Academic literature on the topic 'Coronary Vessels physiology'
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Journal articles on the topic "Coronary Vessels physiology":
1
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.
Abstract:
The branching characteristics of the right coronary artery, acute marginal, posterior descending, left anterior descending, circumflex, and obtuse marginal arteries are compared with those of diagonal branches, left and right ventricular branches, septal, and higher-order branches, to test a newly proposed functional classification of the coronary arteries in which the first group rank as distributing vessels and the second as delivering vessels. According to this classification, the function of the first type is merely to convey blood to the borders of myocardial zones, while the function of the second is to implement the actual delivery of blood into these zones. This functional difference is important in the hemodynamic analysis of coronary heart disease, as it provides an assessment of the role of a vessel within the coronary network and hence an assessment of the functional importance of that vessel in a particular heart. Measurements from casts of human coronary arteries are used to examine the relevant characteristics of these vessels and hence to test the basis of this classification.
2
Greer, 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.
3
Kassab, 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.
Abstract:
To establish a mathematical model of the tree like arteries for the purpose of hemodynamic analysis, a complete set of morphometric data of pig coronary arteries is presented. For the purpose of mathematical modeling, three innovations in morphometry are introduced: 1) a rule for assigning the order numbers of the vessels on the basis of diameter ranges, 2) a connectivity matrix to describe asymmetric branching, and 3) a measurement of the fraction of vessel segments connected in series. The morphometric measurements were made with the silicone elastomer-casting method. Data on smaller vessels were obtained from histological specimens by optical sectioning. Data on larger vessels were obtained from vascular casts. The order number, diameter, length, connectivity matrix, and fractions of the vessels of a given order connected in series were measured for all orders of vessels of the right coronary artery and the left anterior descending and left circumflex branches. The data can be used to analyze the longitudinal distribution of blood pressure and volume and spatial distribution of perfusion in myocardium.
4
Kassab, 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.
Abstract:
The heart muscle is nourished by a complex system of blood vessels that make up the coronary circulation. Here we show that the design of the coronary circulation has a functional hierarchy. A full anatomic model of the coronary arterial tree, containing millions of blood vessels down to the capillary vessels, was simulated based on previously measured porcine morphometric data. A network analysis of blood flow through every vessel segment was carried out based on the laws of fluid mechanics and appropriate boundary conditions. Our results show an abrupt change in cross-sectional area that demarcates the transition from epicardial (EPCA) to intramyocardial (IMCA) coronary arteries. Furthermore, a similar pattern of blood flow was observed with a corresponding transition from EPCA to IMCA. These results suggest functional differences between the two types of vessels. An additional abrupt change occurs in the IMCA in relation to flow velocity. The velocity is fairly uniform proximal to these vessels but drops significantly distal to those vessels toward the capillary branches. This finding suggests functional differences between large and small IMCA. Collectively, these observations suggest a novel functional hierarchy of the coronary vascular tree and provide direct evidence of a structure-function relation.
5
Hoffman, 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.
Abstract:
The blood vessels that run on the surface of the heart and through its muscle are compliant tubes that can be affected by the pressures external to them in at least two ways. If the pressure outside these vessels is higher than the pressure at their downstream ends, the vessels may collapse and become Starling resistors or vascular waterfalls. If this happens, the flow through these vessels depends on their resistance and the pressure drop from their inflow to the pressure around them and is independent of the actual downstream pressure. In the first part of this review, the physics of collapsible tubes is described, and the possible occurrences of vascular waterfalls in the body is evaluated. There is good evidence that waterfall behavior is seen in collateral coronary arteries and in extramural coronary veins, but the evidence that intramural coronary vessels act like vascular waterfalls is inconclusive. There is no doubt that in systole there are high tissue pressures around the intramyocardial vessels, particularly in the subendocardial muscle of the left ventricle. The exact nature and values of the forces that act at the surface of the small intramural vessels, however, are still not known. We are not certain whether radial (compressive) or circumferential and longitudinal (tensile) stresses are the major causes of vascular compression; the role of collagen struts in modifying the reaction of vessel walls to external pressures is unknown but possibly important; direct examination of small subepicardial vessels has failed to show vascular collapse. One of the arguments in favor of intramyocardial vascular waterfalls has been that during a long diastole the flow in the left coronary artery decreases and reaches zero when coronary arterial pressure is still high: it can be as much as 50 mmHg in the autoregulating left coronary arterial bed and approximately 15-20 mmHg even when the vessels have been maximally dilated. These high zero flow pressures, especially during maximal vasodilatation, have been regarded as indicating a high back pressure to flow that is due to waterfall behavior of vessels that are exposed to tissue pressures.(ABSTRACT TRUNCATED AT 400 WORDS)
6
Habazettl, 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.
