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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 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.
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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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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 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.
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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 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.
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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 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)
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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 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.
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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 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.
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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 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.
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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 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.
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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 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.
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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 each segment, the venules have approximately elliptical cross sections, are usually wavy in the longitudinal direction, and often converge like fingers to a hand. Measurements were made with the silicone elastomer casting method on five pig hearts. Data on smaller vessels were obtained from histological specimens by optical sectioning. Data on larger vessels were obtained from vascular casts. Arcading veins and anastomoses on the epicardial surface have a unique topology. Data on the number of vessels in each order, the major and minor axes, length, connectivity matrix, and the fractions of the vessels of a given order connected in series in all orders of vessels of the sinusal and thebesian veins are presented. It is shown that of the blood in the coronary blood vessels of a pig heart 27.4% is in the arteries (> 200 microns), 37.1% is in veins (> 200 microns), and 35.5% is in microcirculation (< 200 microns), of which 89.4% is in the capillaries.
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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, the vessel radii, and the vessel lengths were identified for over 700 vessel segments. The extraction algorithm was based on a topological analysis of a vector field generated by normal vectors of the extracted vessel wall. The diameters, lengths, and angles of the right coronary artery, left anterior descending coronary artery, and left circumflex artery of all vessels ≥1 mm in diameter were tabulated for the respective orders. It was found that bifurcations at orders 9–11 are planar (∼90%). The relations between volume and length and area and length were also examined and found to scale as power laws. Furthermore, the bifurcation angles follow the minimum energy hypothesis but with significant scatter. Some of the applications of the semiautomated extraction of morphometric data in applications to coronary physiology and pathophysiology are highlighted.
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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% glutaraldehyde and casted with a catalyzed silicone-elastomer solution. Arterial and venous vessels were obtained from different transmural locations of the RV and LV, processed for histological analysis, and measured with an imaging software. A larger transmural gradient was found for IMT, IMT-to-R ratio, and diastolic circumferential stress in vessels from the LV than the nearly zero transmural slope in the RV. The IMT of arterial vessels in the LV showed a slope of 0.7 ± 0.5 compared with 0.3 ± 0.3 of arterial vessels in the RV ( P ≤ 0.05). The slope for venous vessels in the LV was 0.14 ± 0.14 vs. 0.06 ± 0.05 in the RV. The present data reflect the local structure-function relation, where the significant gradient in intramyocardial pressure in the LV is associated with a significant gradient of IMT and IMT-to-R ratio, unlike the RV. This has important implications for local adaptation of transmural loading on the vessel wall and vascular remodeling when the loading is perturbed in cardiac hypertrophy or heart failure.
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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 relaxation induced by bradykinin and calcium ionophore A23187 was greater in arteries from antenatal betamethasone-treated lambs than in arteries from control lambs. The relaxation was abolished by N omega-nitro-L-arginine. Nitric oxide induced a greater relaxation in vessels from antenatal betamethasone-treated lambs and in vessels preincubated with betamethasone than in vessels from controls. Coronary arteries from control and antenatal betamethasone-treated lambs relaxed similarly to 8-bromoguanosine 3',5'-cyclic monophosphate. Nitric oxide induced a greater increase in guanosine 3',5'-cyclic monophosphate content in coronary arteries from antenatal betamethasone-treated lambs than in arteries from control lambs. Our data suggest that antenatal betamethasone therapy potentiates nitric oxide-mediated relaxation in coronary arteries from preterm lambs, probably by affecting the activity of soluble guanylate cyclase of vascular smooth muscle cells.
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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 was measured. The vasculature was fixed by perfusing the coronary vessels with a catalyzed polymer. After the polymer hardened, plugs of the myocardium were removed, sectioned, dehydrated, and cleared to render the capillary network visible in a light microscope. The capillaries then were traced by optical sectioning. We designated the capillaries as blood vessels of order number zero; we further designated the capillaries as those fed directly by arterioles (C0a), those drained directly into venules (C0v), and those capillary vessels connected to C0a and C0v. The capillaries are connected in patterns identified as Y, T, H, or hairpin and anastomosed through capillary cross-connections (Ccc). The Ccc vessels may connect adjacent capillaries or capillaries originating from different arterioles. The connection among the capillaries, arteries, and veins is presented in terms of a connectivity matrix. Combining the present data with those for the arterial and venous trees, we have obtained a complete set of statistical data of all the blood vessels of the heart of the pig. Such a data set will serve as the basis of coronary hemodynamics.
