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Journal articles on the topic 'Arterial heterogeneity'

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Published: 26 April 2025

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1

Bowles, D. K., Q. Hu, M. H. Laughlin, and M. Sturek. "Heterogeneity of L-type calcium current density in coronary smooth muscle." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 4 (October 1, 1997): H2083—H2089. http://dx.doi.org/10.1152/ajpheart.1997.273.4.h2083.

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Heterogeneity of vascular responses to physiological and pharmacological stimuli has been demonstrated throughout the coronary circulation. Typically, this heterogeneity is based on vessel size. Although the cellular mechanisms for this heterogeneity are unknown, one plausible factor may be heterogeneous distribution of ion channels important in regulation of vascular tone. Because of the importance of voltage-gated Ca2+ channels in regulation of vascular tone, we hypothesized that these channels would be unequally distributed throughout the coronary arterial bed. To test this hypothesis, voltage-gated Ca2+current was measured in smooth muscle from conduit arteries (>1.0 mm), small arteries (200–250 μm), and large arterioles (75–125 μm) of miniature swine using whole cell voltage-clamp techniques. With 2 mM Ca2+ or 10 mM Ba2+ as charge carrier, voltage-gated Ca2+ current density was inversely related to arterial diameter, i.e., large arterioles > small arteries > conduit. Peak inward currents (10 mM Ba2+) were increased ∼2.5- and ∼1.5-fold in large arterioles and small arteries, respectively, compared with conduit arteries (−5.58 ± 0.53, −3.54 ± 0.34, and −2.26 ± 0.31 pA/pF, respectively). In physiological Ca2+ (2 mM), small arteries demonstrated increased inward current at membrane potentials within the physiological range for vascular smooth muscle (as negative as −40 mV) compared with conduit arteries. In addition, cells from large arterioles showed a negative shift in the membrane potential for half-maximal activation compared with small and conduit arteries (−13.23 ± 0.88, −6.22 ± 1.35, and −8.62 ± 0.81 mV, respectively; P < 0.05). Voltage characteristics and dihydropyridine sensitivity identified this Ca2+ current as predominantly L-type current in all arterial sizes. We conclude that L-type Ca2+ current density is inversely related to arterial diameter within the coronary arterial vasculature. This heterogeneity of Ca2+ current density may provide, in part, the basis for functional heterogeneity within the coronary circulation.
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2

Hao, Hiroyuki, Giulio Gabbiani, and Marie-Luce Bochaton-Piallat. "Arterial Smooth Muscle Cell Heterogeneity." Arteriosclerosis, Thrombosis, and Vascular Biology 23, no. 9 (September 2003): 1510–20. http://dx.doi.org/10.1161/01.atv.0000090130.85752.ed.

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3

Cerecedo, Doris, Ivette Martínez-Vieyra, Edgar Oliver López-Villegas, Arturo Hernández-Cruz, and Arlet del Carmen Loza-Huerta. "Heterogeneity of neutrophils in arterial hypertension." Experimental Cell Research 402, no. 2 (May 2021): 112577. http://dx.doi.org/10.1016/j.yexcr.2021.112577.

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4

Daemen, Mat J. A. P., and Jo G. R. De Mey. "Regional Heterogeneity of Arterial Structural Changes." Hypertension 25, no. 4 (April 1995): 464–73. http://dx.doi.org/10.1161/01.hyp.25.4.464.

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5

Zhao, Yidan, Jenny Peng, Catherine Lu, Michael Hsin, Marco Mura, Licun Wu, Lei Chu, et al. "Metabolomic Heterogeneity of Pulmonary Arterial Hypertension." PLoS ONE 9, no. 2 (February 12, 2014): e88727. http://dx.doi.org/10.1371/journal.pone.0088727.

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6

Ciavarella, Carmen, Ilenia Motta, Miriam Capri, Mauro Gargiulo, and Gianandrea Pasquinelli. "Heterogeneity and Differentiation of the Human Arterial Tree: Focus on microRNA Expression in Vascular Disease." Biomolecules 14, no. 3 (March 12, 2024): 343. http://dx.doi.org/10.3390/biom14030343.

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Human arteries show structural and functional peculiarities according to the nutrient and oxygen needs of a specific vascular district. This architectural heterogeneity is reflected in the pathological setting of cardiovascular diseases (CVDs). Indeed, the responsiveness to cardiovascular risk factors, and the morphological and molecular patterns are discriminating factors among CVDs affecting different vascular beds. MicroRNAs (miRNAs) are endogenous regulators of gene expression and fine-tuners of vascular cell differentiation; thus, these non-coding RNAs can modulate arterial heterogeneity. The identification of an artery-specific miRNA signature would be promising in the therapy of CVDs, especially in patients who are frail and elderly. In the present review, we will provide a concise description of the arterial tree heterogeneity on a structural and cellular basis, mainly in the pathological context. Secondly, we will address the miRNA potential as crucial mediators of arterial heterogeneity, focusing on the abdominal aorta and femoral artery, with the final goal of strengthening the search for more targeted therapies in CVDs and stratification approaches in patients who are frail and elderly.
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7

Titov, V. N. "Phylogenesis, structure, and functional heterogeneity of arterial bed and pathogenesis of arterial hypertension." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 16, no. 3 (June 28, 2010): 333–42. http://dx.doi.org/10.18705/1607-419x-2010-16-3-333-342.

