessel diameter in the absence of carbenoxolone was -6.82 ± 0.09 M and it was significantly different in the presence of carbenoxolone, it was -6.22 ± 0.16 M (student’s t test, p>0.05). The concentration that cause a 20% reduction in the vessel diameter, in the absence of suramin was -6.72 ± 0.18 M and it was significantly different in its presence -6.00 ± 0.15 M (Student’s t test, p>0.05). However, mefloquine and probenecid also inhibited the contraction produced by raising extracellular KCl. The myogenic tone of 3rd order mesenteric arteries was reduced by both pannexin channel inhibitors and purinoceptor antagonists. With the exception of mefloquine, none of the agents had any effect on the myogenic tone of cerebral arteries. The attempt to knock down the Panx1 protein in isolated mesenteric arterial smooth muscle cells and mesenteric arteries was unsuccessful, despite demonstrating that the delivery systems worked. In conclusion, Panx1 and Panx2 proteins are expressed in both mesenteric and cerebral arteries. Some of the observations in this study provide evidence that support the role for pannexin channels in sympathetic nerve responses and those to exogenous NA, these include the inhibitory effects seen with the P2 purinoceptor antagonists, suramin, and NF449 as well as αβ-MeATP on exogenous NA. This effect was also mimicked by the pannexin channel inhibitors, mefloquine, probenecid and carbenoxolone which also inhibited the nerve mediated contractions. Thus the data is consistent with the hypothesis that transduction of responses to NA involves the opening of pannexin channels and the release of ATP as an intercellular messenger, to enable synchronized vasoconstriction of the vascular smooth muscle cells. However, some caution needs to be applied since mefloquine and probenecid also reduced the response to raised extracellular KCl indicating that they may not be selective. In the case of the myogenic tone major differences in the effects of the pannexin channel inhibitors were seen between the cerebral and mesenteric arteries showing that probenecid and carbenoxolone were acting selectively, however mefloquine was non-selective. Thus the effects obtained with probenecid and carbenoxolone coupled with those obtained with P2 purinoceptor antagonists, suramin and NF449 on the myogenic tone of mesenteric arteries suggests a role for pannexin channels as the stress/pressure sensor in mesenteric arteries.
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Vaughan, Gareth D. A. "Pulse propagation in the pulmonary and systemic arteries." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/1785/.
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The one-dimensional model of Olufsen (2000) [*] for blood flow in the systemic arteries has been extended and built upon in a number of ways. Firstly, it has been applied to hypotheses of diseases of the systemic circulation, and that of the microcirculation. With a view to better understanding the microcirculation (the smallest vessels of the systemic circulation) and its diseases, the model has been extended to provide predictions of the propagating pressure pulse and flow rate in small arteries. Secondly, Olufsen’s model has been used as a base upon which to build a model of the pulmonary circulation, incorporating both the pulmonary arterial and venous circulations, with detailed simulations of pressure and flow predicted in the large pulmonary arteries and large pulmonary veins. To this end, a new model has been eveloped to describe a connected network of small arteries and small veins, replacing the small arterial model used as an outflow condition in the original model. A new outflow condition to describe the return of blood from the pulmonary venous system to the left atrium of the heart has also been implemented. Finally, this new pulmonary model has been applied to various hypotheses as to the causes of diseases and disorders of the pulmonary circulation, providing predictions of pressure and flow in the large pulmonary arteries and veins in both normal and abnormal circumstances, and showing agreement with clinical observations. [*] M.S. Olufsen at al. Numerical simulation and experimental validation of blood flow in arteries with structured-tree outflow conditions. Ann Biomed Eng, 28:1281–1299, 2000.
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Payvandi, S. "Mathematical modelling of flow in curved, compliant arteries." Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534971.
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Endesh, Naima Eltuhami M. "Contractile functions of Piezo1 channels in murine arteries." Thesis, University of Leeds, 2018. http://etheses.whiterose.ac.uk/20692/.
