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Journal articles on the topic 'Coronary Vessels physiology'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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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.

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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

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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.

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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.

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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

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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.

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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 dem

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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.

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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 collaps

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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.

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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 s

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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.

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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 ge

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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.

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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 triggere

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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.

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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 vasodilat

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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.

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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 o

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11

Kassab, G. S., D. H. Lin, and Y. C. Fung. "Morphometry of pig coronary venous system." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 6 (December 1, 1994): H2100—H2113. http://dx.doi.org/10.1152/ajpheart.1994.267.6.h2100.

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This is a third part of tripartite morphometric data of the pig coronary blood vessels, giving a complete quantitative description of the arterial tree [Kassab et al., Am. J. Physiol. 265 (Heart Circ. Physiol. 34): H350-H365, 1993], capillary network [Kassab and Fung, Am. J. Physiol. 267 (Heart Circ. Physiol. 36): H319-H325, 1994], and venous tree (this article). Together they provide the quantitative anatomic foundation for coronary hemodynamics. The coronary venules have a unique morphology. Unlike coronary arterioles, which have cylindrical cross sections and a fairly constant diameter in e

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Wischgoll, Thomas, Jenny S. Choy, and Ghassan S. Kassab. "Extraction of morphometry and branching angles of porcine coronary arterial tree from CT images." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 5 (November 2009): H1949—H1955. http://dx.doi.org/10.1152/ajpheart.00093.2009.

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The morphometry (diameters, length, and angles) of coronary arteries is related to their function. A simple, easy, and accurate image-based method to seamlessly extract the morphometry for coronary arteries is of significant value for understanding the structure-function relation. Here, the morphometry of large (≥1 mm in diameter) coronary arteries was extracted from computed tomography (CT) images using a recently validated segmentation algorithm. The coronary arteries of seven pigs were filled with Microfil, and the cast hearts were imaged with CT. The centerlines of the extracted vessels, t

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Choy, Jenny Susana, and Ghassan S. Kassab. "Wall thickness of coronary vessels varies transmurally in the LV but not the RV: implications for local stress distribution." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 2 (August 2009): H750—H758. http://dx.doi.org/10.1152/ajpheart.01136.2008.

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Since the right and left ventricles (RV and LV) function under different loading conditions, it is not surprising that they differ in their mechanics (intramyocardial pressure), structure, and metabolism; such differences may also contribute to differences in the coronary vessel wall. Our hypothesis is that intima-media thickness (IMT), IMT-to-radius (IMT-to-R) ratio, and vessel wall stress vary transmurally in the LV, much more than in the RV. Five normal Yorkshire swine were used in this study. The major coronary arteries were cannulated through the aorta and perfusion fixed with 6.25% gluta

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14

Gao, Y., H. Zhou, and J. U. Raj. "Antenatal betamethasone therapy potentiates nitric oxide-mediated relaxation of preterm ovine coronary arteries." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 2 (February 1, 1996): H538—H544. http://dx.doi.org/10.1152/ajpheart.1996.270.2.h538.

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The present study was designed to test the hypothesis that betamethasone may potentiate nitric oxide-mediated relaxation of coronary arteries of preterm lambs. Isolated coronary arteries were obtained from lambs delivered at 128 days gestation. The lambs were treated intramuscularly with a single dose of betamethasone or saline 48 h before delivery and were killed after 3 h of ventilation after delivery. Vessel rings were suspended in organ chambers filled with modified Krebs-Ringer solution (95% O2-5% CO2, 37 degrees C), and their isometric tension was recorded. The endothelium-dependent rela

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15

Kassab, G. S., and Y. C. Fung. "Topology and dimensions of pig coronary capillary network." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 1 (July 1, 1994): H319—H325. http://dx.doi.org/10.1152/ajpheart.1994.267.1.h319.