Abstract:
We investigated the effects of adenosine and nitroglycerin (NTG) on coronary microvessel diameters (intravital fluorescence microscopy) and coronary perfusion (radioactive microspheres). Measurements were performed during baseline conditions (intravenous piritramid) and during controlled hypotension (mean arterial pressure approximately 60 mmHg) induced by halothane, adenosine, and NTG. Coronary vascular resistance (CVR) remained unchanged during halothane (-7%) but decreased during adenosine (-76%) and NTG (-29%). Coronary arteriolar diameters increased during all experimental steps. In the smallest vessels (20–40 microns), diameters increased by 14, 43, and 42% during halothane-, adenosine-, and NTG-induced hypotension, respectively. Diameter increases were less pronounced in larger vessels. The uniform action of adenosine and NTG in 20- to 500-microns arterial vessels is in contrast to the pronounced differences in reduction of CVR. Preferential dilation of arterioles < 20 microns or recruitment of coronary microvessels by adenosine might account for the more pronounced decrease of CVR during adenosine. Intracoronary application of adenosine (0.8 mg.kg-1.h-1) and NTG (1, 5, and 25 micrograms.kg-1.h-1) equally caused near-maximum dilation of coronary arterioles > 100 microns. However, NTG dilation of arterioles < 100 microns was dose dependent and exceeded large-vessel dilation only with the highest concentration of NTG.
7
Räsänen, 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.
Abstract:
Background: Recent discoveries have indicated that, in the developing heart, sinus venosus and endocardium provide major sources of endothelium for coronary vessel growth that supports the expanding myocardium. Here we set out to study the origin of the coronary vessels that develop in response to vascular endothelial growth factor B (VEGF-B) in the heart and the effect of VEGF-B on recovery from myocardial infarction. Methods: We used mice and rats expressing a VEGF-B transgene, VEGF-B-gene–deleted mice and rats, apelin-CreERT, and natriuretic peptide receptor 3–CreERT recombinase-mediated genetic cell lineage tracing and viral vector–mediated VEGF-B gene transfer in adult mice. Left anterior descending coronary vessel ligation was performed, and 5-ethynyl-2’-deoxyuridine–mediated proliferating cell cycle labeling; flow cytometry; histological, immunohistochemical, and biochemical methods; single-cell RNA sequencing and subsequent bioinformatic analysis; microcomputed tomography; and fluorescent- and tracer-mediated vascular perfusion imaging analyses were used to study the development and function of the VEGF-B–induced vessels in the heart. Results: We show that cardiomyocyte overexpression of VEGF-B in mice and rats during development promotes the growth of novel vessels that originate directly from the cardiac ventricles and maintain connection with the coronary vessels in subendocardial myocardium. In adult mice, endothelial proliferation induced by VEGF-B gene transfer was located predominantly in the subendocardial coronary vessels. Furthermore, VEGF-B gene transduction before or concomitantly with ligation of the left anterior descending coronary artery promoted endocardium-derived vessel development into the myocardium and improved cardiac tissue remodeling and cardiac function. Conclusions: The myocardial VEGF-B transgene promotes the formation of endocardium-derived coronary vessels during development, endothelial proliferation in subendocardial myocardium in adult mice, and structural and functional rescue of cardiac tissue after myocardial infarction. VEGF-B could provide a new therapeutic strategy for cardiac neovascularization after coronary occlusion to rescue the most vulnerable myocardial tissue.
8
Lavallée, 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.