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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 with one-dimensional Navier-Stokes equations, while the smaller-diameter vessels were treated as Womersley-type vessels. Energy losses associated with vessel bifurcations were incorporated in the present analysis. The formulation enables prediction of impedance and pressure and pulsatile flow distribution throughout the entire coronary arterial tree down to the first capillary segments in the arrested, vasodilated state. We found that the nonlinear convective term is negligible and the loss of energy at a bifurcation is small in the larger epicardial vessels of an arrested heart. Furthermore, we found that the flow waves along the trunk or at the primary branches tend to scale (normalized with respect to their mean values) to a single curve, except for a small phase angle difference. Finally, the model predictions for the inlet pressure and flow waves are in excellent agreement with previously published experimental results. This hybrid one-dimensional/Womersley model is an efficient approach that captures the essence of the hemodynamics of a complex large-scale vascular network. The present model has numerous applications to understanding the dynamics of coronary circulation.
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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. Upon heating, vessels developed spontaneous tone and constricted to 72 +/- 3% of their maximum diameter. After a 30-mmHg step change in coronary pressure from 50 to 80 mmHg, there was an initial dilation from 131 +/- 9 to 149 +/- 11 microns, followed by myogenic constriction that returned diameter to the initial value over a period of several minutes (134 +/- 10 microns, P = NS). Directionally opposite peak transients were observed during reductions in pressure. Steady-state diameter remained relatively constant over a pressure range from 100 to 20 mmHg. Although these data demonstrate that myogenic responses are present in resistance arteries that are greater than 100 microns in diameter, their contribution to steady-state coronary resistance changes as pressure is varied is small. This suggests that additional mechanisms contribute to the phenomenon of coronary autoregulation in this class of resistance vessel.
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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 NG-nitro-l-arginine methyl ester (l-NAME) inhibited the dilation to adenosine by ∼50%; subsequent addition of glibenclamide was without effect. Hypoxic dilation was completely inhibited by endothelium removal or l-NAME. We conclude that adenosine- and hypoxia-induced dilation of rat coronary arteries does not appear to involve the KATP channel. Adenosine-induced dilation is partially and hypoxic dilation is completely dependent on endothelium-derived NO.
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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 the support of the surrounding myocardial tissue, which significantly limits distension of the vessel. In this finite-element study, we modeled the nonuniform support by embedding the left anterior descending artery into the myocardium to different depths and analyzed deformation and strain in the vessel wall. Circumferential wall strain was much higher in the untethered than tethered region at physiological pressure. On the basis of the hypothesis that elevated wall strain is the stimulus for remodeling, the simulation results suggest that large epicardial coronary vessels have a greater tendency to become thicker in the absence of myocardial constraint. This study provides a mechanical basis for understanding the local growth and remodeling of vessels subjected to various degrees of surrounding tissue.
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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.
Full textAbstract:
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 (EC50, 0.07 microM; maximum response, 79 +/- 5% relaxation). Hemoglobin was utilized to inactivate endothelium-derived relaxing factor (EDRF), resulting in reversal of acetylcholine vasodilation in both the microvessels (92 +/- 3.2% reversal) and the large epicardial vessels (117 +/- 9%). Hemoglobin had no effect on passively distended or preconstricted microvessels. Vasopressin constricted resistance vessels by 22.3 +/- 5.9 microns at 500 microU/ml. Hemoglobin potentiated this response by 100%, suggesting that vasopressin elicited EDRF release. In large coronary arteries, however, vasopressin elicited endothelium-dependent dilation with maximal relaxation of 36 +/- 9% at 3,000 microU/ml. Thrombin produced endothelium-dependent relaxation of large epicardial arterial rings but only constricted coronary microvessels. The response to thrombin was not altered by hemoglobin. This study demonstrates that the endothelium of coronary microvessels, like that of larger vessels, importantly modulates vascular reactivity to selected agents. Furthermore, major differences exist between large and small coronary arteries in their response to vasopressin and thrombin.
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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.
Full textAbstract:
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-nitro-l-arginine (l-NNA) to block NO production and untreated vessels were pressurized at 60 mmHg for 3 days with and without flow. Endothelium-dependent dilation to 10−7 M bradykinin was preserved in all groups. Tone was significantly less in vessels cultured under flow conditions in the last half of the culture period. Untreated and l-NNA-treated vessels regulated their diameter to yield shear stresses of 10.3 ± 2.1 and 14.0 ± 2.4 (SE) dyn/cm2, respectively (not significantly different). Without l-NNA, passive pressure-diameter curves at the end of the culture period revealed inward remodeling in the control group [to 92.3 ± 1.3% of D0 (SE)] and no remodeling in the vessels cultured under flow conditions (100.2 ± 1.3% of D0); with l-NNA, the group subjected to flow showed inward remodeling (92.1 ± 2.5% of D0). We conclude that pressurized coronary resistance arteries could be maintained in culture for several days with flow. Vessels cultured under flow conditions remained more dilated when NO synthesis was blocked. Inward remodeling occurred in vessels cultured under no-flow conditions and was inhibited by flow-dependent NO synthesis.