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To provide a morphometric basis for any mathematical modeling of the coronary vasculature, data on the network of coronary capillary blood vessels and the topology of the arteriolar supply and venular drainage relative to the capillaries are presented. The diameters, lengths, and branching patterns of the coronary capillary blood vessels in the right and left ventricles of four pigs were measured. The locations of the coronary arterioles and venules were identified, topological maps were constructed, and the mean functional length of capillaries connecting an arteriole to an adjacent venule wa

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16

Huo, Yunlong, and Ghassan S. Kassab. "A hybrid one-dimensional/Womersley model of pulsatile blood flow in the entire coronary arterial tree." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 6 (June 2007): H2623—H2633. http://dx.doi.org/10.1152/ajpheart.00987.2006.

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Using a frequency-domain Womersley-type model, we previously simulated pulsatile blood flow throughout the coronary arterial tree. Although this model represents a good approximation for the smaller vessels, it does not take into account the nonlinear convective energy losses in larger vessels. Here, using Womersley's theory, we present a hybrid model that considers the nonlinear effects for the larger epicardial arteries while simulating the distal vessels (down to the 1st capillary segments) with the use of Womersley's Theory. The main trunk and primary branches were discretized and modeled

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17

Rajagopalan, S., S. Dube, and J. M. Canty. "Regulation of coronary diameter by myogenic mechanisms in arterial microvessels greater than 100 microns in diameter." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 2 (February 1, 1995): H788—H793. http://dx.doi.org/10.1152/ajpheart.1995.268.2.h788.

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We performed the present study to determine the quantitative significance of transient and steady-state myogenic responses in isolated coronary resistance vessels greater than 100 microns in diameter. Small coronary arteries were isolated from freshly excised porcine hearts (n = 14) and were studied under static conditions in a superfused vessel chamber that allowed internal diameter to be assessed continuously using video microscopic techniques. At a mean distending pressure of 50 mmHg, the passive diameter of resistance arteries following sodium nitroprusside averaged 181 +/- 10 (SE) microns

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18

Lynch, F. M., C. Austin, A. M. Heagerty, and A. S. Izzard. "Adenosine and hypoxic dilation of rat coronary small arteries: roles of the ATP-sensitive potassium channel, endothelium, and nitric oxide." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 3 (March 2006): H1145—H1150. http://dx.doi.org/10.1152/ajpheart.00314.2005.

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The aims of the study were to examine the roles of the ATP-sensitive potassium (KATP) channel, the endothelium, and nitric oxide (NO) in the responses of rat coronary small arteries to adenosine and hypoxia. Segments of rat coronary vessel were investigated in vitro using pressure myography; all vessels studied developed stable spontaneous myogenic tone during equilibration. Glibenclamide (a KATP channel inhibitor) reversed pinacidil but not 2-deoxyglucose-induced dilation. Both adenosine and hypoxia dilated the vessels, and glibenclamide did not reverse these responses. Endothelial removal or

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Liu, Yi, Wei Zhang, and Ghassan S. Kassab. "Effects of myocardial constraint on the passive mechanical behaviors of the coronary vessel wall." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 1 (January 2008): H514—H523. http://dx.doi.org/10.1152/ajpheart.00670.2007.

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The large epicardial coronary arteries and veins span the surface of the heart and gradually penetrate into the myocardium. It has recently been shown that remodeling of the epicardial veins in response to pressure overload strongly depends on the degree of myocardial support. The nontethered regions of the vessel wall show significant intimal hyperplasia compared with the tethered regions. Our hypothesis is that such circumferentially nonuniform structural adaptation in the vessel wall is due to nonuniform wall stress and strain. Transmural stress and strain are significantly influenced by th

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Myers, P. R., P. F. Banitt, R. Guerra, and D. G. Harrison. "Characteristics of canine coronary resistance arteries: importance of endothelium." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 2 (August 1, 1989): H603—H610. http://dx.doi.org/10.1152/ajpheart.1989.257.2.h603.

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Canine coronary resistance vessels were studied in vitro to examine the role of the endothelium in modulating responses to acetylcholine, vasopressin, and thrombin and to compare these responses to those found in large epicardial vessels. Acetylcholine had no effect on passively distended microvessels; however, after preconstriction with the thromboxane analogue, U 46619 caused dose-dependent vasodilation [50% effective concentration (EC50), 0.05 microM; maximum response, 97.9 +/- 2.1% relaxation]. Large epicardial arterial rings studied in organ chambers similarly relaxed to acetylcholine (EC

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Pistea, Adrian, Erik N. T. P. Bakker, Jos A. E. Spaan, and Ed VanBavel. "Flow inhibits inward remodeling in cannulated porcine small coronary arteries." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 6 (December 2005): H2632—H2640. http://dx.doi.org/10.1152/ajpheart.00205.2005.