Abstract:
Given that circulating ET levels in heart failure, in particular, may reach physiological threshold for coronary constrictor responses, the primary objective of the present review is to consider coronary vessels as an important target for circulating and locally produced endothelin(s). In healthy vessels, ET-1 causes biphasic coronary responses characterized by a transient dilation of large and small arteries followed by a sustained constriction. ETB receptors are pivotal in the early dilation of resistance vessels, whereas dilation of conductance vessels may be a secondary phenomenon triggered by flow increases. Exogenous ET-1 causes coronary constriction almost exclusively through ETA receptor activation. Human and canine large epicardial coronary vessels display significant baseline ET-1 dependent tone in vitro and in vivo, an ETA-dependent process. In contrast, ETB receptors located on smooth muscle cells are apparently less important for producing constrictor responses. NO production may serve as an important counter-regulatory mechanism to limit ET-dependent effects on coronary vessels. Conversely, in a dysfunctional endothelium, the loss of NO may augment ET-1 production and activity. By lifting the ET-dependent burden from coronary vessels, ET receptor blockade should help to ensure a closer match between cardiac metabolic demand and coronary perfusion.Key words: endothelin, ET receptors, coronary vessels, coronary blood flow, nitric oxide, shear stress, atherosclerosis, humans, animals.
9
Zhang, 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.
Abstract:
This study assessed the effects of nitroglycerin (NTG) on epicardial conductance and blood flow regulatory vessels over a wide dose range (10(-10) to 10(-6) mol NTG) in chronically instrumented awake mongrel dogs. NTG bolus injection caused dose-dependent dilation of both conductance and blood flow regulatory vessels. The dose-response curves for blood flow were shifted markedly to the right of the response of conductance vessels so that the proximal vessels had reached 50% of their maximum vasodilation before significant increases in blood flow. The calculated doses for half-maximal vasodilation were 2.8 x 10(-8) and 7.8 x 10(-7) mol for conductance and blood flow, respectively, indicating an approximately 39 times greater sensitivity of the proximal vessels to NTG. NTG had a striking dose-dependent effect on the duration of vasodilation of conductance vessels but did not have a dose-dependent duration effect on coronary blood flow. Although acetylcholine demonstrated a dose-dependent response effect on the conductance vessels similar to NTG, the conductance and resistance vessels demonstrated the same sensitivity to acetylcholine, supporting the view that differences in the mechanics of vasodilation of the two vessel segments did not account for the differential sensitivities to NTG.
10
Duncker, 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.
Abstract:
Exercise is the most important physiological stimulus for increased myocardial oxygen demand. The requirement of exercising muscle for increased blood flow necessitates an increase in cardiac output that results in increases in the three main determinants of myocardial oxygen demand: heart rate, myocardial contractility, and ventricular work. The approximately sixfold increase in oxygen demands of the left ventricle during heavy exercise is met principally by augmenting coronary blood flow (∼5-fold), as hemoglobin concentration and oxygen extraction (which is already 70–80% at rest) increase only modestly in most species. In contrast, in the right ventricle, oxygen extraction is lower at rest and increases substantially during exercise, similar to skeletal muscle, suggesting fundamental differences in blood flow regulation between these two cardiac chambers. The increase in heart rate also increases the relative time spent in systole, thereby increasing the net extravascular compressive forces acting on the microvasculature within the wall of the left ventricle, in particular in its subendocardial layers. Hence, appropriate adjustment of coronary vascular resistance is critical for the cardiac response to exercise. Coronary resistance vessel tone results from the culmination of myriad vasodilator and vasoconstrictors influences, including neurohormones and endothelial and myocardial factors. Unraveling of the integrative mechanisms controlling coronary vasodilation in response to exercise has been difficult, in part due to the redundancies in coronary vasomotor control and differences between animal species. Exercise training is associated with adaptations in the coronary microvasculature including increased arteriolar densities and/or diameters, which provide a morphometric basis for the observed increase in peak coronary blood flow rates in exercise-trained animals. In larger animals trained by treadmill exercise, the formation of new capillaries maintains capillary density at a level commensurate with the degree of exercise-induced physiological myocardial hypertrophy. Nevertheless, training alters the distribution of coronary vascular resistance so that more capillaries are recruited, resulting in an increase in the permeability-surface area product without a change in capillary numerical density. Maintenance of α- and ß-adrenergic tone in the presence of lower circulating catecholamine levels appears to be due to increased receptor responsiveness to adrenergic stimulation. Exercise training also alters local control of coronary resistance vessels. Thus arterioles exhibit increased myogenic tone, likely due to a calcium-dependent protein kinase C