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During early phylogenesis, each forming paracrine regulated community (future structural and functional units of body organs) included a pool of specialized cells, elements of the interstitial tissue, and local peristaltic pump. In the community the pump performed the biological functions of homeostasis and endoecology (purity of the intercellular medium); the paracrine community regulated the pump via humoral factors. Later on, the development of the biological function of locomotion required a closed circulation system in which the heart and elastic arteries, as a single functional unit, have united millions of much more ancient local peristaltic pumps. We suppose that muscular arterioles are these peristaltic pumps, and the number of paracrine communities equals the number of arterioles in the body. Phylogenetically, arterial bed consists of two segments: proximal (heart and elastic arteries) and distal (muscular arterioles). Proximal segment is regulated by the vasomotor center via sympathetic and parasympathetic innervation, and distal segment (peripheral peristaltic pumps) - by paracrine communities. When the biological function of locomotion is performed, two levels of regulation are coordinated via the mechanosensitivity of the muscular arteriolar endothelium, thus providing intense cell perfusion. In the realization of the biological function of homeostasis two mechanisms of regulation are opposing, which is crucial for the pathogenesis of arterial hypertension.
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8

Rubanyi, Gabor M., and Paul M. Vanhoutte. "Heterogeneity of Endothelium-Dependent Responses to Acetylcholine in Canine Femoral Arteries and Veins." Journal of Vascular Research 25, no. 2 (1988): 75–81. http://dx.doi.org/10.1159/000158721.

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The purpose of this study was to determine whether heterogeneity in endothelium-dependent responses to acetylcholine between canine blood vessels of different anatomical origin reflects variations in endothelial function or in responsiveness of vascular smooth muscle cells. Experiments were conducted in a bioassay system, where segments of femoral artery or vein with endothelium were perfused intraluminally and the perfusate used to superfuse rings of femoral arteries or veins without endothelium. Indomethacin was present in all experiments to prevent the synthesis of prostanoids. The blood vessels were contracted by phenylephrine. Measurement of wall tension in both the perfused segment and bioassay ring allowed simultaneous detection of endothelium-derived relaxing factor(s) released abluminally (segment) and intraluminally (ring). Intraluminal infusion of acetylcholine (ACh) induced relaxations in the perfused artery but not in vein segments. During arterial superfusion ACh induced relaxation in femoral arterial rings but contraction in venous rings. After treatment with atropine the arterial perfusate evoked relaxations in venous rings. Infusion of ACh through the femoral vein evoked only moderate relaxations in arterial rings. These data demonstrate that depressed endothelium-dependent relaxation to ACh in femoral veins compared to femoral arteries is due to a masking effect of the direct stimulating action of ACh and decreased release of the same mediator or the release of a different relaxing factor from venous endothelium.
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9

Jino, Hiroshi, Hachiro Usui, Shinji Temma, and Kazuyoshi Kurahashi. "Heterogeneity of TXA2-receptor in arterial preparation." Japanese Journal of Pharmacology 64 (1994): 109. http://dx.doi.org/10.1016/s0021-5198(19)50078-6.

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10

Eichinger, M. R., and B. R. Walker. "Segmental heterogeneity of NO-mediated pulmonary vasodilation in rats." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 2 (August 1, 1994): H494—H499. http://dx.doi.org/10.1152/ajpheart.1994.267.2.h494.

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Nitric oxide (NO) is known to elicit vasodilation in the preconstricted rat lung. However, the sites of dilation within the pulmonary vasculature remain unknown. We hypothesized that donated NO would dilate all areas of constriction within the pulmonary vasculature, whereas receptor-mediated, NO-induced dilations would correspond to regional binding of agents. Isolated lungs from male Sprague-Dawley rats were perfused at constant flow with physiological saline solution. Pulmonary arterial and pulmonary venous pressures were monitored, while pulmonary microvascular pressures were estimated by vascular occlusion. Lungs were constricted with U-46619, and upon development of a stable degree of vasoconstriction, the NO donor sodium nitroprusside or the endothelium-dependent dilators A23187, arginine vasopressin, or ATP were administered. U-46619 caused constriction of both arterial and venous segments. Administration of sodium nitroprusside and the calcium ionophore A23187 elicited similar dilation of preconstricted arterial and venous segments. Arginine vasopressin significantly dilated both arterial and venous segments, with a greater reversal of venous resistance. In contrast, ATP significantly reduced arterial resistance more than venous. These results demonstrate that donated NO uniformly dilates all constricted regions of the pulmonary vasculature. However, receptor-mediated, endothelium-dependent dilators display characteristic heterogeneities in the sites of decreased pulmonary vascular resistance.
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11

Brogan, Thomas V., H. Thomas Robertson, Wayne J. E. Lamm, Jennifer E. Souders, and Erik R. Swenson. "Carbon dioxide added late in inspiration reduces ventilation-perfusion heterogeneity without causing respiratory acidosis." Journal of Applied Physiology 96, no. 5 (May 2004): 1894–98. http://dx.doi.org/10.1152/japplphysiol.00160.2003.

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We have shown previously that inspired CO2 (3-5%) improves ventilation-perfusion (V̇a/Q̇) matching but with the consequence of mild arterial hypercapnia and respiratory acidosis. We hypothesized that adding CO2 only late in inspiration to limit its effects to the conducting airways would enhance V̇a/Q̇ matching and improve oxygenation without arterial hypercapnia. CO2 was added in the latter half of inspiration in a volume aimed to reach a concentration of 5% in the conducting airways throughout the respiratory cycle. Ten mixed-breed dogs were anesthetized and, in a randomized order, ventilated with room air, 5% CO2 throughout inspiration, and CO2 added only to the latter half of inspiration. The multiple inert-gas elimination technique was used to assess V̇a/Q̇ heterogeneity. Late-inspired CO2 produced only very small changes in arterial pH (7.38 vs. 7.40) and arterial CO2 (40.6 vs. 39.4 Torr). Compared with baseline, late-inspired CO2 significantly improved arterial oxygenation (97.5 vs. 94.2 Torr), decreased the alveolar-arterial Po2 difference (10.4 vs. 15.7 Torr) and decreased the multiple inert-gas elimination technique-derived arterial-alveolar inert gas area difference, a global measurement of V̇a/Q̇ heterogeneity (0.36 vs. 0.22). These changes were equal to those with 5% CO2 throughout inspiration (arterial Po2, 102.5 Torr; alveolar-arterial Po2 difference, 10.1 Torr; and arterial-alveolar inert gas area difference, 0.21). In conclusion, we have established that the majority of the improvement in gas exchange efficiency with inspired CO2 can be achieved by limiting its application to the conducting airways and does not require systemic acidosis.
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12