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The mechanisms of flow-induced vascular remodeling are poorly understood, especially in the coronary microcirculation. We hypothesized that application of flow in small coronary arteries in organoid culture would cause a nitric oxide (NO)-mediated dilation and inhibit inward remodeling. We developed an organoid culture setup to drive a flow through cannulated arterioles at constant luminal pressure via a pressure gradient between the pipettes. Subepicardial porcine coronary arterioles with diameter at full dilation and 60 mmHg ( D0) of 168 ± 10 (SE) μm were cannulated. Vessels treated with Nω-

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Kassab, Ghassan S., Kha N. Le, and Yuan-Cheng B. Fung. "A hemodynamic analysis of coronary capillary blood flow based on anatomic and distensibility data." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 6 (December 1, 1999): H2158—H2166. http://dx.doi.org/10.1152/ajpheart.1999.277.6.h2158.

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An understanding of cardiac health and disease requires knowledge of the various factors that control coronary capillary blood flow. An analysis of coronary capillary blood flow based on a complete set of actual data on the capillary anatomy and elasticity does not exist. Previously, a complete set of data on the branching pattern and the vascular geometry of the pig coronary capillary network were obtained in our laboratory. In the present study, we obtained distensibility data on the coronary capillary blood vessels on the epicardial surface in the form of a pressure-diameter relationship us

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Kaimovitz, Benjamin, Yoram Lanir, and Ghassan S. Kassab. "A full 3-D reconstruction of the entire porcine coronary vasculature." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 4 (October 2010): H1064—H1076. http://dx.doi.org/10.1152/ajpheart.00151.2010.

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We have previously reconstructed the entire coronary arterial tree of the porcine heart down to the first segment of capillaries. Here, we extend the vascular model through the capillary bed and the entire coronary venous system. The reconstruction was based on comprehensive morphometric data previously measured in the porcine heart. The reconstruction was formulated as a large-scale optimization process, subject to both global constraints relating to the location of the larger veins and to local constraints of measured morphological features. The venous network was partitioned into epicardial

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Namani, Ravi, Ghassan S. Kassab, and Yoram Lanir. "Integrative model of coronary flow in anatomically based vasculature under myogenic, shear, and metabolic regulation." Journal of General Physiology 150, no. 1 (December 1, 2017): 145–68. http://dx.doi.org/10.1085/jgp.201711795.

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Coronary blood flow is regulated to match the oxygen demand of myocytes in the heart wall. Flow regulation is essential to meet the wide range of cardiac workload. The blood flows through a complex coronary vasculature of elastic vessels having nonlinear wall properties, under transmural heterogeneous myocardial extravascular loading. To date, there is no fully integrative flow analysis that incorporates global and local passive and flow control determinants. Here, we provide an integrative model of coronary flow regulation that considers the realistic asymmetric morphology of the coronary net

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Kassab, Ghassan S., Edith Pallencaoe, Amy Schatz, and Yuan-Cheng B. Fung. "Longitudinal position matrix of the pig coronary vasculature and its hemodynamic implications." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 6 (December 1, 1997): H2832—H2842. http://dx.doi.org/10.1152/ajpheart.1997.273.6.h2832.

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Hemodynamic analysis of coronary blood flow must be based on a statistically valid geometric model of the coronary vasculature. We have previously developed a diameter-defined Strahler model for the arterial and venous trees and a network model for the capillaries. A full set of data describing the geometric properties of the porcine coronary vasculature was given. The order number, diameter, length, connectivity matrix [ m,n] (CM), and parallel-series features were measured for all orders of vessels of the right coronary artery (RCA), left anterior descending artery (LAD), left circumflex art

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Liesmaa, Inka, Antti Kuoppala, Naotaka Shiota, Jorma O. Kokkonen, Karam Kostner, Mikko Mäyränpää, Petri T. Kovanen, and Ken A. Lindstedt. "Increased expression of bradykinin type-1 receptors in endothelium of intramyocardial coronary vessels in human failing hearts." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 5 (May 2005): H2317—H2322. http://dx.doi.org/10.1152/ajpheart.00815.2004.