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Piezo1 proteins are Na+ and Ca2+ permeable mechanosensitive ion channels. Expressed on endothelial cell membranes, where they sense the shear stress forces created by blood flow, Piezo1 channels are essential for vascular development. The functional significance of vascular Piezo1 channels in adult physiology and pathology, however, remains largely unexplored. Therefore, using an inducible, endothelial-specific Piezo1 knock-out mouse line this study sought to identify and investigate the functional role of this channel in adult arterial vessels. Four morphologically and physiologically distinct arteries, the aorta, mesenteric, saphenous and carotid arteries, were selected and their responses to the vasoconstrictor phenylephrine (PE) and the vasorelaxant acetylcholine (ACh) were assessed using wire myography. While loss of endothelial Piezo1 did not alter or had only a small effect on the overall sensitivity or responsiveness of these vessels to either PE or ACh, further investigation revealed a significant increase in the endothelium-derived hyperpolarizing factor (EDHF) component of ACh-induced relaxation in mesenteric arteries. This anti-EDHF effect of Piezo1 was vascular bed specific, no difference between control or knock-out mice being observed in saphenous or carotid arteries. This finding led to the identification of a flow-stimulated vasoconstriction response in mesenteric vessels and furthermore provided an explanation for the reduced elevation in blood pressure detected in endothelial Piezo1 knock-out mice during exercise. Mesenteric arteries contract during exercise, enabling blood to be directed to tissues actively involved in physical movement. The data support the hypothesis that Piezo1 channels have specific importance in whole body physical exercise, sensing increased blood flow at the endothelium to elevate tone in the underlying vascular smooth muscle cells of visceral arteries, thus redirecting blood to the muscles.
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Banerjee, Rusha. "Fatigue Analysis of Arteries Using Finite Element Method." Thesis, North Dakota State University, 2012. https://hdl.handle.net/10365/26532.
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In this thesis, the fatigue response of arteries to four specific physiological conditions representative of various morphological changes that artery undergo during its lifetime, was explored. Single layered nonlinear elastic micromechanical model of artery was developed for this purpose.
A comparative study was completed on fatigue response, in the form of available life and shear stress accumulation, between hypertensive and normotensive arteries.
The effects of morphological changes of ageing arteries on the fatigue response of the artery were studied. Change in stiffness, arterial dilation and remodeling were taken into consideration.
The effect of undulation of the artery, due to weakening of arterial walls with age or hypertension, on fatigue response, is the third aspect of this study.
Lastly, the contribution of the surrounding linear elastic tissue material on fatigue response of the artery was investigated to reflect the in-vivo condition of artery where it is always surrounded by different tissues.
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Locke, Victoria. "AMPK ACTIVATORS REGULATE CONTRACTILE FUNCTION OF MESENTERIC ARTERIES." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3332.
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Vasoconstrictor tone in the splanchnic circulation redistributes blood flow during hemorrhage and resuscitation. A metabolic sensor, 5’adenosine monophosphate-activated protein kinase (AMPK), has been proposed to relax arteries by inhibiting myosin light chain (MLC) kinase (MLCK) and rho kinase (ROCK) activities. Because AMPK activation might be beneficial in re-establishing splanchnic blood flow during resuscitation, we sought to explore the relative ability of AMPK activators (AICAR, A769662, berberine (BBR) and simvastatin (SIMV)) to relax mesenteric artery (MA) contraction. Our data revealed that these drugs caused vasorelaxation when tissues were stimulated either with KCl (producing primarily a Ca2+ dependent contraction) or phenylephrine (PE; producing a primarily Ca2+ independent contraction). We further investigated the potential mechanisms by which BBR induced mesenteric artery relaxation. We found that BBR did not inhibit MLC phosphorylation, nor did it phosphorylate AMPK, and therefore is likely working through another mechanism to cause vasorelaxation. Notably, PE induced an increase in AMPK phosphorylation and, of all the AMPK activators examined, only AICAR phosphorylated AMPK in rabbit mesenteric artery, which provides a guide for future studies.
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Chen, Weiwei. "A coupled left ventricle and systemic arteries model." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/7037/.