Espitia, Olivier, Mathias Chatelais, Marja Steenman, Céline Charrier, Blandine Maurel, Steven Georges, Rémi Houlgatte, et al. "Implication of molecular vascular smooth muscle cell heterogeneity among arterial beds in arterial calcification." PLOS ONE 13, no. 1 (January 26, 2018): e0191976. http://dx.doi.org/10.1371/journal.pone.0191976.

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13

Karch, Rudolf, Friederike Neumann, Bruno K. Podesser, Martin Neumann, Paul Szawlowski, and Wolfgang Schreiner. "Fractal Properties of Perfusion Heterogeneity in Optimized Arterial Trees." Journal of General Physiology 122, no. 3 (August 11, 2003): 307–22. http://dx.doi.org/10.1085/jgp.200208747.

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Regional blood flows in the heart muscle are remarkably heterogeneous. It is very likely that the most important factor for this heterogeneity is the metabolic need of the tissue rather than flow dispersion by the branching network of the coronary vasculature. To model the contribution of tissue needs to the observed flow heterogeneities we use arterial trees generated on the computer by constrained constructive optimization. This method allows to prescribe terminal flows as independent boundary conditions, rather than obtaining these flows by the dispersive effects of the tree structure. We study two specific cases: equal terminal flows (model 1) and terminal flows set proportional to the volumes of Voronoi polyhedra used as a model for blood supply regions of terminal segments (model 2). Model 1 predicts, depending on the number Nterm of end-points, fractal dimensions D of perfusion heterogeneities in the range 1.20 to 1.40 and positively correlated nearest-neighbor regional flows, in good agreement with experimental data of the normal heart. Although model 2 yields reasonable terminal flows well approximated by a lognormal distribution, it fails to predict D and nearest-neighbor correlation coefficients r1 of regional flows under normal physiologic conditions: model 2 gives D = 1.69 ± 0.02 and r1 = −0.18 ± 0.03 (n = 5), independent of Nterm and consistent with experimental data observed under coronary stenosis and under the reduction of coronary perfusion pressure. In conclusion, flow heterogeneity can be modeled by terminal positions compatible with an existing tree structure without resorting to the flow-dispersive effects of a specific branching tree model to assign terminal flows.
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14

Orlandi, Augusto, Arianna Francesconi, Alessandro Ciucci, Marcella Marcellini, and Luigi Giusto Spagnoli. "PHENOTYPIC HETEROGENEITY AND APOPTOSIS OF ARTERIAL SMOOTH MUSCLE CELLS." Cardiovascular Pathology 13, no. 3 (May 2004): 161. http://dx.doi.org/10.1016/j.carpath.2004.03.486.

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15

Bochaton-Piallat, Marie-Luce, Patricia Ropraz, Françoise Gabbiani, and Giulio Gabbiani. "Phenotypic Heterogeneity of Rat Arterial Smooth Muscle Cell Clones." Arteriosclerosis, Thrombosis, and Vascular Biology 16, no. 6 (June 1996): 815–20. http://dx.doi.org/10.1161/01.atv.16.6.815.

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16

Stremmel, Christopher, Konstantin Stark, and Christian Schulz. "Heterogeneity of Macrophages in Atherosclerosis." Thrombosis and Haemostasis 119, no. 08 (June 26, 2019): 1237–46. http://dx.doi.org/10.1055/s-0039-1692665.

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AbstractAtherosclerosis is a prevalent inflammatory condition and a frequent cause of morbidity and mortality worldwide. Macrophages are among the key immune cells driving lesion formation in the arterial wall. They have therefore evolved as potential targets for therapeutic strategies. Understanding of the different macrophage phenotypes and functions seems to be of pivotal importance for the development of treatments to target these immune cells. This review highlights the complexity of the mononuclear phagocyte system and summarizes important features of macrophage biology contributing to atherosclerosis.
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17

Kolbeck, Ralph C., and William A. Speir Jr. "Regional contractile responses in pulmonary artery to α- and β-adrenoceptor agonists." Canadian Journal of Physiology and Pharmacology 65, no. 6 (June 1, 1987): 1165–70. http://dx.doi.org/10.1139/y87-184.

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Contractile sensitivity and reactivity to α- and β-adrenoceptor stimulation was studied in incubated rabbit pulmonary artery cylindrical segments of differing diameters. Distinct differences were noted between the responses of extra- and intra-pulmonary pulmonary arteries to norepinephrine and isoproterenol. The sensitivity to norepinephrine was largest in the intrapulmonary pulmonary arteries. Arterial reactivity to norepinephrine was greatest in the larger of the intrapulmonary vessel segments, diminishing considerably as the vessels became smaller. Cocaine did not cause substantial alterations in the response of any of the arterial segments to the α-agonist. Phentolamine, however, exerted its influence primarily in the smaller arterial segments. Vascular sensitivity to isoproterenol was least in the intrapulmonary pulmonary arteries. These smaller vessel segments, however, were more reactive to isoproterenol than were the extrapulmonary pulmonary arterial segments. Propranolol, at a concentration of 10−8 M, was an effective antagonist of the β-agonist; at a concentration of 10−7 M, however, this antagonist was related to isoproterenol-induced arterial contraction, apparently by stimulation of α-receptor sites. The results of this study demonstrated a regional heterogeneity in the contractile response of the pulmonary artery to α- and β-stimulation. The extrapulmonary arterial segments were found to be more sensitive to β-stimulation than were the smaller, intrapulmonary, segments. The intrapulmonary arterial segments, on the other hand, were found to be more sensitive to α-stimulation than were the extrapulmonary segments.
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18

Ohlsson, J., M. Middaugh, and M. P. Hlastala. "Reduction of lung perfusion increases VA/Q heterogeneity." Journal of Applied Physiology 66, no. 5 (May 1, 1989): 2423–30. http://dx.doi.org/10.1152/jappl.1989.66.5.2423.