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In experimental animals, bradykinin type-1 receptors (BK-1Rs) are induced during inflammation and ischemia, and, by exerting either cardioprotective or cardiotoxic effects, they may contribute to the pathogenesis of heart failure. Nothing is known about the expression of BK-1Rs in human heart failure. Human heart tissue was obtained from excised hearts of patients undergoing cardiac transplantation ( n = 13), due to idiopathic dilated cardiomyopathy (IDC; n = 7) or to coronary heart disease (CHD; n = 6), and from normal hearts ( n = 6). The expression of BK-1Rs was analyzed by means of competi

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Clark, Shawn G., and Leslie C. Fuchs. "BKCa channels compensate for loss of NOS-dependent coronary artery relaxation in cardiomyopathy." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 6 (December 1, 2000): H2598—H2603. http://dx.doi.org/10.1152/ajpheart.2000.279.6.h2598.

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Previously, we showed that development of myocardial necrotic lesions is associated with impaired endothelium-dependent coronary artery relaxation in young cardiomyopathic hamsters. Since active necrosis declines with aging, this study was designed to determine whether coronary artery endothelium-dependent relaxation to ACh is restored and to identify the mechanisms mediating this effect. Intraluminal diameter was recorded in coronary arteries (150–250 μm) from control (C, 297 ± 5 days old) and cardiomyopathic (M, 296 ± 4 days old) hamsters. Relaxation to ACh (10−9–3 × 10−5M) was similar in ve

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Merkus, Daphne, Marleen Visser, Birgit Houweling, Zhichao Zhou, Jessica Nelson, and Dirk J. Duncker. "Phosphodiesterase 5 inhibition-induced coronary vasodilation is reduced after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 10 (May 15, 2013): H1370—H1381. http://dx.doi.org/10.1152/ajpheart.00410.2012.

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The balance between the production and removal of cGMP in coronary vascular smooth muscle is of critical importance in determining coronary vasomotor tone and thus in the regulation of coronary blood flow. cGMP production by soluble guanylyl cyclase is activated by nitric oxide (NO), whereas cGMP breakdown occurs through phosphodiesterase 5 (PDE5). We hypothesized that myocardial infarction (MI) alters the balance between the production and removal of cGMP in the coronary vasculature and thereby alters the control of coronary vasomotor tone. Chronically instrumented swine with and without a 2-

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Hader, Shelby N., Natalya Zinkevich, Laura E. Norwood Toro, Alison J. Kriegel, Amanda Kong, Julie K. Freed, David D. Gutterman, and Andreas M. Beyer. "Detrimental effects of chemotherapy on human coronary microvascular function." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 4 (October 1, 2019): H705—H710. http://dx.doi.org/10.1152/ajpheart.00370.2019.

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Chemotherapy (CT) is a necessary treatment to prevent the growth and survival of cancer cells. However, CT has a well-established adverse impact on the cardiovascular (CV) system, even years after cessation of treatment. The effects of CT drugs on tumor vasculature have been the focus of much research, but little evidence exists showing the effects on the host microcirculation. Microvascular (MV) dysfunction is an early indicator of numerous CV disease phenotypes, including heart failure. The goal of this study was to evaluate the direct effect of doxorubicin (Dox) on human coronary MV functio

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Huo, Yunlong, Xuefeng Zhao, Yana Cheng, Xiao Lu, and Ghassan S. Kassab. "Two-layer model of coronary artery vasoactivity." Journal of Applied Physiology 114, no. 10 (May 15, 2013): 1451–59. http://dx.doi.org/10.1152/japplphysiol.01237.2012.