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Mathematical modelling and computational simulation are effective tools in studying the function of the cardiovascular system and diagnosing the progress of diseases in this system, especially when clinical experiments or measurements are limited or not capable to proceed. A variety of models have been developed related to different segments in the cardiovascular system, such as the heart, the valves, the systemic arteries and the pulmonary arteries, etc. Among these studies, modelling the left ventricle (LV) and systemic arteries (SA) have drawn a great deal of attention in the last several decade due to the high pressure and high morbidity of the systemic circulation. The recent models range from lumped-parameter models, one-dimensional models to three-dimensional models,which expand our understanding of the function of the left ventricle and systemic arteries respectively, but few of them considered the interaction between two parts. Thus, the propose of this thesis is to develop a dynamic cardiac-vascular model to study the pressure and flow wave interactions in the systemic circulation. Here we employs two advanced models, a three-dimensional finite-strain structure-based LV, and a one-dimensional dynamic physiologically-based model for the systemic arteries, to complete a coupled LV-SA model. The LV model is based on Gao et al. [35]’s work. In this model, the fluid-structure interaction (FSI) is described by an Immersed Boundary (IB) approach, in which an incompressible solid is immersed in a viscous incompressible fluid, and solved by a Lagrangian Finite Element (FE) method [40]. The systemic circulation model is employed from Olufsen et al. [90]’s work, which consists of two groups of arteries, the large arteries and the small arteries or vascular beds. The large-arteries model uses a LaxWendroff scheme to compute the cross-sectional area-averaged flow and pressure based on physiological parameters of the arterial tree. The vascular beds are modelled as asymmetric structured tree, to provide outflow boundary conditions at the end of each terminal vessel in the network of large arteries. The coupling is achieved by matching the pressure and flow rate at the aortic root, i.e. the circulation model feeds back the pressure as a boundary condition to the LV model, and the flow rate from the LV is used as the inflow for the circulation model. The function of the aortic valve (AV) is modelled as follows: the AV opens when the pressure in the LV just exceeds the pressure in the proximal aorta adjacent to the valve; the AV closes when the flow rate is negative (referring to backflow) at the boundary plane in the LV proximal to the AV. The governing equations of the system is solved by a combined immersed boundary finite element (IB/FE) method, and the LaxWendroff scheme of Olufsen et al. [90]. To investigate the cardio-vascular interactions under different conditions in the LV-SA system, this thesis first simulate a standard case defined by using parameters based on measurements of healthy LV and healthy systemic arteries from two healthy subjects, and then simulating four disease-related cases based on different pathological conditions in the LV-SA model, i.e. stiffening of the large arteries, functional rarefaction, increasing heart beat rate (by shortening the systemic diastolic phase) and varied end-of-diastolic pressure. The results of pathological cases are compared with the standard case to provide a more insightful change of the pressure/flow interaction, and the change of LV contractility. To better understand the cardiac-valvular-vascular interactions, a lumped-parameter AV model is coupled in the LV-SA model to further develop it into a more detailed LV-AV-SA model. Compared to the LV-SA model (no AV), when a normal AV condition is used in the coupled LV-AV-SA model, the active tension of the LV and the peak LV pressure at early systole slightly increases, but the peak flow rate and the cardiac output barely changed. While, when a mild stenosis AV condition is applied in the LV-AV-SA model, the LV function changes dramatically, especially a dramatically increase of the peak LV pressure and the peak active tension of the LV. This indicates that the valve condition is also important in studying cardiac-vascular interactions, especially for diseased valve conditions that the effects are huge and cannot be ignored. In order to study how the valvular region affects the cross-valve pressure difference, we reconstruct the valvular region in the LV based on the mid-systolic CMR images, which shows a 93% increase of the cross-sectional area in the valvular region than early systole. The cross-valve pressure drop decreases dramatically with a expanded valvular region compared with the narrower valvular region in previous LV-SA model. This indicates that the a local stenosis in the valvular region may have significant effects on the heart function, and a better description of modelling the expanding procedure of the valvular region is needed to predict more physiological results. This thesis is a step forward for studying the cardiac-valvular-vascular interactions in the systemic circulation, and can provide dynamic pressure and flow waveforms in the LV and long the systemic arteries. Moreover, this model not only verifies the effects of pethological conditions but also quantifies change of pressure, flow rate and ventricular inotropy in the LV-SA system, which is important progress and has barely been studied before. Further approach of this work is to develop a patient-specific model in the future to diagnose the progress of disease, as well as providing practical treatment strategy.