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This study addresses the hypothesis that decreases in lung perfusion rate independently worsen gas exchange efficiency in an isolated left lower lobe in zone 2 conditions. In seven anesthetized dogs, the left lower lobe was isolated, leaving the bronchus and bronchial vasculature intact. Blood was taken from the femoral arteries and reinfused at a controlled rate into the pulmonary artery of the left lower lobe. The flow rate was varied between 100 and 400 ml/min. The multiple inert gas elimination technique was used to quantitate the matching of ventilation to perfusion. Reduction in lobe blood flow resulted in a significant increase in perfusion-related indexes of alveolar ventilation-perfusion heterogeneity, such as the log standard deviation of the perfusion distribution, the retention component of the arterial-alveolar difference area, and the retention dispersion index. The increased heterogeneity suggests a worsening of the intraregional matching between the ventilation and the perfusion when perfusion is less than normal.
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19

Domino, K. B., B. L. Eisenstein, F. W. Cheney, and M. P. Hlastala. "Pulmonary blood flow and ventilation-perfusion heterogeneity." Journal of Applied Physiology 71, no. 1 (July 1, 1991): 252–58. http://dx.doi.org/10.1152/jappl.1991.71.1.252.

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We studied the independent influence of changes in perfusion on pulmonary gas exchange in the left lower lobe (LLL) of anesthetized dogs. Blood flow to the LLL (QLLL) was raised 50% (increased QLLL) or reduced 50% (decreased QLLL) from baseline by partial occlusion of the right or left pulmonary artery, respectively. Minute ventilation and alveolar PCO2 of the LLL remained constant throughout the study. We determined ventilation-perfusion distributions of the LLL using the multiple inert gas elimination technique. Increased QLLL impaired LLL pulmonary gas exchange. All dispersion indexes and all arterial-alveolar difference areas increased (P less than 0.01). Decreased QLLL increased the log standard deviation of the perfusion distribution (P less than 0.05) and reduced the log standard deviation of the ventilation distribution (P less than 0.01) but did not affect the dispersion indexes or alveolar-arterial difference areas. We conclude that ventilation-perfusion heterogeneity is increased by independent changes in perfusion from normal baseline blood flow, even when ventilation and alveolar gas composition remain constant.
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20

Titov, V. "PHYLOGENESIS, ANATOMIC, FUNCTIONAL HETEROGENEITY OF THE ARTERIAL BED AND PATHOGENESIS OF ARTERIAL HYPERTENSION: PP.8.333." Journal of Hypertension 28 (June 2010): e149-e150. http://dx.doi.org/10.1097/01.hjh.0000378657.99849.6a.

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21

Shin, Donghun, and David J. Anderson. "Isolation of arterial-specific genes by subtractive hybridization reveals molecular heterogeneity among arterial endothelial cells." Developmental Dynamics 233, no. 4 (2005): 1589–604. http://dx.doi.org/10.1002/dvdy.20479.

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22

Stroeva, V. S., and O. F. Kalev. "The clinico-functional heterogeneity of changes in the coronary and cerebral blood circulation with the arterial hypertonia of the I stage." Regional blood circulation and microcirculation 14, no. 2 (June 30, 2015): 56–62. http://dx.doi.org/10.24884/1682-6655-2015-14-2-56-62.

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Purpose of this investigation: to determine the early signs of the typological disturbances of coronary and cerebral blood circulation with the arterial hypertonia of the I stage. Materials and the methods. Is carried out a study of cardio-cerebrovascular system in 147 men in the age of 30-59 years with the arterial hypertonia of the I stage, control group they composed 37 clinically healthy men at the age from 29 to 42 years. Results and their consideration. Substantial changes in the coronary and cerebral blood flow with the I stage of arterial hypertonia to the development of the clinical manifestations of the defeat of the vessels of heart and brain are revealed. Is carried out daily monitoring arterial pressure and electrocardiogram, rhythmocardiography, bicycle ergometry, echocardiography, transcranial dopplerography, ultrasonic diagnostics of the main arteries of head and neck. Statistical processing of the results of a study is carried out by the standard methods within the framework of software Statistica for Windows, version 6 and recommended in the management on the biomedical statistics. Obtained by us data give grounds for expanding the criteria, which characterize the defeat of the target organs at the early stage arterial hypertonia. To these criteria we carried the clinical signs of the initial manifestations of the insufficiency of the blood supply of brain and discirculatory encephalopathy of the I stage, and also painless ischemia of the myocardium in the absence of stenocardia and its equivalents, presence of the minimum signs of the disturbance extra and intracranial blood flow (high-speed indices and the asymmetry of blood flow, the index of cerebrovascular reactivity and the presence of microembolic signals). Conclusions. The clinico-functional heterogeneity of changes in the coronary and cerebral blood circulation with the arterial hypertonia of the I stage requires the revision of the standards of the inspection of patients with the development of the increased numbers of arterial pressure, and also start of the new criteria of the early defeat of heart and brain in clinical recommendations.
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23

Bakker, Erik N. T. P., Gergely Groma, Léon J. A. Spijkers, Judith de Vos, Angela van Weert, Henk van Veen, Vincent Everts, Silvia M. Arribas, and Ed VanBavel. "Heterogeneity in Arterial Remodeling among Sublines of Spontaneously Hypertensive Rats." PLoS ONE 9, no. 9 (September 24, 2014): e107998. http://dx.doi.org/10.1371/journal.pone.0107998.