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Since vascular tone is regulated by smooth muscle cells in the media layer, a multilayer mechanical model is required for blood vessels. Here, we performed biaxial mechanical tests in the intima-media layer of right coronary artery to determine the passive and active properties in conjunction with the passive properties of adventitia for a full vessel wall model. A two-layer (intima-media and adventitia) model was developed to determine the transmural stress and stretch across the vessel wall. The mean ± SE values of the outer diameters of intima-media layers at transmural pressure of 60 mmHg

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Parker, Janet L., Mildred L. Mattox, and M. Harold Laughlin. "Contractile responsiveness of coronary arteries from exercise-trained rats." Journal of Applied Physiology 83, no. 2 (August 1, 1997): 434–43. http://dx.doi.org/10.1152/jappl.1997.83.2.434.

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Parker, Janet L., Mildred L. Mattox, and M. Harold Laughlin.Contractile responsiveness of coronary arteries from exercise trained rats. J. Appl. Physiol. 83(2): 434–443, 1997.—The purpose of this study was to determine whether exercise training alters vasomotor reactivity of rat coronary arteries. In vitro isometric microvessel techniques were used to evaluate vasomotor properties of proximal left anterior artery rings (1 ring per animal) from exercise-trained rats (ET; n = 10) subjected to a 12-wk treadmill training protocol (32 m/min, 15% incline, 1 h/day, 5 days/wk) and control rats (C; n =

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Goto, M., K. Tsujioka, Y. Ogasawara, Y. Wada, S. Tadaoka, O. Hiramatsu, M. Yanaka, and F. Kajiya. "Effect of blood filling in intramyocardial vessels on coronary arterial inflow." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 4 (April 1, 1990): H1042—H1048. http://dx.doi.org/10.1152/ajpheart.1990.258.4.h1042.

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The influence of the filling condition of the unstressed volume (UV) of intramyocardial vessels on the diastolic coronary arterial pressure-flow relationship was analyzed. UV is defined as the blood volume at zero transmural pressure. In seven anesthetized, paced dogs with induced heart block, coronary artery inflow was occluded so that blood in the UV was displaced into the coronary vein by myocardial contraction. After pacing was turned off, coronary perfusion pressure was increased stepwise to seven target pressures (20-90 mmHg). After reperfusion, left anterior descending coronary arterial

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Choy, Jenny Susana, and Ghassan S. Kassab. "A novel strategy for increasing wall thickness of coronary venules prior to retroperfusion." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 2 (August 2006): H972—H978. http://dx.doi.org/10.1152/ajpheart.00235.2006.

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The sudden exposure of veins to arterial pressures during coronary venous retroperfusion may cause rupture of small venules. Our rationale is to first occlude the coronary vein, which will cause an increase in pressure intermediate to arterial and venous values, and hence lead to remodeling and increased wall thickness of the veins prior to retroperfusion. To accomplish this objective, five pigs were subjected to left anterior descending (LAD) vein ligation while six pigs served as sham. Myocardial tissue samples were obtained from the area adjacent to the LAD vein at four transmural locations

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Jahangiri, Bijan, Charlotte Greer, Jackie Sutherland, Cameron McAlister, Toby Verryt, John Elliott, James Blake, Dougal McClean, David Smyth, and Aniket Puri. "Cut-off Values in Coronary Physiology: Does One Size Fit All Vessels?" Heart, Lung and Circulation 27 (2018): S26. http://dx.doi.org/10.1016/j.hlc.2018.05.158.

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Jahangiri, B., C. Greer, J. Sutherland, C. McAlister, T. Verryt, J. Elliott, D. McClean, J. Blake, D. Smyth, and A. Puri. "Cut-Off Values in Coronary Physiology: Does One Size Fit All Vessels?" Heart, Lung and Circulation 27 (2018): S490—S491. http://dx.doi.org/10.1016/j.hlc.2018.06.1018.

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Spaan, Jos, Christina Kolyva, Jeroen van den Wijngaard, Rene ter Wee, Pepijn van Horssen, Jan Piek, and Maria Siebes. "Coronary structure and perfusion in health and disease." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 366, no. 1878 (June 17, 2008): 3137–53. http://dx.doi.org/10.1098/rsta.2008.0075.