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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.
Full textAbstract:
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 using intravital microscopy. A mathematical model of the coronary capillary blood flow was then constructed on the basis of measured anatomic and elasticity data of the coronary capillary network, rheology of blood, physical laws governing blood flow, and appropriate boundary conditions. The constructed model was used to examine the heterogeneity of the spatial distribution of coronary blood flow, which is an important issue in coronary physiology. One interesting result of the model is that the dispersions of pressure and flow are significantly reduced in the presence of capillary cross-connections, and the resistance to flow is reduced as well. Finally, we found that the compliance of the epicardial surface capillary vessels is so small that its effect on the blood pressure drop is negligible in the diastolic state. However, the compliance of the intramyocardial capillaries remains unknown, and the interaction of the muscle contraction and blood vessel elasticity in systole remains to be studied.
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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.
Full textAbstract:
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, transmural, and perfusion functional subnetworks. The epicardial portion was generated by a simulated annealing search for the optimal coverage of the area perfused by the arterial epicardial vessels. The epicardial subnetwork and coronary arterial capillary network served as boundary conditions for the reconstruction of the in-between transmural and perfusion networks, which were generated to optimize vascular homogeneity. Five sets of full coronary trees, which spanned the entire network down to the capillary level, were reconstructed. The total number of reconstructed venous segments was 17,148,946 ± 1,049,498 ( n = 5), which spanned the coronary sinus ( order −12) to the first segment of the venous capillary ( order 0v). Combined with the reconstructed arterial network, the number of vessel segments for the entire coronary network added up to 27,307,376 ± 1,155,359 ( n = 5). The reconstructed full coronary vascular network agreed with the gross anatomy of coronary networks in terms of structure, location of major vessels, and measured morphometric statistics of native coronary networks. This is the first full model of the entire coronary vasculature, which can serve as a foundation for realistic large-scale coronary flow analysis.
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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.
Full textAbstract:
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 network, the dynamic myocardial loading on the vessels embedded in it, and the combined effects of local myogenic effect, local shear regulation, and conducted metabolic control driven by venous O2 saturation level. The model predicts autoregulation (approximately constant flow over a wide range of coronary perfusion pressures), reduced heterogeneity of regulated flow, and presence of flow reserve, in agreement with experimental observations. Furthermore, the model shows that the metabolic and myogenic regulations play a primary role, whereas shear has a secondary one. Regulation was found to have a significant effect on the flow except under extreme (high and low) inlet pressures and metabolic demand. Novel outcomes of the model are that cyclic myocardial loading on coronary vessels enhances the coronary flow reserve except under low inlet perfusion pressure, increases the pressure range of effective autoregulation, and reduces the network flow in the absence of metabolic regulation. Collectively, these findings demonstrate the utility of the present biophysical model, which can be used to unravel the underlying mechanisms of coronary physiopathology.
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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.
Full textAbstract:
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 artery (LCX), and coronary venous system. The purpose of the present study is to present another feature of the branching pattern of the coronary vasculature: the longitudinal position matrix [ m,n] (LPM), whose component in row m and column n is the fractional longitudinal position of the branch point on vessels of order n at which vessels of order m branch off ( m ≤ n). The LPM of the pig RCA, LAD and LCX arterial trees, as well as the coronary sinusal and thebesian venous trees, are presented. The hemodynamic implications of the LPM are illustrated by comparing two kinds of circuits: one, the CM + LPM model, simulates the mean data on the morphology (diameters, lengths, and numbers), CM, and LPM of vessels, whereas the other, the CM model, simulates the mean data on the morphology and CM without considering the LPM. We found that the LPM affects the hemodynamics of coronary blood flow especially with regard to the nonuniformity or dispersion of flow distribution.
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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.
Full textAbstract:
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 competitive RT-PCR, Western blot analysis, and immunohistochemistry. Expression of BK-1R mRNA was increased in both IDC (2.8-fold) and CHD (2.1-fold) hearts compared with normal hearts. The observed changes were verified at the protein level. Expression of BK-1Rs in failing hearts localized to the endothelium of intramyocardial coronary vessels and correlated with an increased expression of TNF-α in the vessel wall. Treatment of human coronary artery endothelial cells with TNF-α increases their BK-1R expression. These novel results show that BK-1Rs are induced in the endothelium of intramyocardial coronary vessels in failing human hearts and so may participate in the pathogenesis of heart failure.
