Academic literature on the topic 'Coronary Vessels physiology'
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Journal articles on the topic "Coronary Vessels physiology"
Zamir, M. "Distributing and delivering vessels of the human heart." Journal of General Physiology 91, no. 5 (May 1, 1988): 725–35. http://dx.doi.org/10.1085/jgp.91.5.725.
Full textGreer, C., A. Puri, J. Sutherland, J. Blake, D. McClean, J. Elliott, and D. Smyth. "Borderline Coronary Physiology – Are All Vessels Equal?" Heart, Lung and Circulation 28 (2019): S387. http://dx.doi.org/10.1016/j.hlc.2019.06.588.
Full textKassab, G. S., C. A. Rider, N. J. Tang, and Y. C. Fung. "Morphometry of pig coronary arterial trees." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 1 (July 1, 1993): H350—H365. http://dx.doi.org/10.1152/ajpheart.1993.265.1.h350.
Full textKassab, Ghassan S. "Functional hierarchy of coronary circulation: direct evidence of a structure-function relation." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 6 (December 2005): H2559—H2565. http://dx.doi.org/10.1152/ajpheart.00561.2005.
Full textHoffman, J. I., and J. A. Spaan. "Pressure-flow relations in coronary circulation." Physiological Reviews 70, no. 2 (April 1, 1990): 331–90. http://dx.doi.org/10.1152/physrev.1990.70.2.331.
Full textHabazettl, H., B. Vollmar, M. Christ, H. Baier, P. F. Conzen, and K. Peter. "Heterogeneous microvascular coronary vasodilation by adenosine and nitroglycerin in dogs." Journal of Applied Physiology 76, no. 5 (May 1, 1994): 1951–60. http://dx.doi.org/10.1152/jappl.1994.76.5.1951.
Full textRäsänen, Markus, Ibrahim Sultan, Jennifer Paech, Karthik Amudhala Hemanthakumar, Wei Yu, Liqun He, Juan Tang, et al. "VEGF-B Promotes Endocardium-Derived Coronary Vessel Development and Cardiac Regeneration." Circulation 143, no. 1 (January 5, 2021): 65–77. http://dx.doi.org/10.1161/circulationaha.120.050635.
Full textLavallée, Michel, and Eric Thorin. "Role of ET-1 in the regulation of coronary circulation." Canadian Journal of Physiology and Pharmacology 81, no. 6 (June 1, 2003): 570–77. http://dx.doi.org/10.1139/y03-014.
Full textZhang, J., M. Somers, and F. R. Cobb. "Heterogeneous effects of nitroglycerin on the conductance and resistance coronary arterial vasculature." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 6 (June 1, 1993): H1960—H1968. http://dx.doi.org/10.1152/ajpheart.1993.264.6.h1960.
Full textDuncker, Dirk J., and Robert J. Bache. "Regulation of Coronary Blood Flow During Exercise." Physiological Reviews 88, no. 3 (July 2008): 1009–86. http://dx.doi.org/10.1152/physrev.00045.2006.
Full textDissertations / Theses on the topic "Coronary Vessels physiology"
Warner, Anke Sigrid. "The expression, regulation and effects of inducible nitric oxide synthase in hibernating myocardium." Title page, contents and summary only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phw279.pdf.
Full textWikenheiser, Jamie Christopher. "Altered Hypoxia-Inducible Factor-1 Alpha Levels Correlate with Coronary Artery Anomalies." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1216218122.
Full textWang, Ruoya. "Novel theoretical and experimental frameworks for multiscale quantification of arterial mechanics." Diss., Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/47718.
Full textSarkar, Nondita. "Myocardial angiogenesis induced by plasmid VEGF-A165 gene transfer : experimental and clinical studies /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-196-2/.
Full text"Cellular electrophysiological and mechanical effects of organ preservation solutions on endothelial function in resistance coronary and pulmonary arteries: implications in heart and lung transplantation." 2006. http://library.cuhk.edu.hk/record=b5892759.
Full textThesis (M.Phil.)--Chinese University of Hong Kong, 2006.
Includes bibliographical references (leaves 87-114).
Abstracts in English and Chinese.