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Blood flow is distributed through the heart muscle via a system of vessels forming the coronary circulation. The perfusion of the myocardium can be hampered by atherosclerosis creating localized obstructions in the epicardial vessels or by microvascular disease. In early stages of the disease, these impediments to blood flow are offset by dilation of the resistance vessels, which normally compensates for a decrease in perfusion pressure or increased metabolism. However, this dilatory reserve can become exhausted, which in general occurs first at the deeper layers of the heart wall where intram

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Symons, J. David, Stephen V. Rendig, Charles L. Stebbins, and John C. Longhurst. "Microvascular and myocardial contractile responses to ischemia: influence of exercise training." Journal of Applied Physiology 88, no. 2 (February 1, 2000): 433–42. http://dx.doi.org/10.1152/jappl.2000.88.2.433.

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We hypothesized that exercise training preserves endothelium-dependent relaxation, lessens receptor-mediated constriction of coronary resistance arteries, and reduces myocardial contractile dysfunction in response to ischemia. After 10 wk of treadmill running or cage confinement, regional and global indexes of left ventricular contractile function were not different between trained and sedentary animals in response to three 15-min periods of ischemia (long-term; n = 17), one 5-min bout of ischemia (short-term; n = 18), or no ischemia (sham-operated; n = 24). Subsequently, coronary resistance v

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de Beer, Vincent J., Oana Sorop, Daniël A. Pijnappels, Dick H. Dekkers, Frans Boomsma, Jos M. J. Lamers, Dirk J. Duncker, and Daphne Merkus. "Integrative control of coronary resistance vessel tone by endothelin and angiotensin II is altered in swine with a recent myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 5 (May 2008): H2069—H2077. http://dx.doi.org/10.1152/ajpheart.01163.2007.

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Several studies have indicated an interaction between the renin-angiotensin (ANG II) system and endothelin (ET) in the regulation of vascular tone. Previously, we have shown that both ET and ANG II exert a vasoconstrictor influence on the coronary resistance vessels of awake normal swine. Here, we investigated whether the interaction between ANG II and ET exists in the control of coronary resistance vessel tone at rest and during exercise using single and combined blockade of angiotensin type 1 (AT1) and ETA/ETB receptors. Since both circulating ANG II and ET levels are increased after myocard

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Heaps, Cristine L., and Janet L. Parker. "Effects of exercise training on coronary collateralization and control of collateral resistance." Journal of Applied Physiology 111, no. 2 (August 2011): 587–98. http://dx.doi.org/10.1152/japplphysiol.00338.2011.

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Coronary collateral vessels serve as a natural protective mechanism to provide coronary flow to ischemic myocardium secondary to critical coronary artery stenosis. The innate collateral circulation of the normal human heart is typically minimal and considerable variability occurs in extent of collateralization in coronary artery disease patients. A well-developed collateral circulation has been documented to exert protective effects upon myocardial perfusion, contractile function, infarct size, and electrocardiographic abnormalities. Thus therapeutic augmentation of collateral vessel developme

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Klassen, Gerald A., J. Andrew Armour, and J. Barry Garner. "Coronary circulatory pressure gradients." Canadian Journal of Physiology and Pharmacology 65, no. 4 (April 1, 1987): 520–31. http://dx.doi.org/10.1139/y87-089.

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The pressure gradients of the canine coronary circulation were measured in 37 dogs during control and following eight interventions: left stellate ganglion or left vagosympathetic trunk stimulation, as well as isoproterenol, acetylcholine, noradrenaline, adenosine, phenylephrine, or adrenaline infusions. During control, pressure gradients in the epicardial coronary arteries (measured from the aorta to coronary artery branch) were 15.2 ± 1 mmHg(1 mmHg = 133.32 Pa) during systole and 10.6 ± 1.5 mmHg during diastole. Adrenaline increased this systolic gradient, while acetylcholine and phenylephri

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Parent, R., R. Pare, and M. Lavallee. "Contribution of nitric oxide to dilation of resistance coronary vessels in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 1 (January 1, 1992): H10—H16. http://dx.doi.org/10.1152/ajpheart.1992.262.1.h10.