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Sun, Nanfeng. "Mathematical modelling of mass transport in large arteries." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/1313.
Full textAbstract:
Atherosclerosis is a major cause of morbidity and mortality in the western world. The focal depletion of oxygen and accumulation of macromolecules are believed to initiate, accelerate and complicate the development of atherosclerosis. However, species concentrations in vessel walls are difficult to measure in vivo non-invasively. Therefore, it is essential to obtain detailed concentration profiles of atherogenic molecules to gain further understanding of the mass transfer mechanisms within arterial walls. In the present study, comprehensive mathematical models describing species transport in large arteries are developed and presented. Existing mathematical models are reviewed and reconciled. A fluid phase model, a single-layered and a multilayered fluid-wall models are employed to simulate the mass transfer processes in proatherosclerotic arteries. Since trans-endothelial transport is considered to be an important sub-process in the system and is dependent on wall shear stress (WSS) imposed on the endothelial surface, shear-dependent transport properties are derived from relevant experimental data in the literature. A novel approach, which exploits the optimisation theory, is proposed and used to determine model parameters based on the experimental data. Furthermore, numerical schemes to accommodate the effects of pulsatile flow on lipid transport in the arterial wall are presented in the thesis. Mathematical models and numerical schemes are tested and compared using idealised computational geometries. Then the models are applied to realistic geometries to investigate: 1) oxygen transport in a normal human abdominal aorta and an abdominal aortic aneurysm (AAA) with intralumenal thrombus (ILT); 2) macromolecular transport in a mildly stenosed human right coronary artery (RCA). Based on the model predictions, mechanisms inducing hypoxia and macromolecular accumulation are discussed in depth.
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Stoll, Scott Thomas. "Naloxone Potentiation of Epinephrine Induced Vasoconstriction in Canine Skeletal Muscle Arteries." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc277685/.
Full textAbstract:
Naloxone (NX) potentiated epinephrine (EPI) induced submaximal vasoconstriction in canine renal and skeletal muscle arterial segments, yet had no vasoconstrictor action alone. Developed tension generated in-vitro by 4 x 1mm. O.D. rings from 1st degree branches of canine femoral arteries was expressed as % of KCI induced maximum response. NX (10^-5 M) potentiated EPI induced submaximal contractions (34.2%) significantly more than contractions induced by norepinephrine, phenylephrine, lofexidine, ADH, KCI and serotonin (13.8,13.4,4.7,13.5,14.4 and 11.4% respectively). The NX response was unaffected by beta-adrenergic blockade and NX did not reverse an isoproterenol mediated vasodilation. Alphaadrenergic blockade with phentolamine completely eliminated EPI plus NX induced vasoconstriction. After washout, vessels exposed to EPI plus NX relaxed by 50% significantly faster than vessels exposed to EPI alone (18.5 and 27.9 min respectively). EPI induced vasoconstrictions were potentiated by 10^-5 M corticosterone (49.0%) which inhibits extraneuronal catecholamine uptake, but not by 10^-7 M desipramine (1.1%) which inhibits neuronal uptake. EPI induced vasoconstrictions were also potentiated by 10^-4 M pyrogallol (33.0%) which inhibits catechol-o-methyl transferase activity, but not by 10^-5 M pargyline (-1.1%) which inhibits monoamine oxidase activity. The NX effect was endothelium independent. The dose-response of various opioid receptor agonists and antagonists were compared to the NX response. A specific opioid receptor subclass could not be identified as the mediator of the NX effect. The ED_50s for NX (3.7x^-6 M) and (+)NX (8.1x^-7M) indicated a significant stereoselectivity for the (+)enantiomer. A variety of sigma receptor ligands, steroids and steroid metabolites were tested for the ability to augment EPI vasoconstrictions. Several of the opioid, sigma and steroid ligands, all with polycyclic structures, induced responses similarto those of NX. NX exerted its effect independent of traditional opiate receptors and may have influenced the cellular uptake or degradation of EPI. Endogenous compounds with sigma or steroid activity may modulate these processes in-vivo.