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24

De Backer, Daniel, and Ashish K. Khanna. "The Ideal Mean Arterial Pressure Target Debate: Heterogeneity Obscures Conclusions*." Critical Care Medicine 52, no. 9 (August 15, 2024): 1495–98. http://dx.doi.org/10.1097/ccm.0000000000006331.

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25

Zhao, Lan, Ali Ashek, Lei Wang, Wei Fang, Swati Dabral, Olivier Dubois, John Cupitt, et al. "Heterogeneity in Lung 18 FDG Uptake in Pulmonary Arterial Hypertension." Circulation 128, no. 11 (September 10, 2013): 1214–24. http://dx.doi.org/10.1161/circulationaha.113.004136.

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26

Vakhovskaya, T. V., M. I. Tripoten, O. A. Pogorelova, T. V. Balakhonova, M. M. Loukianov, and S. A. Boytsov. "Local rigidity of the walls of the carotid artery at the site of formation of atherosclerotic plaques in patients with arterial hypertension." Systemic Hypertension 11, no. 4 (December 15, 2014): 49–52. http://dx.doi.org/10.26442/sg29050.

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Aim: To study the local elastic properties of the arterial wall at the site of atherosclerotic plaque and adjacent areas «healthy» wall of the common carotid artery in patients with arterial hypertension (AH).Materials and methods. The study included 25 patients (3 men, 22 women) with AH 1-2 grad in combination with moderate carotid atherosclerosis and lipid metabolism disorders. All patients underwent conventional ultrasound duplex scanning of the carotid arteries to determine the severity of atherosclerotic carotid arteries and the structure of atherosclerotic plaque. Determination of parameters of the local rigidity - the elasticity of the arterial wall and the atherosclerotic plaque, was carried out on the ultrasound system ALOKA a7. Was scanned and the surroundingarea atherosclerotic plaque sections of the arterial wall in the B/M mode using echo-tracking method.Results. A significant increase in the hardness of the arterial wall in atherosclerotic plaque as in the adventitia and its surface, as compared with the adjacent «healthy» wall of the carotid artery. Atherosclerotic plaque base has significantly greater rigidity and less flexibility than its surface. Conclusion. The formation of atheroma by the action of arterial pulse pressure develops heterogeneity elastic properties carotid wall not only along the artery, but in the atherosclerotic plaque (between its base and the surface). This indicates of different mobility plots artery and plaque and can lead to the formation of the mechanical instability of atherosclerotic plaque in patients with hypertension.
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Speck, Nancy, Qin Zhu, Peng Gao, Joanna Tober, Laura Bennett, Changya Chen, Yasin Uzun, Yan Li, and Kai Tan. "Developmental Biology of the Blood System." Blood 134, Supplement_1 (November 13, 2019): SCI—29—SCI—29. http://dx.doi.org/10.1182/blood-2019-121283.

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Hematopoietic stem and progenitor cells (HSPCs) in the bone marrow are derived from a small population of hemogenic endothelial (HE) cells located in the yolk sac and major caudal arteries of the mammalian embryo. HE cells undergo an endothelial to hematopoietic cell transition, giving rise to HSPCs that accumulate in intra-arterial clusters before colonizing the fetal liver. To examine the molecular transitions between endothelial cells, HE, and intra-arterial cluster cells, and the heterogeneity of HSPCs within the intra-arterial clusters, we profiled ~40,000 cells from the caudal arteries (dorsal aorta, umbilical, vitelline) of embryonic day 9.5 to 11.5 mouse embryos by single-cell RNA sequencing (scRNA-seq) and single-cell chromatin accessibility sequencing (scATAC-Seq). A continuous developmental trajectory leads from endothelial cells to intra-arterial cluster cells, with identifiable intermediate stages between endothelial cells and HE. The intermediate endothelial stages most proximal to HE are characterized by elevated expression of genes regulated by GATA and SOX transcription factors. Developmental bottlenecks separate endothelial cells from HE cells, with the efficiency of transit through one of the last bottleneck regulated by RUNX1 dosage. Distinct developmental trajectories within intra-arterial cluster cells result in two populations of CD45+HSPCs; an initial wave of multi-lineage committed progenitors followed by precursors of hematopoietic stem cells (pre-HSCs). These and other insights gained from single cell analyses of HSPC formation from arterial endothelium will be presented. Disclosures No relevant conflicts of interest to declare.
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28

Thijssen, Dick H. J., Ellen A. Dawson, Mark A. Black, Maria T. E. Hopman, N. Timothy Cable, and Daniel J. Green. "Heterogeneity in conduit artery function in humans: impact of arterial size." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 5 (November 2008): H1927—H1934. http://dx.doi.org/10.1152/ajpheart.00405.2008.