Declaration --- p.i
Acknowledgement --- p.ii
Publication list --- p.iii
Abstract (English) --- p.xi
Abstract (Chinese) --- p.xiv
Abbreviations --- p.xvi
List of figures / tables --- p.xviii
Chapter Chapter 1. --- General Introduction --- p.1
Chapter 1.1 --- Endothelial function in the regulation of vascular tone --- p.1
Chapter 1.1.1 --- NO --- p.2
Chapter 1.1.2 --- PGI2 --- p.5
Chapter 1.1.3 --- EDHF --- p.6
Chapter 1.2 --- Alteration of endothelial functions after preservation with cardioplegia /organ preservation solutions in the coronary and pulmonary microcirculations --- p.18
Chapter 1.2.1 --- Cardioplegia/organ preservation solutions --- p.21
Chapter 1.2.2 --- Effect of Cardioplegia/organ preservation solutions on endothelial function --- p.22
Chapter 1.2.2.1 --- Effect of K+ on endothelial function --- p.23
Chapter 1.2.2.2 --- Effect of other components on endothelial function --- p.24
Chapter Chapter 2. --- Materials and Methods --- p.26
Chapter 2.1 --- Isometric force study in coronary/pulmonary resistance arteries --- p.26
Chapter 2.1.1 --- Preparation of vessels --- p.26
Chapter 2.1.1.1 --- Preparation of porcine coronary small arteries --- p.26
Chapter 2.1.1.2 --- Preparation of porcine pulmonary small arteries --- p.26
Chapter 2.1.2 --- Technique of setting up --- p.29
Chapter 2.1.2.1 --- Mounting of small vessels --- p.29
Chapter 2.1.2.2 --- Normalization procedure for small vessels --- p.29
Chapter 2.1.3 --- EDHF-mediated vasorelaxation --- p.30
Chapter 2.1.3.1 --- Precontraction and stimuli of EDHF --- p.30
Chapter 2.1.3.2 --- """True"" response of EDHF" --- p.31
Chapter 2.1.4 --- Data acquisition and analysis --- p.32
Chapter 2.2 --- Electrophysiological study --- p.32
Chapter 2.2.1 --- Preparation of small porcine coronary/pulmonary arteries --- p.32
Chapter 2.2.2 --- Preparation of microelectrode --- p.32
Chapter 2.2.3 --- Impaling of microelectrode --- p.33
Chapter 2.2.4 --- Recording of membrane potential --- p.33
Chapter 2.3 --- Statistical analysis --- p.34
Chapter 2.4 --- Chemicals --- p.34
Chapter Chapter 3. --- Effects of Celsior Solution on Endothelial Function in Resistance Coronary Arteries Compared to St. Thomas' Hospital Solution --- p.37
Chapter 3.1 --- Abstract --- p.37
Chapter 3.2 --- Introduction --- p.38
Chapter 3.3 --- Experimental design and analysis --- p.40
Chapter 3.3.1 --- Vessel preparation --- p.40
Chapter 3.3.2 --- Normalization --- p.40
Chapter 3:3.3 --- "Relaxation study: BK-induced, EDHF-mediated relaxation" --- p.41
Chapter 3.3.4 --- Cellular electrophysiological study: EDHF-mediated cellular hyperpolarization and associated relaxation --- p.41
Chapter 3.3.5 --- Data analysis --- p.42
Chapter 3.4 --- Results --- p.43
Chapter 3.4.1 --- Relaxation study --- p.43
Chapter 3.4.1.1 --- Resting force --- p.43
Chapter 3.4.1.2 --- U46619-induced precontraction --- p.43
Chapter 3.4.1.3 --- EDHF-mediated relaxation --- p.43
Chapter 3.4.2 --- Electrophysiological studies --- p.44
Chapter 3.4.2.1 --- Resting membrane potential --- p.44
Chapter 3.4.2.2 --- EDHF-mediated cellular hyperpolarization --- p.45
Chapter 3.4.2.3 --- Cellular hyperpolarization-associated relaxation --- p.45
Chapter 3.5 --- Discussion --- p.46
Chapter 3.5.1 --- Effects of Celsior solution on endothelial function --- p.47
Chapter 3.5.2 --- Effects of ST solution on EDHF-mediated function --- p.48
Chapter 3.5.3 --- Comparison between Celsior and ST solutions on EDHF-mediated function --- p.48
Chapter 3.5.4 --- Clinical implications --- p.49
Chapter Chapter 4. --- Effects of Perfadex and Celsior Solution on Endothelial Function in Resistance Pulmonary Arteries --- p.57
Chapter 4.1 --- Abstract --- p.57
Chapter 4.2 --- Introduction --- p.58
Chapter 4.3 --- Experimental design and analysis --- p.59
Chapter 4.3.1 --- Vessel Preparation --- p.59
Chapter 4.3.2 --- Normalization --- p.60
Chapter 4.3.3 --- Isometric force study --- p.60
Chapter 4.3.4 --- Electrophysiological studies --- p.61
Chapter 4.3.5 --- Data analysis --- p.61
Chapter 4.4 --- Results --- p.62
Chapter 4.4.1 --- Relaxation study: EDHF-mediated relaxation --- p.62
Chapter 4.4.1.1 --- Resting force --- p.62
Chapter 4.4.1.2 --- U46619-induced precontraction --- p.62
Chapter 4.4.1.3 --- EDHF-mediated relaxation --- p.62
Chapter 4.4.2 --- Electrophysiological studies --- p.63
Chapter 4.4.2.1 --- Resting membrane potential --- p.63
Chapter 4.4.2.2 --- EDHF-mediated cellular hyperpolarization --- p.64