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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 vessels from C and M hamsters. However, mechanisms mediating relaxation to ACh were altered. Inhibition of nitric oxide synthase (NOS) activity with N-nitro-l-arginine (1 mM) had a greater inhibitory effect in vessels from C hamsters, indicating a reduction in NOS-dependent relaxation in vessels from M hamsters. Conversely, inhibition of large Ca2+-dependent K+ (BKCa) channels with charybdotoxin (CTX, 0.1 μM) had a greater inhibitory effect in vessels from M hamsters. In the presence of both N-nitro-l-arginine and CTX, relaxation to ACh was abolished in both groups. CTX (0.1 μM) produced a 50 ± 4 and 30 ± 3% contraction of vessels from M and C hamsters, respectively, indicating an enhanced role for BKCa channels in regulation of coronary artery tone in M hamsters. Finally, vasodilatory cyclooxygenase products contributed to ACh-induced relaxation in vessels from M, but not C, hamsters. In conclusion, NOS-dependent relaxation of coronary small arteries is reduced in the late stage of cardiomyopathy. An increase in relaxation mediated by BKCa channels and vasodilatory cyclooxygenase products compensates for this effect.
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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.
Full textAbstract:
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-wk-old MI were exercised on a treadmill in the absence and presence of the PDE5 inhibitor EMD-360527 (300 μg·kg−1·min−1 iv). Inhibition of PDE5 produced coronary resistance vessel dilation, which was more pronounced at rest than during exercise in normal swine. PDE5 gene expression was markedly reduced in coronary resistance vessels isolated from the remote myocardium of MI swine, which was accompanied by a similarly marked attenuation of coronary vasodilation by PDE5 inhibition in MI swine. The coronary vasoconstriction produced by inhibition of NO synthesis with Nω-nitro-l-arginine (20 mg/kg iv) was only slightly smaller in swine with MI. Interestingly, inhibition of NO synthesis reduced the vasodilator response to subsequent PDE5 inhibition in normal swine but not in MI swine. Conversely, PDE5 inhibition enhanced the coronary vasoconstriction produced by NO synthesis inhibition in normal swine but not in MI swine, suggesting that downregulation of PDE5 mitigated the loss of NO vasodilator influence. In conclusion, the expression and vasoconstrictor influence of PDE5 are markedly attenuated in coronary resistance vessels in the remote myocardium after MI, which appears to serve as a compensatory mechanism to mitigate the loss of NO vasodilator influence.
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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.
Full textAbstract:
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 function. To study the effect of CT on the cardiac MV function, flow-mediated dilation (FMD), pharmacologically-induced endothelial dependent dilation to acetylcholine (ACh), and smooth muscle-dependent dilation to papaverine were investigated. Vessels were freshly isolated from atrial appendages of adult patients undergoing cardiopulmonary bypass surgery or from cardiac tissue of pediatric patients, collected at the time of surgery to repair congenital heart defects. Isolated vessels were incubated in endothelial culture medium containing vehicle or Dox (100 nm, 15–20 h) and used to measure dilator function by video microscopy. Ex vivo treatment of adult human coronary microvessels with Dox significantly impaired flow-mediated dilation (FMD). Conversely, in pediatric coronary microvessels, Dox-induced impairment of FMD was significantly reduced in comparison with adult subjects. In both adult and pediatric coronary microvessels, ACh-induced constriction was reversed into dilation in the presence of Dox. Smooth muscle-dependent dilation remained unchanged in all groups tested. In vessels from adult subjects, acute treatment with Dox in clinically relevant doses caused significant impairment of coronary arteriolar function, whereas vessels from pediatric subjects showed only marginal impairment to the same stressor. This interesting finding might explain the delayed onset of future adverse CV events in children compared with adults after anthracycline therapy. NEW & NOTEWORTHY We have characterized, for the first time, human microvascular responses to acute ex vivo exposure to doxorubicin in coronary vessels from patients without cancer. Our data show an augmented impairment of endothelial function in vessels from adult subjects compared with pediatric samples.
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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.