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To determine whether conduit artery size affects functional responses, we compared the magnitude, time course, and eliciting shear rate stimulus for flow-mediated dilation (FMD) in healthy men ( n = 20; 31 ± 7 yr). Upper limb (brachial and radial) and lower limb (common and superficial femoral) FMD responses were simultaneously assessed, whereas popliteal responses were measured in the same subjects during a separate visit. Glyceryl trinitrate (GTN)-mediated responses were similarly examined. Edge detection and wall tracking of high-resolution B-mode arterial ultrasound images, combined with synchronized Doppler waveform envelope analysis, were used to calculate conduit artery diameter, blood flow, and shear rate continuously across the cardiac cycle. Baseline artery size correlated inversely with the FMD response ( r = −0.57, P < 0.001). Within-artery comparisons revealed a significant inverse correlation between artery size and FMD% for the radial ( r = −0.66, P = 0.001), brachial ( r = −0.55, P = 0.01), and popliteal artery ( r = −0.48, P = 0.03), but not for the superficial and common femoral artery. Normalization of FMD responses for differences in eliciting shear rate did not abolish the between-artery relationship for artery function and size ( r = −0.48, P < 0.001), suggesting that differences between artery function responses were not entirely due to size-related differences in shear rate. This was reinforced by a significant between-artery correlation for GTN responses and baseline artery size ( r = −0.74, P < 0.001). In summary, systematic differences exist in vascular function responses of conduit arteries that differ in size. This raises the possibility that differences in artery size within or between individuals may influence functional responses.
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Reyes Gamonal, Jacqueline M., Robert Malpartida Palomino, Fiorella E. Zuzunaga-Montoya, Jenny R. Torres-Malca, Alfredo J. Chiappe Gonzalez, Víctor J. Vera-Ponce, and Jhony A. De La Cruz-Vargas. "Hypertriglyceridemic waist and arterial hypertension in adults: a systematic review and meta-analysis." Revista de la Facultad de Medicina Humana 22, no. 1 (September 7, 2022): 743–53. http://dx.doi.org/10.25176/rfmh.v22i4.5092.

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Objective: To develop a systematic review and meta-analysis to determine the association between hypertriglyceridemic waist (CHTG) and arterial hypertension (HBP) in adults. Materials: The present study is a systematic review (SR) with meta-analysis of analytical cross-sectional observational studies. Search strategies will be used in different databases, which will be Pubmed, SCOPUS, Web of Science, Embase. The qualitative analysis was presented in a table with the characteristics of each study. For quantitative analysis, random-effects meta-analysis was performed due to the heterogeneity of the studies. These variables were compared using Odds Ratios (OR) as a measure of association with their corresponding 95% confidence interval. Results: Five studies were included for statistical analysis. Overall, a statistically significant association was found between both variables (OR: 1.36; 95% CI 1.07 to 1.71). In turn, there was a high heterogeneity (I squared 92%). Conclusions: This SR found that CHTG is associated with the presence of hypertension. However, given the few studies found, it is recommended to carry out more primary studies with a prospective design before carrying out a next SR on the subject, and with standardized cut-off points to make a more homogeneous comparability.
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Zhang, Yi, Patrick Lacolley, Athanase D. Protogerou, and Michel E. Safar. "Arterial Stiffness in Hypertension and Function of Large Arteries." American Journal of Hypertension 33, no. 4 (February 15, 2020): 291–96. http://dx.doi.org/10.1093/ajh/hpz193.

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Abstract BACKGROUND Arterial stiffness—typically assessed from non-invasive measurement of pulse wave velocity along a straight portion of the vascular tree between the right common carotid and femoral arteries—is a reliable predictor of cardiovascular risk in patients with essential hypertension. METHODS We reviewed how carotid-femoral pulse wave velocity increases with age and is significantly higher in hypertension (than in age- and gender-matched individuals without hypertension), particularly when hypertension is associated with diabetes mellitus. RESULTS From the elastic aorta to the muscular peripheral arteries of young healthy individuals, there is a gradual but significant increase in stiffness, with a specific gradient. This moderates the transmission of pulsatile pressure towards the periphery, thus protecting the microcirculatory network. The heterogeneity of stiffness between the elastic and muscular arteries causes the gradient to disappear or be inversed with aging, particularly in long-standing hypertension. CONCLUSIONS In hypertension therefore, pulsatile pressure transmission to the microcirculation is augmented, increasing the potential risk of damage to the brain, the heart, and the kidney. Furthermore, elevated pulse pressure exacerbates end-stage renal disease, particularly in older hypertensive individuals. With increasing age, the elastin content of vessel walls declines throughout the arterial network, and arterial stiffening increases further due to the presence of rigid wall material such as collagen, but also fibronectin, proteoglycans, and vascular calcification. Certain genes, mainly related to angiotensin and/or aldosterone, affect this aging process and contribute to the extent of arterial stiffness, which can independently affect both forward and reflected pressure waves.
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31

Lautt, W. Wayne, Joshua Schafer, and Dallas J. Legare. "Hepatic blood flow distribution: consideration of gravity, liver surface, and norepinephrine on regional heterogeneity." Canadian Journal of Physiology and Pharmacology 71, no. 2 (February 1, 1993): 128–35. http://dx.doi.org/10.1139/y93-018.

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Blood flow distribution within the livers of cats and dogs was assessed using 15-μm microspheres injected into the hepatic artery and portal vein. Representative vertical core samples (n = 11–18) were taken from the thickest part of each liver. Heterogeneity was assessed in several ways. The difference in total flow to different lobes was greater in dogs than in cats, and in dogs, those lobes with highest portal venous flow had lowest hepatic arterial flow. Overall flow variance was very high in both species, with adjacent surface samples in a single lobe showing variance of 15–22% for both vessels. The ratio of highest to lowest flow within core samples averaged 2.1–3.4 for both vessels in both species. The hepatic arterial flow was highest to the surface 2 mm of the liver. Portal flow most often (31% of all samples) showed a pattern of highest flow to the top, graduating down to lowest flow to the bottom (dorsal side) of the vertical cores. However, this pattern appeared much more frequently in the most ventral liver lobes and very seldom in the lobes lying beneath the liver mass. Norepinephrine reduced heterogeneity. Hepatic arterial occlusion for 10 min produced minor and inconsistent reduction of heterogeneity. Rotating cats from back to front and again to back disrupted patterns of distribution but not in a way that could be interpreted as due to effects of gravity. Flow patterns changed with time. The heterogeneity of perfusion appears to be under dynamic and multiple interacting forces.Key words: blood flow distribution, blood flow heterogeneity, hepatic artery, portal vein, liver.
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Kawai, Yasuaki, and Toshio Ohhashi. "Heterogeneity in responses of isolated monkey arteries and veins to atrial natriuretic peptide." Canadian Journal of Physiology and Pharmacology 67, no. 4 (April 1, 1989): 326–30. http://dx.doi.org/10.1139/y89-053.