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Kölegård, Roger. "Distensibility in Arteries, Arterioles and Veins in Humans : Adaptation to Intermittent or Prolonged Change in Regional Intravascular Pressure." Doctoral thesis, KTH, Omgivningsfysiologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-25965.
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The present series of in vivo experiments in healthy subjects, were performed to investigate wall stiffness in peripheral vessels and how this modality adapts to iterative increments or sustained reductions in local intravascular pressures. Vascular stiffness was measured as changes in arterial and venous diameters, and in arterial flow, during graded increments in distending pressures in the vasculature of an arm or a lower leg. In addition, effects of intravascular pressure elevation on flow characteristics in veins, and on limb pain were elucidated. Arteries and veins were stiffer (i.e. pressure distension was less) in the lower leg than in the arm. The pressure-induced increase in arterial flow was substantially greater in the arm than in the lower leg, indicating a greater stiffness in the arterioles of the lower leg. Prolonged reduction of intravascular pressures in the lower body, induced by 5 wks of sustained horizontal bedrest (BR), decreased stiffness in the leg vasculature. BR increased pressure distension in the tibial artery threefold and in the tibial vein by 86 %. The pressure-induced increase in tibial artery flow was greater post bedrest, indicating reduced stiffness in the arterioles of the lower leg. Intermittent increases of intravascular pressures in one arm (pressure training; PT) during a 5-wk period decreased vascular stiffness. Pressure distension and pressure-induced flow in the brachial artery were reduced by about 50 % by PT. PT reduced pressure distension in arm veins by 30 to 50 %. High intravascular pressures changed venous flow to arterial-like pulsatile patterns, reflecting propagation of pulse waves from the arteries to the veins either via the capillary network or through arteriovenous anastomoses. High vascular pressures induced pain, which was aggravated by BR and attenuated by PT; the results suggest that the pain was predominantly caused by vascular overdistension. In conclusion, vascular wall stiffness constitutes a plastic modality that adapts to meet demands imposed by a change in the prevailing local intravascular pressure. That increased intravascular pressure leads to increased arteriolar wall stiffness supports the notion that local pressure load may serve as a “prime mover” in the development of vascular changes in hypertension.medicine doktorsexamen QC 20101109
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Zhou, Xiaowei. "Investigation of ultrasound-measured blood flow related parameters in radial and ulnar arteries." Thesis, University of Dundee, 2017. https://discovery.dundee.ac.uk/en/studentTheses/cb2a68cb-949a-413f-b561-c137b7605583.