Chapter 4.4.2.3 --- Cellular hyperpolarization-associated relaxation --- p.64
Chapter 4.5 --- Discussion --- p.65
Chapter 4.5.1 --- Effects of Celsior solution on endothelial function during cardiopulmonary surgery --- p.65
Chapter 4.5.2 --- Effects of Perfadex solution on EDHF-mediated endothelial function --- p.66
Chapter 4.5.3 --- Comparison between Celsior and Perfadex solutions on EDHF-mediated function --- p.66
Chapter 4.5.4 --- Clinical implications --- p.67
Chapter Chapter 5. --- Exploration of the Nature of EDHF - the Effect of H2O2 on the Membrane Potential in the Rat Small Mesenteric Arteries --- p.73
Chapter Chapter 6. --- General Discussion --- p.75
Chapter 6.1 --- EDHF-mediated endothelial function in porcine coronary and pulmonary circulation --- p.75
Chapter 6.1.1 --- Role of EDHF in the regulation of porcine coronary arterial tone --- p.75
Chapter 6.1.2 --- Role of EDHF in the regulation of porcine pulmonary arterial tone --- p.76
Chapter 6.2 --- Alteration of EDHF-mediated endothelial functions after exposure to organ preservation solutions --- p.77
Chapter 6.2.1 --- Effects of hyperkalemic solution on EDHF-mediated endothelial function in coronary and pulmonary circulation --- p.78
Chapter 6.2.2 --- Effects of low-potassium-based preservation solution on EDHF-mediated endothelial function in pulmonary circulation --- p.79
Chapter 6.2.3 --- Comparison between hyperkalemic solution and low-potassium-based preservation solution on EDHF-mediated endothelial function --- p.80
Chapter 6.2.4 --- Effects of other component of organ preservation solutions on EDHF-mediated endothelial function --- p.81
Chapter 6.3 --- Clinical implications --- p.82
Chapter 6.4 --- The effect of H202 on the membrane potential in rat small mesenteric arteries --- p.83
Chapter 6.5 --- Limitation of the study --- p.84
Chapter 6.6 --- Future investigations --- p.85
Chapter 6.7 --- Conclusions --- p.85
References --- p.87
Noblet, Jillian Nicole. "Coronary perivascular adipose tissue and vascular smooth muscle function: influence of obesity." Diss., 2016. http://hdl.handle.net/1805/9815.
Full textFactors released from coronary perivascular adipose tissue (PVAT), which surrounds large coronary arteries, have been implicated in the development of coronary disease. However, the precise contribution of coronary PVAT-derived factors to the initiation and progression of coronary vascular dysfunction remains ill defined. Accordingly, this investigation was designed to delineate the mechanisms by which PVAT-derived factors influence obesity-induced coronary smooth muscle dysfunction. Isometric tension studies of coronary arteries from lean and obese swine demonstrated that both lean and obese coronary PVAT attenuate vasodilation via inhibitory effects on smooth muscle K+ channels. Specifically, lean coronary PVAT attenuated KCa and KV7 channel-mediated dilation, whereas obese coronary PVAT impaired KATP channel-mediated dilation. Importantly, these effects were independent of alterations in underlying smooth muscle function in obese arteries. The PVAT-derived factor calpastatin impaired adenosine dilation in lean but not obese arteries, suggesting that alterations in specific factors may contribute to the development of smooth muscle dysfunction. Further studies tested the hypothesis that leptin, which is expressed in coronary PVAT and is upregulated in obesity, acts as an upstream mediator of coronary smooth muscle dysfunction. Long-term administration (3 day culture) of obese concentrations of leptin markedly altered the coronary artery proteome, favoring pathways associated with calcium signaling and cellular proliferation. Isometric tension studies demonstrated that short-term (30 min) exposure to leptin potentiated depolarization-induced contraction of coronary arteries and that this effect was augmented following longer-term leptin administration (3 days). Inhibition of Rho kinase reduced leptin-mediated increases in coronary artery contractions. Acute treatment was associated with increased Rho kinase activity, whereas longer-term exposure was associated with increases in Rho kinase protein abundance. Alterations in Rho kinase signaling were also associated with leptin-mediated increases in coronary vascular smooth muscle proliferation. These findings provide novel mechanistic evidence linking coronary PVAT with vascular dysfunction and further support a role for coronary PVAT in the pathogenesis of coronary disease.