Full textAbstract:
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 in active state were 3.17 ± 0.16 and 3.07 ± 0.18 mm at axial stretch ratio of 1.2 and 1.3, respectively, which were significantly smaller than those in passive state (i.e., 3.62 ± 0.19 and 3.49 ± 0.22 mm, respectively, P < 0.05). The inner and outer diameters in no-load state of intima-media layers were 1.17 ± 0.09 and 2.08 ± 0.09 mm, respectively. The opening angles in zero-stress state had values of 159 ± 21° for intima-media layers and 98 ± 15° for adventitia layers, which suggests a residual strain between the two layers. There were slightly decreased active circumferential stresses (<10%), but significantly decreased active axial stresses (>25%) in the intima-media layer compared with those in the intact vessel. This suggests that the adventitia layer affects vascular contraction. The two-layer analysis showed that the intima-media layer bears the majority of circumferential tensions, in contrast to the adventitia layer, while contraction results in decreased stress and stretch in both layers.
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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.
Full textAbstract:
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 = 6) restricted to cage activity. No differences in passive length-tension characteristics or internal diameter (158 ± 9 and 166 ± 9 μm) were observed between vessesls of C and ET rats. Concentration-response curves to K+ (5–100 mM), prostaglandin F2α(10−8–10−4M), and norepinephrine (10−8–10−4) were unaltered ( P > 0.05) in coronary rings from ET rats compared with C rats; however, lower values of the concentration producing 50% of the maximal contractile response in rings from ET rats ( P = 0.05) suggest that contractile sensitivity to norepinephrine was enhanced. Vasorelaxation responses to sodium nitroprusside (10−9-10−4M) and adenosine (10−9-10−4M) were not different ( P > 0.05) between vessels of C and ET rats. However, relaxation responses to the endothelium-dependent vasodilator acetylcholine (ACh; 10−10-10−4M) were significantly blunted ( P < 0.001) in coronary rings from ET animals; maximal ACh relaxation averaged 90 ± 5 and 46 ± 12%, respectively, in vessels of C and ET groups. In additional experiments, two coronary rings (proximal and distal) were isolated from each C ( n = 7) and ET ( n = 7) animal. Proximal coronary artery rings from ET animals demonstrated decreased relaxation responses to ACh; however, ACh-mediated relaxation of distal coronary rings was not different between C and ET groups. N G-monomethyl-l-arginine (inhibitor of nitric oxide synthase) blocked ACh relaxation of all rings. l-Arginine (substrate for nitric oxide synthase) did not improve the blunted ACh relaxation in proximal coronary artery rings from ET rats. These studies suggest that exercise-training selectively decreases endothelium-dependent (ACh) but not endothelium-independent (sodium nitroprusside) relaxation responses of rat proximal coronary arteries; endothelium-dependent relaxation of distal coronary arteries is unaltered by training.
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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 (LAD) flow reached an initial quasi-steady level, but great cardiac venous (GCV) flow was absent (UV-unfilled phase). With reappearance of the GCV flow (UV-filled phase), LAD flow decreased to a final steady level. Pressure-flow relationships during both phases were linear (r = 0.97-0.99). The inverse of the slope of the pressure-flow relationship during the UV-filled phase, 0.69 +/- 0.08 mmHg.min.ml-1, was significantly higher than that during the UV-unfilled phase, 0.55 +/- 0.06 mmHg.min.ml-1 (P less than 0.01), although the zero-flow pressure intercepts were similar (18.9 +/- 1.8 mmHg for UV filled vs. 19.9 +/- 2.2 for UV unfilled). These results indicate that diastolic coronary arterial inflow is impeded by a blood volume within intramyocardial vessels that exceeds the UV.
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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.
Full textAbstract:
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 of the left ventricular free wall: epicardial surface, subepicardium, midmyocardium, and endocardium. Arterioles and venules from the experimental and sham control groups were photographed, and the following measurements were made: inner and outer circumferences, inner and outer areas, major and minor diameters, and intima-media thickness. Each vessel was categorized in four different orders according to lumen diameter. Our results show that intima-media thickness was larger in the experimental group in all four regions of the heart and in all four orders of the vessels, although venules from the epicardial region showed the largest increase in thickness. The intima-media thickness-to-radius ratio was also larger in the experimental group and decreased from epicardial to endocardial region of the heart and from order 1 to order 4 of the vessels. The present study provides a rationale for the development of coronary retroperfusion strategy that avoids vessel rupture and hemorrhage in the postcapillary venules.
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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.
Full textAbstract:
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 intramural vessels are subjected to compressive forces related to heart contraction. In the catheterization laboratory, guide wires of 0.33 mm diameter are available that are equipped with a pressure and flow velocity sensor at the tip, which can be positioned distal to the stenosis. These signals provide information about the impediment of the stenosis on coronary flow and allow for the evaluation of the status of the microcirculation. However, the interpretation of these signals is strongly model-dependent and therefore it is of paramount importance to develop realistic models reflecting the anatomy and unique physiology of the coronary circulation.