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Endothelium-dependent relaxation of conductance coronary vessels involves nitric oxide formation from L-arginine. The present study examines whether a similar mechanism intervenes in the vasomotor control of resistance coronary vessels. In conscious dogs, the excess of coronary blood flow (CBF) created by intracoronary acetylcholine (3.0 ng/kg) averaged 7.2 +/- 1.1 ml. Intracoronary adenosine (100 ng/kg) increased CBF by 12.4 +/- 1.4 ml. Intracoronary nitroglycerin (175 ng/kg) increased CBF by 7.4 +/- 1.2 ml. CBF repayment-to-debt ratio after a 15-s coronary arterial occlusion averaged 2.8 +/-

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Huang, Qiaobing, Mac Wu, Cynthia Meininger, Katherine Kelly, and Yuan Yuan. "Neutrophil-dependent augmentation of PAF-induced vasoconstriction and albumin flux in coronary arterioles." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 4 (October 1, 1998): H1138—H1147. http://dx.doi.org/10.1152/ajpheart.1998.275.4.h1138.

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Platelet-activating factor (PAF) has been implicated in the pathogenesis of ischemic heart disease, reperfusion injury, and inflammatory reactions. Although neutrophils have been shown to primarily mediate PAF-induced microvascular dysfunction, the vasoactive effect of PAF and its neutrophil-dependent mechanism have not been directly and systematically studied in coronary resistance vessels. Therefore, the aim of this study was to examine the effects of PAF on coronary arteriolar function and neutrophil dynamics using an isolated and perfused microvessel preparation. Topical application of PAF

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Beyar, R., and S. Sideman. "Time-dependent coronary blood flow distribution in left ventricular wall." American Journal of Physiology-Heart and Circulatory Physiology 252, no. 2 (February 1, 1987): H417—H433. http://dx.doi.org/10.1152/ajpheart.1987.252.2.h417.

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A mathematical model of the coronary circulation in the left ventricular (LV) wall, which describes the time-dependent local blood perfusion throughout the myocardium and the coronary flow in the epicardial vessels, is presented. The myocardial perfusion is essentially controlled by the intramyocardial resistance and the coronary pressure driving force, whereas the epicardial arterial flow is dominated by the epicardial and intramyocardial arterial capacitance and the local transmural pressure on the vessels. The temporal and spatial intramural pressure [P im(y,t)], calculated based on a neste

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Oltman, Christine L., Laura L. Richou, Eric P. Davidson, Lawrence J. Coppey, Donald D. Lund, and Mark A. Yorek. "Progression of coronary and mesenteric vascular dysfunction in Zucker obese and Zucker diabetic fatty rats." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 4 (October 2006): H1780—H1787. http://dx.doi.org/10.1152/ajpheart.01297.2005.

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We investigated the progression of vascular dysfunction associated with the metabolic syndrome with and without hyperglycemia in lean, Zucker obese, and Zucker diabetic fatty (ZDF) rats. Responses of aorta and small coronary and mesenteric arteries were measured to endothelium-dependent and -independent vasodilators. Indices of oxidative stress were increased in serum from ZDF rats throughout the study, whereas values were increased in Zucker obese rats later in the study [thiobarbituric acid reactive substances: 0.45 ± 0.02, 0.59 ± 0.03 ( P < 0.05), and 0.58 ± 0.03 ( P < 0.05) μg/ml in

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Kang, T., J. Resar, and J. D. Humphrey. "Heat-Induced Changes in the Mechanical Behavior of Passive Coronary Arteries." Journal of Biomechanical Engineering 117, no. 1 (February 1, 1995): 86–93. http://dx.doi.org/10.1115/1.2792274.

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We performed in vitro pressure-diameter and axial force-length experiments on nondiseased, passive bovine coronary arteries subjected to bath temperatures from 21 to 80° C for 90 s to 4 hr. Over the strain ranges studied, we found that: (a) vessel behavior remained the same over 20 min of testing at 21 to 55° C, (b) vessels stiffened multiaxially after 5 min of exposure to 60° C and continued to stiffen over 20 min of testing, (c) dramatic multiaxial vessel stiffening and shrinkage occurred after 90 s of exposure to 70 and 80° C, and (d) heat-induced changes at 70° C depended on the intralumin

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Sellke, F. W., Y. Kagaya, R. G. Johnson, T. Shafique, F. J. Schoen, W. Grossman, and R. M. Weintraub. "Endothelial modulation of porcine coronary microcirculation perfused via immature collaterals." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 6 (June 1, 1992): H1669—H1675. http://dx.doi.org/10.1152/ajpheart.1992.262.6.h1669.