signaling-mediated alteration in voltage-gated calcium channel activity in response to stretch. Conversely, training augments endothelium-dependent vasodilation throughout the coronary microcirculation. This enhanced responsiveness appears to result principally from an increased expression of nitric oxide (NO) synthase. Finally, physical conditioning decreases extravascular compressive forces at rest and at comparable levels of exercise, mainly because of a decrease in heart rate. Impedance to coronary inflow due to an epicardial coronary artery stenosis results in marked redistribution of myocardial blood flow during exercise away from the subendocardium towards the subepicardium. However, in contrast to the traditional view that myocardial ischemia causes maximal microvascular dilation, more recent studies have shown that the coronary microvessels retain some degree of vasodilator reserve during exercise-induced ischemia and remain responsive to vasoconstrictor stimuli. These observations have required reassessment of the principal sites of resistance to blood flow in the microcirculation. A significant fraction of resistance is located in small arteries that are outside the metabolic control of the myocardium but are sensitive to shear and nitrovasodilators. The coronary collateral system embodies a dynamic network of interarterial vessels that can undergo both long- and short-term adjustments that can modulate blood flow to the dependent myocardium. Long-term adjustments including recruitment and growth of collateral vessels in response to arterial occlusion are time dependent and determine the maximum blood flow rates available to the collateral-dependent vascular bed during exercise. Rapid short-term adjustments result from active vasomotor activity of the collateral vessels. Mature coronary collateral vessels are responsive to vasodilators such as nitroglycerin and atrial natriuretic peptide, and to vasoconstrictors such as vasopressin, angiotensin II, and the platelet products serotonin and thromboxane A2. During exercise, ß-adrenergic activity and endothelium-derived NO and prostanoids exert vasodilator influences on coronary collateral vessels. Importantly, alterations in collateral vasomotor tone, e.g., by exogenous vasopressin, inhibition of endogenous NO or prostanoid production, or increasing local adenosine production can modify collateral conductance, thereby influencing the blood supply to the dependent myocardium. In addition, vasomotor activity in the resistance vessels of the collateral perfused vascular bed can influence the volume and distribution of blood flow within the collateral zone. Finally, there is evidence that vasomotor control of resistance vessels in the normally perfused regions of collateralized hearts is altered, indicating that the vascular adaptations in hearts with a flow-limiting coronary obstruction occur at a global as well as a regional level. Exercise training does not stimulate growth of coronary collateral vessels in the normal heart. However, if exercise produces ischemia, which would be absent or minimal under resting conditions, there is evidence that collateral growth can be enhanced. In addition to ischemia, the pressure gradient between vascular beds, which is a determinant of the flow rate and therefore the shear stress on the collateral vessel endothelium, may also be important in stimulating growth of collateral vessels.
Dissertations / Theses on the topic "Coronary Vessels physiology":
1
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.
Abstract:
Amendments inserted at back. "May 2002" Includes bibliographical references (leaves 237-290) Experiments described in this thesis address the potential role of inducible nitric oxide synthase (iNOS) in hibernating myocardium. Specifically it was sought to establish a cellular model of hibernating myocardium and investigate the expression, regulation and effects of iNOS in this model. Experiments were performed using primary cultures of neonatal rat ventricular myocytes.
2
Wikenheiser, 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.
3
Wang, Ruoya. "Novel theoretical and experimental frameworks for multiscale quantification of arterial mechanics." Diss., Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/47718.
Abstract:
The mechanical behavior of the arterial wall is determined by the composition and structure of its internal constituents as well as the applied traction-forces, such as pressure and axial stretch. The purpose of this work is to develop new theoretical frameworks and experimental methodologies to further the understanding of arterial mechanics and role of the various intrinsic and extrinsic mechanically motivating factors. Specifically, residual deformation, matrix organization, and perivascular support are investigated in the context of their effects on the overall and local mechanical behavior of the artery. We propose new kinematic frameworks to determine the displacement field due to residual deformations previously unknown, which include longitudinal and shearing residual deformations. This allows for improved predictions of the local, intramural stresses of the artery. We found distinct microstructural differences between the femoral and carotid arteries from non-human primates. These arteries are functionally and mechanically different, but are geometrically and compositionally similar, thereby suggesting differences in their microstructural alignments, particularly of their collagen fibers. Finally, we quantified the mechanical constraint of perivascular support on the coronary artery by mechanically testing the artery in-situ before and after surgical exposure.