Owen, Meredith Kohr. "Effect of coronary perivascular adipose tissue on vascular smooth muscle function in metabolic syndrome." Thesis, 2013. http://hdl.handle.net/1805/3789.
Full textObesity increases cardiovascular disease risk and is associated with factors of the “metabolic syndrome” (MetS), a disorder including hypertension, hypercholesterolemia and/or impaired glucose tolerance. Expanding adipose and subsequent inflammation is implicated in vascular dysfunction in MetS. Perivascular adipose tissue (PVAT) surrounds virtually every artery and is capable of releasing factors that influence vascular reactivity, but the effects of PVAT in the coronary circulation are unknown. Accordingly, the goal of this investigation was to delineate mechanisms by which lean vs. MetS coronary PVAT influences vasomotor tone and the coronary PVAT proteome. We tested the hypothesis that MetS alters the functional expression and vascular contractile effects of coronary PVAT in an Ossabaw swine model of the MetS. Utilizing isometric tension measurements of coronary arteries in the absence and presence of PVAT, we revealed the vascular effects of PVAT vary according to anatomical location as coronary and mesenteric, but not subcutaneous adipose tissue augmented coronary artery contractions to KCl. Factors released from coronary PVAT increase baseline tension and potentiate constriction of isolated coronary arteries relative to the amount of adipose tissue present. The effects of coronary PVAT are elevated in the setting of MetS and occur independent of endothelial function. MetS is also associated with substantial alterations in the coronary PVAT proteome and underlying increases in vascular smooth muscle Ca2+ handling via CaV1.2 channels, H2O2-sensitive K+ channels and/or upstream mediators of these ion channels. Rho-kinase signaling participates in the increase in coronary artery contractions to PVAT in lean, but not MetS swine. These data provide novel evidence that the vascular effects of PVAT vary according to anatomic location and are influenced by the MetS phenotype.
Deep, Debanjan. "A study of blood flow in normal and dilated aorta." Thesis, 2013. http://hdl.handle.net/1805/4440.
Full textAtherosclerotic lesions of human beings are common diagnosed in regions of arte- rial branching and curvature. The prevalence of atherosclerosis is usually associated with hardening and ballooning of aortic wall surfaces because of narrowing of flow path by the deposition of fatty materials, platelets and influx of plasma through in- timal wall of Aorta. High Wall Shear Stress (WSS) is proved to be the main cause behind all these aortic diseases by physicians and researchers. Due to the fact that the atherosclerotic regions are associated with complex blood flow patterns, it has believed that hemodynamics and fluid-structure interaction play important roles in regulating atherogenesis. As one of the most complex flow situations found in cardio- vascular system due to the strong curvature effects, irregular geometry, tapering and branching, and twisting, theoretical prediction and in vivo quantitative experimental data regarding to the complex blood flow dynamics are substantial paucity. In recent years, computational fluid dynamics (CFD) has emerged as a popular research tool to study the characteristics of aortic flow and aim to enhance the understanding of the underlying physics behind arteriosclerosis. In this research, we study the hemo- dynamics and flow-vessel interaction in patient specific normal (healthy) and dilated (diseased) aortas using Ansys-Fluent and Ansys-Workbench. The computation con- sists of three parts: segmentation of arterial geometry for the CFD simulation from computed tomography (CT) scanning data using MIMICS; finite volume simulation of hemodynamics of steady and pulsatile flow using Ansys-Fluent; an attempt to perform the Fluid Structure Simulation of the normal aorta using Ansys-Workbench. Instead of neglecting the branching or smoothing out the wall for simplification as a lot of similar computation in literature, we use the exact aortic geometry. Segmen- tation from real time CT images from two patients, one young and another old to represent healthy and diseased aorta respectively, is on MIMICS. The MIMICS seg- mentation operation includes: first cropping the required part of aorta from CT dicom data of the whole chest, masking of the aorta from coronal, axial and saggital views of the same to extract the exact 3D geometry of the aorta. Next step was to perform surface improvement using MIMICS 3-matic module to repair for holes, noise shells and overlapping triangles to create a good quality surface of the geometry. A hexahe- dral volume mesh was created in T-Grid. Since T-grid cannot recognize the geometry format created by MIMICS 3-matic; the required step geometry file was created in Pro-Engineer. After the meshing operation is performed, the mesh is exported to Ansys Fluent to perform the required fluid simulation imposing adequate boundary conditions accordingly. Two types of study are performed for hemodynamics. First is a steady flow driven by specified parabolic velocity at inlet. We captured the flow feature such as skewness of velocity around the aortic arch regions and vortices pairs, which are in good agreement with open data in literature. Second is a pulsatile flow. Two pulsatile velocity profiles are imposed at the inlet of healthy and diseased aorta respectively. The pulsatile analysis was accomplished for peak systolic, mid systolic and diastolic phase of the entire cardiac cycle. During peak systole and mid-systole, high WSS was found at the aortic branch roots and arch regions and diastole resulted in flow reversals and low WSS values due to small aortic inflow. In brief, areas of sudden geometry change, i.e. the branch roots and irregular surfaces of the geom- etry experience more WSS. Also it was found that dilated aorta has more sporadic nature of WSS in different regions than normal aorta which displays a more uniform WSS distribution all over the aorta surface. Fluid-Structure Interaction simulation is performed on Ansys-WorkBench through the coupling of fluid dynamics and solid mechanics. Focus is on the maximum displacement and equivalent stress to find out the future failure regions for the peak velocity of the cardiac cycle.