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Regional differences in responses of isolated monkey arteries and veins to atrial natriuretic peptide were investigated by recording isometric tension. Addition of atrial natriuretic peptide (4 × 10−12 to 4 × 10−8 M) produced a concentration-dependent relaxation in isolated monkey arteries and veins. No significant difference was observed between the responses to rat and human atrial natriuretic peptides. A marked heterogeneity in responses to rat atrial natriuretic peptide, however, was observed in arterial preparations. The decreasing order of the response was as follows: renal > pulmonary > femoral = mesenteric > coronary > middle cerebral > basilar arteries. A heterogeneity in the relaxation produced by atrial natriuretic peptide was also observed in monkey veins. The decreasing order of the response was as follows: pulmonary > mesenteric = portal > femoral > renal = inferior caval veins. On the other hand, 10−5 M sodium nitroprusside caused a maximal relaxation in all monkey arteries and veins used. In the middle cerebral, basilar, and coronary arteries, the relaxant effects of rat atrial natriuretic peptide on KCl-induced contraction were significantly smaller than those on the preparations contracted by an agonist such as prostaglandin F2α. These results suggest that there exist profound regional vasorelaxant selectivities of atrial natriuretic peptide in isolated monkey arteries and veins.Key words: atrial natriuretic peptide, artery, vein, vasodilation, monkey.
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33

Peterson, S. J., and R. J. Okamoto. "Effect of Residual Stress and Heterogeneity on Circumferential Stress in the Arterial Wall." Journal of Biomechanical Engineering 122, no. 4 (March 22, 2000): 454–56. http://dx.doi.org/10.1115/1.1288210.

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Quantifying the stress distribution through the arterial wall is essential to studies of arterial growth and disease. Previous studies have shown that both residual stress, as measured by opening angle, and differing material properties for the media-intima and the adventitial layers affect the transmural circumferential stress σθ distribution. Because a lack of comprehensive data on a single species and artery has led to combinations from multiple sources, this study determined the sensitivity of σθ to published variations in both opening angle and layer thickness data. We fit material properties to previously published experimental data for pressure–diameter relations and opening angles of rabbit carotid artery, and predicted σθ through the arterial wall at physiologic conditions. Using a one-layer model, the ratio of σθ at the internal wall to the mean σθ decreased from 2.34 to 0.98 as the opening angle increased from 60 to 130 deg. In a two-layer model using a 95 deg opening angle, mean σθ in the adventitia increased (112 percent for 25 percent adventitia) and mean σθ in the media decreased (47 percent for 25 percent adventitia). These results suggest that both residual stress and wall layers have important effects on transmural stress distribution. Thus, experimental measurements of loading curves, opening angles, and wall composition from the same species and artery are needed to accurately predict the transmural stress distribution in the arterial wall. [S0148-0731(00)02204-4]
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Lomas-Neira, Joanne, Daithi Heffernan, Alfred Ayala, and Chun-Shiang Chung. "Pulmonary vascular heterogeneity: microvascular vs. arterial generation of angiopoietin-2 (IRC5P.633)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 58.16. http://dx.doi.org/10.4049/jimmunol.194.supp.58.16.

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Abstract Endothelial cell (EC) growth factors, Angiopoietin (Ang)-1 and Ang-2, are important mediators of EC function. Bound to a shared receptor, Tie2, expressed on ECs, they have opposing effects on EC activation. Ang-1/Tie2 promotes a quiescent while Ang-2/Tie2 promotes an activated phenotype and increased vascular permeability. Ang-2, stored preformed in EC Weibel Palade bodies (WPbs), is rapidly released from activated ECs. We have reported increased Ang-2 in the blood of trauma patients with ARDS, representing a potential therapeutic target. To assess lung EC activation and release of Ang-2, we used human pulmonary arterial ECs (hPAECs) and microvascular ECs (hPMECs) grown on electric cell-substrate impedance sensing arrays. These arrays measure changes in EC monolayer integrity in response to inflammatory stimulus. We show that, in response to TNF-a stimulation, hPMECs exhibited increased loss of barrier function compared to hPAECs. Also, Ang-2 in culture supernatant increased in both hPAECs and hPMECs compared to untreated controls. While ECs in larger vessels (arteries), contain WPbs, they are not observed in microvascular ECs (&lt;10um diam). To further investigate, we inhibited WPb vesicle exocytosis. Our findings show that inhibition of WPb release decreased Ang-2 in supernatant from hPAECs, but not significantly from hPMECs, suggesting that the microvascular is a region with distinct responses potentially associated with their location and anatomic structure.
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Hernandez-Gonzalez, Ignacio, Jair Tenorio, Julian Palomino-Doza, Amaya Martinez Meñaca, Rafael Morales Ruiz, Mauro Lago-Docampo, María Valverde Gomez, et al. "Clinical heterogeneity of Pulmonary Arterial Hypertension associated with variants in TBX4." PLOS ONE 15, no. 4 (April 29, 2020): e0232216. http://dx.doi.org/10.1371/journal.pone.0232216.

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36

Hu, Zhan, Wendao Liu, Xiumeng Hua, Xiao Chen, Yuan Chang, Yiqing Hu, Zhenyu Xu, and Jiangping Song. "Single-Cell Transcriptomic Atlas of Different Human Cardiac Arteries Identifies Cell Types Associated With Vascular Physiology." Arteriosclerosis, Thrombosis, and Vascular Biology 41, no. 4 (April 2021): 1408–27. http://dx.doi.org/10.1161/atvbaha.120.315373.