4
Sarkar, 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/.
5
"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.
Abstract:
Wu Min.Thesis (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
6
Noblet, Jillian Nicole. "Coronary perivascular adipose tissue and vascular smooth muscle function: influence of obesity." Diss., 2016. http://hdl.handle.net/1805/9815.
Abstract:
Indiana University-Purdue University Indianapolis (IUPUI)Factors 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.
7
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.
Abstract:
Indiana University-Purdue University Indianapolis (IUPUI)Obesity 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.
8
Deep, Debanjan. "A study of blood flow in normal and dilated aorta." Thesis, 2013. http://hdl.handle.net/1805/4440.
Abstract:
Indiana University-Purdue University Indianapolis (IUPUI)Atherosclerotic 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":
1
International Union of Angiology. World Congress. 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. Edited by Maurer Peter Carl and Deutsche Gesellschaft für Angiologie. Jahrestagung. München: W. Zuckschwerdt Verlag, 1986.
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Mohl, W. Coronary sinus interventions in cardiac surgery. 2nd ed. Georgetown, Tex: Landes Bioscience, 2000.
3
Pijls, Nico H. J. Coronary pressure. Dordrecht: Kluwer Academic Publishers, 1997.
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Pijls, Nico H. J. Coronary pressure. 2nd ed. Dordrecht: Kluwer Academic Publishers, 2000.
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Seccombe, John F. Vasoactive factors produced by the endothelium: Physiology and surgical implications. Austin: R.G. Landes, 1994.
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Tomanek, Robert J. Coronary Vasculature: Development, Structure-Function, and Adaptations. Springer, 2012.
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Tomanek, Robert J. Coronary Vasculature: Development, Structure-Function, and Adaptations. Springer, 2012.
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Pijls, N. H. Coronary Pressure. Springer, 2010.
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Pijls, N. H., and B. de Bruyne. Coronary Pressure (DEVELOPMENTS IN CARDIOVASCULAR MEDICINE Volume 227) (Developments in Cardiovascular Medicine). Springer, 2000.
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Li, John K.-J. The Arterial Circulation: Physical Principles and Clinical Applications. Humana Press, 2000.
Book chapters on the topic "Coronary Vessels physiology":
1
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.
Abstract:
Cardiac tumors are rarely encountered in clinical practice; however, because they affect vital structures, they can have significant consequences. Cardiac tumors are categorized as either primary tumors originating from cardiac tissue or metastatic tumors migrated from other sites; they may infiltrate the atria, ventricles, valves, and coronary arteries, resulting in considerable changes to normal physiology. They may extend beyond the myocardium to the pericardium, great vessels, and mediastinum. Advances in the development of imaging modalities have allowed for expedited diagnostic evaluation of cardiac tumors. Prompt treatment, which often includes surgical intervention, is essential to both alleviate symptoms and prevent harmful sequelae. The intraoperative anesthetic management of a patient with a cardiac mass presents a number of challenges due to altered cardiovascular physiology. Because these tumors occur so infrequently, standardized, evidence-based diagnostic and treatment guidelines have not been developed. The existing data were derived mainly from small case series and case reports. The aggressive nature of the disease warrants further investigation to improve the accuracy of diagnostic modalities and the efficacy of treatment regimens.
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Becker, 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.