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Porcine hearts have relatively few native collateral vessels and lack the propensity to develop normal perfusion to the collateral-dependent myocardium. To examine microvascular responses in the collateral-dependent region, collateral vessels were stimulated in pigs by the Ameroid constrictor technique. After 4–7 wk, isolated microarterial vessels (90–170 microns ID) were studied in a pressurized (40 mmHg), no-flow state. Microvessels from noninstrumented pigs were used as controls for vascular studies. Although myocardium in the collateral-dependent region showed minimal evidence of infarctio

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Mittal, N., Y. Zhou, C. Linares, S. Ung, B. Kaimovitz, S. Molloi, and G. S. Kassab. "Analysis of blood flow in the entire coronary arterial tree." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (July 2005): H439—H446. http://dx.doi.org/10.1152/ajpheart.00730.2004.

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A hemodynamic analysis of coronary blood flow must be based on the measured branching pattern and vascular geometry of the coronary vasculature. We recently developed a computer reconstruction of the entire coronary arterial tree of the porcine heart based on previously measured morphometric data. In the present study, we carried out an analysis of blood flow distribution through a network of millions of vessels that includes the entire coronary arterial tree down to the first capillary branch. The pressure and flow are computed throughout the coronary arterial tree based on conservation of ma

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Okajima, Masaki, Robert Parent, Eric Thorin та Michel Lavallée. "Pathophysiological plasma ET-1 levels antagonize β-adrenergic dilation of coronary resistance vessels in conscious dogs". American Journal of Physiology-Heart and Circulatory Physiology 287, № 4 (жовтень 2004): H1476—H1483. http://dx.doi.org/10.1152/ajpheart.00297.2004.

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On the basis of in vitro experiments showing that endothelin (ET)-1 interferes with smooth muscle ATP-sensitive K+ (KATP) channel opening, which is pivotal in β-adrenergic coronary dilation, we hypothesized that pathophysiological plasma ET-1 levels impair β-adrenergic dilation of resistance coronary vessels. In conscious instrumented dogs, graded intravenous doses of dobutamine caused the expected inotropic responses. As myocardial O2 consumption (MV̇o2) increased, the disproportionate rise in coronary sinus (CS) Po2 indicates that increases in coronary blood flow (CBF) exceeded metabolic req

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Conklin, D. J., and K. R. Olson. "Angiotensin II relaxation of rainbow trout vessels in vitro." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 6 (June 1, 1994): R1856—R1860. http://dx.doi.org/10.1152/ajpregu.1994.266.6.r1856.

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The effects of salmonid angiotensin II ([Asn1,Val5]ANG II) were examined in isolated trout arteries [celiacomesenteric (CMA), coronary (COA), 3rd or 4th gill arch epibranchial (EBA), ventral aorta (VA)] and veins [anterior cardinal (ACV) and ductus Cuvier strips (DOC)]. ANG II (10(-10)-10(-6) M) produced modest (< 50% other agonists) transient contractions in otherwise unstimulated COA but was a poor agonist in other vessels. In precontracted vessels, ANG II responses were triphasic; transient contraction (P1), relaxation (P2), and partial recovery (P3) and vessel specific. P1 was similar t

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Godo, Shigeo, and Hiroaki Shimokawa. "Gender Differences in Endothelial Function and Coronary Vasomotion Abnormalities." Gender and the Genome 4 (January 1, 2020): 247028972095701. http://dx.doi.org/10.1177/2470289720957012.

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Introduction: Structural and functional abnormalities of coronary microvasculature, referred to as coronary microvascular dysfunction (CMD), have been implicated in a wide range of cardiovascular diseases and have gained growing attention in patients with chest pain with no obstructive coronary artery disease, especially in females. The central mechanisms of coronary vasomotion abnormalities encompass enhanced coronary vasoconstrictive reactivity (ie, coronary spasm), reduced endothelium-dependent and -independent coronary vasodilator capacities, and increased coronary microvascular resistance

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