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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.
Full textAbstract:
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 vessels (∼106 ± 4 μm ID) were isolated and studied using wire myographs. Maximal ACh-evoked relaxation was ∼25, 40, and 60% of KCl-induced preconstriction after the long-term, short-term, and sham-operated protocols, respectively, and was similar between groups. Maximal sodium nitroprusside-evoked relaxation also was similar between groups among all protocols, and vasoconstrictor responses to endothelin-1 and U-46619 were not different in trained and sedentary rats after short-term ischemia or sham operation. We did observe that, after long-term ischemia, maximal tension development in response to endothelin-1 and U-46619 was blunted ( P < 0.05) in trained animals by ∼70 and ∼160%, respectively. These results support our hypothesis that exercise training lessens receptor-mediated vasoconstriction of coronary resistance vessels after ischemia and reperfusion. However, training did not preserve endothelial function of coronary resistance vessels, or myocardial contractile function, after ischemia and reperfusion.
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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.
Full textAbstract:
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 myocardial infarction (MI), we investigated if the interaction between these systems is altered after MI. In awake healthy swine, coronary vasodilation in response to ETA/ETB receptor blockade in the presence of AT1 blockade was similar to vasodilation produced by ETA/ETB blockade under control conditions. In awake swine with a 2- to 3-wk-old MI, coronary vasodilator responses to individual AT1 and ETA/ETB receptor blockade were virtually abolished, despite similar coronary arteriolar AT1 and ETA receptor expression compared with normal swine. Unexpectedly, in the presence of AT1 blockade (which had no effect on circulating ET levels), ETA/ETB receptor blockade elicited a coronary vasodilator response. These findings suggest that in normal healthy swine the two vasoconstrictor systems contribute to coronary resistance vessel control in a linear additive manner, i.e., with negligible cross-talk. In contrast, in the remodeled myocardium, cross-talk between ANG II and ET emerges, resulting in nonlinear redundant control of coronary resistance vessel tone.
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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.
Full textAbstract:
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 development and/or functional adaptations in collateral and collateral-dependent arteries to reduce resistance into the ischemic myocardium represent a desirable goal in the management of coronary artery disease. Tremendous evidence has provided documentation for the therapeutic benefits of exercise training programs in patients with coronary artery disease (and collateralization); mechanisms that underlie these benefits are numerous and multifaceted, and currently under investigation in multiple laboratories worldwide. The role of enhanced collateralization as a major beneficial contributor has not been fully resolved. This topical review highlights literature that examines the effects of exercise training on collateralization in the diseased heart, as well as effects of exercise training on vascular endothelial and smooth muscle control of regional coronary tone in the collateralized heart. Future directions for research in this area involve further delineation of cellular/molecular mechanisms involved in effects of exercise training on collateralized myocardium, as well as development of novel therapies based on emerging concepts regarding exercise training and coronary artery disease.
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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 phenylephrine decreased it. In contrast, the pressure gradients in the small coronary arteries (from the branch of an epicardial artery to the pressure in an obstructed coronary artery) were 56 ± 1.3 mmHg during systole and 63.7 ± 1.3 mmHg during diastole. These gradients were increased by phenylephrine during both systole and diastole, noradrenaline and adrenaline during diastole and decreased by isoproterenol (systolic), left vagosympathetic trunk stimulation (diastolic), acetylcholine (systolic and diastolic), and adrenosine (diastolic). The microcirculation and small vein gradients during control were 16.4 ± 1.2 mmHg during systole and 8.5 ± 0.8 mmHg during diastole. Decreases in this gradient were produced by isoproterenol, acetylcholine, and adenosine during systole and adenosine during diastole. These observations are consistent with the concept that the coronary circulation has considerable regulatory capacity in all of its component parts. Specifically, epicardial arteries appear to function as both conduits and as resistance vessels, small arteries as major resistance vessels, and the microcirculation and small veins as both capacitors and resistors.
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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.
Full textAbstract:
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 +/- 0.2. After an intracoronary N omega-nitro-L-arginine dose (10 micrograms.kg-1.min-1 x 12 min) was given to inhibit nitric oxide formation, baseline CBF was not altered. CBF increases with acetylcholine averaged 2.4 +/- 0.5 and 6.4 +/- 0.7 ml with adenosine, both less (P less than 0.01) than responses before the arginine analogue. CBF increases with nitroglycerin averaged 7.2 +/- 1.1 ml, similar to control responses. CBF repayment-to-debt ratio during reactive hyperemic responses fell (P less than 0.01) to 1.7 +/- 0.1. L-Arginine (1.0 mg.kg-1.min-1 x 12 min) partially reversed the inhibitory effect of the arginine analogue on CBF responses to acetylcholine. Thus nitric oxide formed in resistance coronary vessels is a major mediator of coronary vasodilation to acetylcholine, adenosine and transient ischemia.