Abstract:
For over a century astute clinicians have recognized that prodromal symptoms often precede acute myocardial infarction (MI). The evolution of symptoms was subsequently found to correlate with changes in atherosclerotic plaque composition, morphology, and thrombogenicity, leading to the classification of symptoms that are currently categorized to better delineate diagnostic and management strategies. Acute coronary syndromes (ACSs) are traditionally divided into two separate categories—ST-segment elevation and non–ST-segment elevation ACS—based on the presenting electrocardiogram. The latter category is then subdivided into unstable angina and non–ST-segment elevation MI, based on the absence or presence of elevated cardiac biomarkers, respectively. This chapter considers ST-segment elevation MI and non–ST-segment elevation ACS based on pharmacologic and clinical (diagnostics and routine management) constructs. ST-segment elevation MI (STEMI), in a vast majority of cases, is caused by occlusive thrombosis at a site of plaque rupture. In others, particularly when the stimulus for thrombosis is strong, occlusion may follow minor disruption of the plaque surface (erosion) or occur in areas of endothelial cell injury (activation with inflammatory features and concomitantly impaired vascular thromboresistance). Coronary arterial spasm, in the absence of intrinsic vascular disease (as may be seen with cocaine use), can also impair restrictive blood flow to the myocardium, resulting in cellular death. The goal of pharmacology-based therapy (and mechanical intervention) is to restore myocardial blood flow as quickly and completely as possible. The “open vessel hypotheses” predicts that rapid, complete, and sustained myocardial perfusion through the prompt restoration of physiologic blood flow will minimize (salvage) myocardium, promote ventricular performance, and reduce mortality. Strong support for the open-vessel hypothesis can be traced to the Thrombolysis and Myocardial Infarction (TIMI) trial performed in the 1980s (Dalen et al., 1988; TIMI Study Group, 1985). Patients with patent infarct-related coronary arteries 90 minutes after the initiation of fibrinolytic therapy had an 8.1% mortality at 1 year, compared to a 14.8% mortality among those with an occluded vessel. Since that time, several large-scale clinical trials have confirmed the importance of an open infarct-related coronary artery for early, intermediate, and long-term outcome.
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Becker, 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.
Abstract:
The failure of fibrinolytic therapy to restore physiologic myocardial perfusion in upward of 40% of patients supports the development of strategies to improve response rates to percutaneous coronary intervention (PCI) in those requiring early procedures. The construct of facilitated PCI (pharmacoinvasive therapy) provides a platform for utilizing the strengths of existing therapies and treatment modalities. The Heparin in Early Patency (HEAP) trial (Zijlstra et al., 2002) included 1,702 patients treated with primary PCI for myocardial infarction (MI); 860 patients received aspirin (500 mg IV) and UFH (≥5,000 U IV) before being transported to the hospital and 842 patients received the same antithrombotic therapy in the hospital. TIMI 2 or 3 flow rates were higher in the pretreated group (31% vs. 20%; p = .001), and patients with TIMI 2 or 3 flow initially had a higher PCI success rate (94% vs. 89%; p <.001) and a lower 30-day mortality (1.6% vs. 3.4%; p = .04). The Plasminogen Activator Angioplasty Compatibility Trial (PACT) randomized 606 patients to receive a 50-mg bolus of alteplase or placebo, followed by immediate angiography and angioplasty if needed (Ross et al., 1999). TIMI flow rates on arrival to the catheterization laboratory were 33% and 15%, respectively. Facilitated PCI and primary PCI restored TIMI 3 flow in occluded vessels equally (77% and 79%, respectively). There were no differences in major bleeding. Left ventricular ejection fraction was highest in those with TIMI 3 flow on arrival to the catheterization laboratory or following PCI within 1 hour of alteplase administration. Full-dose fibrinolytic therapy with alteplase or reteplase followed by coronary angiography and PCI (if no clinical evidence of reperfusion) was evaluated retrospectively in the Global Use of Strategies to Open Occluded Arteries (GUSTO) III trial (Miller et al., 1999). Among those undergoing PCI (n = 392), 87 patients received in-laboratory abciximab. A trend toward reduced mortality was observed in abciximab-treated patients, but at a higher cost of hemorrhagic complications. In the Strategies for Patency Enhancement in the Emergency Department (SPEED) trial (Herrmann et al., 2000), 323 patients who underwent PCI had an 88% procedural success rate and a 30-day composite of death, reinfarction, or revascularization of 5.6%.
Conference papers on the topic "Coronary Vessels physiology":
1
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.