Full textAbstract:
The incidence of disease of the cardiovascular system is very high and increasing worldwide, especially in the developing world. The radial and ulnar arteries are implicated in some important ailments where blood flow related parameters such as flow rate (FR), wall shear rate (WSR), arterial wall motion (AWM) and pressure, all of which can be measured using ultrasound techniques, are useful in diagnosis and patient management. However these measurements are prone to error due to the manner of image formation and the complex flow conditions within the vessels. In this thesis, the errors in ultrasound-measured parameters in the radial and ulnar arteries are investigated using experimental phantoms, computer simulation and on volunteers. Using the Womersley theory, FR and WSR were estimated using a clinical ultrasound scanner with the pulsed wave (PW) mode and B mode. Experimental flow phantoms were designed to evaluate those measurements under different circumstances. A simulation technique which combined image-based computational fluid dynamics and ultrasound simulation was also used to evaluate ultrasound estimation of these parameters. A case study was then conducted on healthy volunteers to evaluate the method of measuring FR and WSR in-vivo. For the AWM in the radial artery, an auto-correlation method was used based on the radio-frequency (RF) data and validations were done by a flow phantom, simulation, and in-vivo trial. The blood pressure waveform in a volunteer’s radial artery was derived from the ultrasound measured AWM and compared with the waveform from a tonometry. FR and WSR were both found to be overestimated by up to 50%, mainly due to the beam-vessel angle in the PW Doppler ultrasound. Measurement of the vessel diameter and assumption of the blood flow direction can also influence the estimations. Other factors, such as flow amplitude, vessel size, imaging depth and flow waveforms, do not seem to affect the estimation of these two parameters. Results taken from the flow phantoms agree with those from simulation and the estimations from the in-vivo case study also agree with the published data. The auto-correlation method for the AWM was validated from the phantom and simulation. It is able to detect motion amplitude of about tens of micrometres. The trial on volunteers proved the feasibility of this motion detection method. Blood pressure waveforms at the radial artery of a volunteer, derived from this ultrasound-measured wall motion and from the tonometry, were very similar. The Womersley-based method is able to estimate the FR and WSR in the radial and ulnar arteries with high accuracy. Sources of the error and their magnitudes in estimation of the two parameters by ultrasound pointed out in this thesis are beam-vessel angle, vessel diameter measurement and flow direction assumption. Researchers and clinicians using these measurements in practice and research should be aware. The capability of ultrasound imaging to measure arterial AWM in the radial artery is demonstrated and it is found that the blood pressure waveform can also be derived from the arterial AWM.
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Dye, Wendy Watson. "Altered biomechanical properties of large arteries in muscular dystrophy." Texas A&M University, 2005. http://hdl.handle.net/1969.1/4304.
Full textAbstract:
Muscular dystrophy is a disease characterized by skeletal muscle weakness and wasting,
but little is known of alterations in the vascular system that occur with this disease. The culprit in
many muscular dystrophies is a defective dystrophin-glycoprotein complex (DGC). The DGC is
a group of transmembrane proteins that connects the cytoskeleton of muscle cells to the
extracellular matrix; it plays a role in mechanotransduction and the maintenance of structural
integrity of these cells, and includes the proteins dystrophin and sarcoglycan-delta. The absence
of these proteins results in severe muscular dystrophies in humans, and thus knockout mice
lacking the genes encoding for dystrophin (mdx mice) and sarcoglycan-delta (sgcd-/- mice) were
studied to detect any vascular alterations that occur as a result of a defective DGC. Acute biaxial
biomechanical data were obtained through pressure-diameter and axial force-length tests on
common carotid arteries of mdx, sgcd-/-, and wild-type mice in the active and passive smooth
muscle state. Functional response to the vasoreactive compounds phenylephrine,
carbamylcholine chloride, and sodium nitroprusside was also tested. We found significant
biomechanical differences between the knockout and wild-type mouse arteries: the mdx and
sgcd-/- arteries had decreased distensibilities in pressure-diameter tests, with mdx arteries also
having increased circumferential stresses, and the knockout arteries generated increased axial
loads and stresses in the axial force-length tests. The mdx and sgcd-/- arteries also differed from
the wild-type in that their âÂÂhomeostaticâ axial stretch, at which the axial force remains constant upon pressurization, was significantly decreased. We conclude that the loss of DGC proteins
does trigger changes in vascular smooth muscle cells or their interactions with the extracellular
matrix, yet that the altered vascular system was able to adapt and function without the DGC.
Knowledge of alterations to the vascular system (and adaptations to these changes) of patients
with muscular dystrophy could help physicians customize their treatment to extend and enhance
their lives, especially as medical advances extend the lifespan of these patients and they begin to
suffer from diseases such as hypertension and atherosclerosis that affect the normal aging
population.
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Geraghty, Annie. "Experiments on the Calcium-Sensing Receptor in Rat Arteries." Thesis, University of Manchester, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518446.