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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.
Full textAbstract:
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 to the vessels induced a dose-dependent decrease in the diameter but an increase in the apparent permeability coefficient of albumin. Disruption of the endothelium abolished the vasomotor response to PAF, and perfusion of neutrophils significantly augmented PAF-induced changes in vasomotor tone and permeability. Furthermore, the interaction between neutrophils and the endothelium was studied in the intact perfused coronary arterioles. Under control conditions, there were no adherent neutrophils observed in the vessels at varied intraluminal flow velocities. However, administration of PAF caused neutrophil adhesion to the endothelium of coronary arterioles at low flow velocities. Western blot analysis indicated that PAF upregulated the expression of intercellular adhesion molecule-1 in cultured coronary microvascular endothelial cells. Taken together, the results suggest that 1) PAF induces vasoconstriction and hyperpermeability in coronary arterioles via an endothelium-dependent and neutrophil-mediated mechanism, and 2) PAF is able to stimulate neutrophil adhesion in coronary arterioles under a condition of low flow rate.
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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.
Full textAbstract:
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 nested-shell spheroidal model of the LV, is used to evaluate the local intramural resistance to flow and the corresponding zero flow pressure. The calculation of the instantaneous flow in each layer is based on a local, time-dependent modification of the back-pressure concept. A function representing the local tonus of the small blood vessels [T wf(y)] is used to adjust the average coronary flow rate to the metabolic demand of each layer. The calculated results are compared with experimental data, and the assumptions of the model are examined against a variety of experimental conditions. The model provides a qualitative tool for comprehending the distributed flow phenomenon within the myocardium and its relation to cardiac mechanics and autoregulation.
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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.
Full textAbstract:
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 serum from 28- to 40-wk-old lean, Zucker obese, and ZDF rats, respectively]. Acetylcholine (ACh)-induced relaxation was not altered in vessels from lean animals from 8–40 wk. ACh-induced relaxation was nearly abolished in coronary arteries from 28- to 36-wk-old Zucker obese rats and by 16–36 wk in ZDF rats and was attenuated in aorta and mesenteric vessels from ZDF rats [%relaxation to 10 μM ACh: 72.2 ± 7.1, 17.9 ± 5.9 ( P < 0.05), and 23.0 ± 4.5 ( P < 0.05) in coronary vessels; and 67.9 ± 9.2, 50.1 ± 5.5, and 42.3 ± 4.7 ( P < 0.05) in mesenteric vessels from 28- to 40-wk-old lean, Zucker obese, and ZDF rats, respectively]. The attenuated ACh-induced relaxation was improved when vessels were incubated with tiron, suggesting superoxide as a mechanism of endothelial dysfunction. Sodium nitroprusside-induced relaxation was not altered in aorta or coronary arteries and was potentiated in mesenteric arteries from Zucker obese rats. Our data suggest that diabetes enhances the progression of vascular dysfunction. Increases in indices of oxidative stress precede the development of dysfunction and may serve as a marker of endothelial damage.
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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 intraluminal pressure during heating. Thus, passive bovine coronary arteries exhibit a complex thermomechanical behavior that depends on the temperature, duration of thermal exposure, and the mechanical loads applied during heating.
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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.
Full textAbstract:
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 infarction, percent systolic shortening was reduced at rest and after pacing compared with myocardium in the normally perfused region. Relaxations to the receptor-mediated endothelium-dependent agents ADP and bradykinin were impaired in collateral-dependent coronary microvessels. Relaxations to the calcium ionophore A23187, which acts through a non-receptor-mediated mechanism, were similar in control and Ameroid microvessels. Relaxations to the endothelium-independent agent sodium nitroprusside were markedly enhanced in microvessels from the collateral-dependent region compared with microvessels from control hearts. In conclusion, receptor-mediated endothelium-dependent relaxation is impaired and endothelium-independent relaxation to sodium nitroprusside is enhanced in microvessels from myocardium perfused by immature collateral vessels.
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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.