Abstract:
Transposition of the great arteries (TGA) is a congenital heart disease characterized by abnormal spatial arrangement of the two main vessels, with the aorta arising from the pulmonary valve and the main pulmonary artery arising from the aortic valve. TGA surgical repair with the arterial switch operation (ASO) involves physically repositioning the aorta and the pulmonary artery in their correct anatomical location, as well as separately moving the coronary arteries. Following ASO, decreased aortic distensibility and enlarged aortic root have been observed, together with late complications such as coronary artery obstruction, neoaortic valvar insufficiency, and arrhythmia [1]. Clearly, further knowledge of the hemodynamics in the neoaorta following ASO can be helpful in understanding the physiology of repaired-TGA. We suggest that engineering tools can provide access to such knowledge, both experimentally and computationally. 4D flow data from magnetic resonance (MR) imaging can generate excellent maps of velocity streamlines and — to our knowledge — has never been applied to this clinical problem. In addition, 4D MR flow data gathered in-vitro (hence more reproducible and more stable than in-vivo) can be a resourceful tool for validating a computational fluid dynamics (CFD) model of the same problem. The experimental model, lacking respiration effects and concerns about scanning time, can also be used for exploring the optimal spatial and temporal resolution for improving the quality of the data. Ultimately, we suggest that a synergistic approach (experimental 4D MR flow + CFD study) carried out at a patient-specific level can provide knowledge about the hemodynamics in the neoaorta following ASO. For this purpose, we present two comparisons: (a) TGA anatomy vs. an age-matched healthy subject (b) in-vitro vs. in-silico.
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Albal, 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.
Abstract:
Left ventricular assist devices (LVADs) are mechanical pumps that provide full or partial support of the circulation in patients with varying degrees of heart failure (HF). This simulation study explores the hemodynamic effects of a continuous flow pump deployed in the Ascending Aorta (AAo) specifically focusing on: (a) perfusion of the coronary arterial circulation and (b) the effect of induced non-physiologic, swirling flow discharged by the pump on perfusion to head-neck vessels of the aortic arch.
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Fayssal, 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.
Abstract:
There is discordance between the anatomic severities of the coronary narrowing and their corresponding functional significance. Fractional Flow Reserve (FFR) is among the physiological parameters invasively measured to assess the hemodynamic significance of a stenosis during maximal hyperemia. FFR values ≤ 0.8 indicate that the downstream heart tissue perfused by this vessel is at risk for ischemia. While measuring FFR is an invasive procedure that is expensive, time consuming, and not without complications, recently, noninvasive estimation of FFR was shown to be possible from comprehensive predictive techniques allowing the computation of in-vivo FFR. However, these non-invasive methods are associated with high computational cost and require high performance computing technology, thus, reducing their wide adoption in clinics. This paper is steered to achieve two main goals: (1) to develop a fast numerical method to aid clinicians assessing ischemia level and determine if coronary revascularization (PCI) is required in human diseased coronary arteries with minimum time and computer resources; (2) to develop a robust method which allows predicting the patient FFR independently of the actual in-vivo physiologic conditions (mainly pressure) of the specific patient. The numerical framework was designed by adopting the finite volume method to generate the discrete model of the Reynolds average form of conservation equations used to predict blood hemodynamics. Two strategies were investigated to reduce computational cost while retaining solution accuracy. The first strategy is based on isolating the diseased artery from its branch tree and simulating it separately without implicitly integrating other arterial segments. A lumped dynamic model with special numerical treatment is coupled to the 3D domain outlet boundary to account for the downstream effects from the vascular bed. The second strategy is based on replacing a full transient simulation by a steady state one performed under mean conditions of pressure and blood volume flow rate. The strategy was applied on a healthy (hypothetical) and stenosed arterial segments with different stenosis severities simulated under rest and hyperemic conditions. An excellent agreement was achieved for FFR values computed from full transient simulations with the ones obtained from steady state simulation (error < 0.2 % was obtained for all test cases). The computational cost for the mean condition scenario was 0.1 that of a full transient simulation. The robustness of the method was tested by varying inflow conditions and reporting their effect on FFR. Interestingly, the predicted ischemia level was not altered when the inlet pressure was increased by 10 % from the base case. An analytical model was derived to explain the FFR independency of patient in-vivo coronary pressure. These promising findings from the numerical tests performed on idealized healthy and stenosed arterial models could significantly impact the applicability of the developed methodology and translating it into future practical clinical applications.