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Satha, Ganarupan. "Goal Function Approach to Growth and Remodeling of Arteries." Licentiate thesis, Linköpings universitet, Mekanik, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-104188.
Full textAbstract:
In this thesis we develop a new goal function approach to investigate stability of the growth processes in blood vessels and cost-optimal composition and geometry of these vessels. In the vascular system of a healthy individual, the living composition of the arterial wall must regenerate and remodel continuously during the entire lifetime to maintain itself. In some cases the system destabilizes due to disease, injury or other complex processes. To understand how and when this happens, several mathematical models have been developed. These models have included an evolution equation for mass fractions of the vessel wall, describing how the vessel develops from an actual state to a target state. These works are based on constrained mixture theory (CMT), which takes care of production and removal of arterial constituents. The cost-optimal design of blood vessels has been studied previously by Murray. The aim of this thesis is to contribute to stability analyses of the growth process by formulating a new goal function approach, making it possible to examine under which conditions instability arises. We also aim to analyze changes in the optimum material composition and geometry of the vessel wall, using a more realistic, nonlinear material model. The blood vessel is modeled as a thin-walled tube and the constituents that form the vessel wall are assumed to deform together (CMT). The growth dynamics of the composite material of the vessel wall is described by an evolution equation, where the effective area of each constituent changes in the direction of steepest descent of a goal function. This goal function is formulated in such way that the constituents grow toward a target potential energy and a target composition. The response of the evolution equation is simulated for several dierent material models. These simulations suggest that elastin-decient vessels are more prone to growth instability, but that increased vessel stiness gives a more stable growth process. Another important nding is that an increased rate of degradation of materials impairs growth stability. By extending Murray's law to include effects of nonlinear mechanics of the artery wall and a growth and remodeling mechanism based on CMT, and at the same time having the system satisfy an equilibrium equation, we study cost-optimal compositions and geometries of the vessel wall. This gives new insight into the wall's architecture under optimal conditions.
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Wishah, Mahmoud I. "Simulation of blood flow through stenotic and branched arteries." Thesis, University of Salford, 2007. http://usir.salford.ac.uk/26966/.
Full textAbstract:
Mathematical and physical models have been developed in order to study blood flow through arteries, numerically and experimentally. The aim of these models was to understand, apply and verify using realistic models how both flow and geometry interact through and downstream of stenosed and branched arteries. This interaction is examined in two ways; initially by investigating the influence of stenosis and branches on flow and then by examining the influence of flow haemodynamics parameters such as Reynolds number, stenosis severity, stenosis shape and bifurcation area ratio on the development of stenosis. In addition, a parametric study was performed to determine the actual influence of the geometry on flow and vice versa. The ability to describe the flow through a stenosed artery provides the possibility of developing imaging enhancement that gives medical staff the ability to diagnose the disease with high accuracy in its early stages and the opportunity of treatment before atherosclerosis becomes severe and dangerous. At the end we conclude that, sites of high wall shear stress just upstream of the stenosis throat, were factors in the process of the development of stenosis through platelet activation, as well as in the rupture of the stenosis cap triggering the process of thrombosis. Low shear stress plays a significant role in initiating the disease in the region of flow stagnation where flow cannot follow the geometry of arteries. The results presented, favour and support the theory of low wall shear stress and its important role in the initiation of atherosclerosis, and the high shear stress theory in the development of the disease. CFD in conjunction with flow visualisation and MRI can be used in the early prediction of artery stenosis and gives more accurate and reliable estimates of the stenosis severity.
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Haeck, Luc Bernard Arthur. "C W Doppler audiospectrum analysis in the iliac arteries." [Maastricht : Maastricht : Rijksuniversiteit Limburg] ; University Library, Maastricht University [Host], 1989. http://arno.unimaas.nl/show.cgi?fid=5512.
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Boonen, Henricus Cornelis Matjeu. "Excitation-contraction coupling in small arteries: role in hypertension." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1992. http://arno.unimaas.nl/show.cgi?fid=6510.
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