Full textAbstract:
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 mass and momentum and appropriate pressure boundary conditions. We found a power law relationship between the diameter and flow of each vessel branch. The exponent is ∼2.2, which deviates from Murray’s prediction of 3.0. Furthermore, we found the total arterial equivalent resistance to be 0.93, 0.77, and 1.28 mmHg·ml−1·s−1·g−1 for the right coronary artery, left anterior descending coronary artery, and left circumflex artery, respectively. The significance of the present study is that it yields a predictive model that incorporates some of the factors controlling coronary blood flow. The model of normal hearts will serve as a physiological reference state. Pathological states can then be studied in relation to changes in model parameters that alter coronary perfusion.
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Okajima, Masaki, Robert Parent, Eric Thorin, and 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, no. 4 (October 2004): H1476—H1483. http://dx.doi.org/10.1152/ajpheart.00297.2004.
Full textAbstract:
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 requirements, consistent with β-adrenergic dilation. ET-1 intravenous infusions, to reach pathophysiological plasma levels, reduced slopes of the Po2-MV̇o2 and CBF-MV̇o2 relations. In contrast, the first derivative of left ventricular pressure over time responses to dobutamine were not impaired during ET-1 delivery. Clazosentan, an ETA receptor blocker, prevented reduction of the slope of Po2-MV̇o2 and CBF-MV̇o2 relations. After ganglionic blockade to exclude reflex influences, ET-1 still reduced slopes of Po2-MV̇o2 and CBF-MV̇o2 relations. To assess effects of ET-1 on endothelium-dependent and -independent coronary vascular responses, intracoronary ACh and nitroglycerin were given to directly target coronary vessels. CBF responses to ACh and nitroglycerin were maintained during ET-1 delivery. In contrast, responses to intracoronary KATP channel-dependent dilators adenosine and lemakalim were impaired by ET-1. In conclusion, pathophysiological levels of ET-1 impaired β-adrenergic dilation of resistance coronary vessels through an ETA receptor-dependent process. In contrast, left ventricular inotropic responses to dobutamine were not impaired during ET-1 delivery. Our data suggest that ET-1 may interfere with smooth muscle KATP channels to impair β-adrenergic coronary dilation.
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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 to uncontracted vessels. With 10(-6) MANG II, %P2 was: EBA, 60.3 +/- 8.3% (n = 22); CMA, 48.8 +/- 8.8% (n = 4); ACV, 38.8 +/- 5.3% (n = 29); VA, 29.4 +/- 4.9% (n = 8); DOC, 25.5 +/- 2.4% (n = 14); COA, 13.2 +/- 6.7% (n = 4). P2 in EBA and ACV was dose dependent [EBA vs. ACV: mean effective concentration (EC50) = 3.6 x 10(-9) +/- 8.1 x 10(-10) M, n = 7 vs. 6.2 x 10(-8) +/- 2.3 x 10(-8) M, n = 8, respectively; P < or = 0.05] and inhibited by indomethacin but unaffected by propranolol, NG-monomethyl-L-arginine, saralasin, PD-123177, or DuP-753. Removal of EBA endothelium also inhibited relaxation. By comparison, ANG II did not relax bullfrog arteries (dorsal aorta, systemic arch, CMA) or femoral veins. These results show that, in large vessels of trout, the predominant effect of ANG II is an endothelium-dependent, prostanoid-mediated relaxation that is unaffected by classical ANG II-receptor antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)
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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.
Full textAbstract:
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. The 2 major endothelium-derived relaxing factors, nitric oxide (NO) and endothelium-dependent hyperpolarization (EDH) factors, modulate vascular tone in a distinct vessel size–dependent manner; NO mainly mediates vasodilatation of relatively large, conduit vessels, while EDH factors in small resistance vessels. Endothelium-dependent hyperpolarization–mediated vasodilatation is more prominent in female resistance arteries, where estrogens exert beneficial effects on endothelium-dependent vasodilatation via multiple mechanisms. In the clinical settings, therapeutic approaches targeting NO are disappointing for the treatment of various cardiovascular diseases, where endothelial dysfunction and CMD are substantially involved. Significance: In this review, we will discuss the current knowledge on the pathophysiology and molecular mechanisms of endothelial function and coronary vasomotion abnormalities from bench to bedside, with a special reference to gender differences. Results: Recent experimental and clinical studies have demonstrated distinct gender differences in endothelial function and coronary vasomotion abnormalities with major clinical implications. Moreover, recent landmark clinical trials regarding the management of stable coronary artery disease have questioned the benefit of percutaneous coronary intervention, supporting the importance of the coronary microvascular physiology. Conclusion: Further characterization and a better understanding of the gender differences in basic vascular biology as well as those in cardiovascular diseases are indispensable to improve health care and patient outcomes in cardiovascular medicine.