Books on the topic "Coronary Vessels physiology"
Carl, Maurer Peter, and Deutsche Gesellschaft für Angiologie. Jahrestagung, eds. What is new in angiology?: Trends and controversies : proceedings, 14th World Congress, International Union of Angiology, 15th Annual Meeting, German Society of Angiology, July 6-11, 1986, Munich, West Germany. München: W. Zuckschwerdt Verlag, 1986.
Find full textMohl, W. Coronary sinus interventions in cardiac surgery. 2nd ed. Georgetown, Tex: Landes Bioscience, 2000.
Find full textde, Bruyne Bernard, ed. Coronary pressure. Dordrecht: Kluwer Academic Publishers, 1997.
Find full textde, Bruyne Bernard, ed. Coronary pressure. 2nd ed. Dordrecht: Kluwer Academic Publishers, 2000.
Find full textV, Schaff Hartzell, ed. Vasoactive factors produced by the endothelium: Physiology and surgical implications. Austin: R.G. Landes, 1994.
Find full textTomanek, Robert J. Coronary Vasculature: Development, Structure-Function, and Adaptations. Springer, 2012.
Find full textCoronary Vasculature: Development, Structure-Function, and Adaptations. Springer, 2012.
Find full textPijls, N. H. Coronary Pressure. Springer, 2010.
Find full textPijls, N. H., and B. de Bruyne. Coronary Pressure (DEVELOPMENTS IN CARDIOVASCULAR MEDICINE Volume 227) (Developments in Cardiovascular Medicine). Springer, 2000.
Find full textLi, John K.-J. The Arterial Circulation: Physical Principles and Clinical Applications. Humana Press, 2000.
Find full textBook chapters on the topic "Coronary Vessels physiology"
Kozarek, Katherine, and Ryan Hood. "Cardiac Tumors." In Cardiac Anesthesia: A Problem-Based Learning Approach, edited by Mohammed M. Minhaj, 42–47. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190884512.003.0005.
Full textBecker, Richard C., and Frederick A. Spencer. "Acute Coronary Syndromes." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0025.
Full textBecker, Richard C., and Frederick A. Spencer. "Facilitated Percutaneous Coronary Intervention." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0018.
Full textConference papers on the topic "Coronary Vessels physiology"
Biglino, Giovanni, Daria Cosentino, Matteo Castelli, Lorenzo De Nova, Hopewell N. Ntsinjana, Jennifer A. Steeden, Andrew M. Taylor, and Silvia Schievano. "Combining 4D MR Flow Experimental Data and Computational Fluid Dynamics to Study the Neoaorta in Patients With Repaired Transposition of the Great Arteries." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14456.
Full textAlbal, Priti G., and Prahlad G. Menon. "MRI and CT Image-Fusion Based Aorta and Coronary Artery Model for In-Silico Feasibility Evaluation of Perfusion With an Ascending Aortic Pump, Using Computational Fluid Dynamics." In ASME 2013 Conference on Frontiers in Medical Devices: Applications of Computer Modeling and Simulation. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/fmd2013-16105.
Full textFayssal, Iyad, Fadl Moukalled, Samir Alam, Robert Habib, and Hussain Ismaeel. "The Development of a Robust Low Computational Cost Diagnostic Tool to Evaluate Stenosis Functional Significance in Human Coronary Arteries." In ASME 2015 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/imece2015-51532.
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