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Objective: Although cellular heterogeneity within arterial walls has been explored in mice and nonhuman primates, the cellular composition of human arterial walls remains unclear. Approach and Results: The cellular composition of nondiseased cardiac arteries (3 aortas, 2 pulmonary arteries and 9 coronary arteries) from 3 heart transplantation patients were investigated by single-cell sequencing of >10 5 cells. Clustering analysis identified 25 subpopulations representing the 10 main arterial cell types: vascular smooth muscle cell (4 clusters), fibroblast (4 clusters), macrophage (Mφ, 4 clusters), T cell (4 clusters), endothelial cell (4 clusters), NK cell (2 clusters), mast cell (1 cluster), myofibroblast (1 cluster), oligodendrocyte (1 cluster), and B/plasma cells (1 cluster). Vascular smooth muscle cell was the largest cell population in cardiac arteries, followed by fibroblast, Mφ, T cell, endothelial cell, NK cell, and so on. We compared cellular composition among different arteries and found some artery-specific vascular smooth muscle cell and fibroblast subpopulations. The communication between vascular smooth muscle cell and fibroblast was predominant in nondiseased condition. Atherosclerosis-associated genes were particularly enriched in endothelial cell and Mφ, and intercellular communication between endothelial cell and immune cells was predicted to increase in atherosclerosis. The interaction between ICAM1 / VCAM1 (EC1) and ITGB2 (immune cells, especially inflammatory Mφ) was speculated to be essential for the pathogenesis of atherosclerosis. Conclusions: We created a cell atlas of human nondiseased cardiac arteries, and characterized the cellular compositions in different cardiac arteries. Our results could be used as a reference to identify vascular disease-associated cell populations and help investigate new therapeutic strategies for vascular diseases.
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37

Cuthbertson, Iona, Nicholas W. Morrell, and Paola Caruso. "BMPR2 Mutation and Metabolic Reprogramming in Pulmonary Arterial Hypertension." Circulation Research 132, no. 1 (January 6, 2023): 109–26. http://dx.doi.org/10.1161/circresaha.122.321554.

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Abstract: Pulmonary arterial hypertension forms the first and most severe of the 5 categories of pulmonary hypertension. Disease pathogenesis is driven by progressive remodeling of peripheral pulmonary arteries, caused by the excessive proliferation of vascular wall cells, including endothelial cells, smooth muscle cells and fibroblasts, and perivascular inflammation. Compelling evidence from animal models suggests endothelial cell dysfunction is a key initial trigger of pulmonary vascular remodeling, which is characterised by hyperproliferation and early apoptosis followed by enrichment of apoptosis-resistant populations. Dysfunctional pulmonary arterial endothelial cells lose their ability to produce vasodilatory mediators, together leading to augmented pulmonary arterial smooth muscle cell responses, increased pulmonary vascular pressures and right ventricular afterload, and progressive right ventricular hypertrophy and heart failure. It is recognized that a range of abnormal cellular molecular signatures underpin the pathophysiology of pulmonary arterial hypertension and are enhanced by loss-of-function mutations in the BMPR2 gene, the most common genetic cause of pulmonary arterial hypertension and associated with worse disease prognosis. Widespread metabolic abnormalities are observed in the heart, pulmonary vasculature, and systemic tissues, and may underpin heterogeneity in responsivity to treatment. Metabolic abnormalities include hyperglycolytic reprogramming, mitochondrial dysfunction, aberrant polyamine and sphingosine metabolism, reduced insulin sensitivity, and defective iron handling. This review critically discusses published mechanisms linking metabolic abnormalities with dysfunctional BMPR2 (bone morphogenetic protein receptor 2) signaling; hypothesized mechanistic links requiring further validation; and their relevance to pulmonary arterial hypertension pathogenesis and the development of potential therapeutic strategies.
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38

Levin, David L., Richard B. Buxton, James P. Spiess, Tatsuya Arai, Jamal Balouch, and Susan R. Hopkins. "Effects of age on pulmonary perfusion heterogeneity measured by magnetic resonance imaging." Journal of Applied Physiology 102, no. 5 (May 2007): 2064–70. http://dx.doi.org/10.1152/japplphysiol.00512.2006.

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Normal aging is associated with a decline in pulmonary function and efficiency of gas exchange, although the effects on the spatial distribution of pulmonary perfusion are poorly understood. We hypothesized that spatial pulmonary perfusion heterogeneity would increase with increasing age. Fifty-six healthy, nonsmoking subjects (ages 21–76 yr) underwent magnetic resonance imaging with arterial spin labeling (ASL) using a Vision 1.5-T whole body scanner (Siemens Medical Systems, Erlangen, Germany). ASL uses a magnetically tagged bolus to generate perfusion maps where signal intensity is proportional to regional pulmonary perfusion. The spatial heterogeneity of pulmonary blood flow was quantified by the relative dispersion (RD = SD/mean, a global index of heterogeneity) of signal intensity for voxels within the right lung and by the fractal dimension ( Ds). There were no significant sex differences for RD ( P = 0.81) or Ds ( P = 0.43) when age was considered as a covariate. RD increased significantly with increasing age by ∼0.1/decade until age 50–59 yr, and there was a significant positive relationship between RD and age ( R = 0.48, P < 0.0005) and height ( R = 0.39, P < 0.01), but not body mass index ( R = 0.07, P = 0.67). Age and height combined in a multiple regression were significantly related to RD ( R = 0.66, P < 0.0001). There was no significant relationship between RD and spirometry or arterial oxygen saturation. Ds was not related to age, height, spirometry, or arterial oxygen saturation. The lack of relationship between age and Ds argues against an intrinsic alteration in the pulmonary vascular branching with age as being responsible for the observed increase in global spatial perfusion heterogeneity measured by the RD.
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39

Slavik, Zdenek, Rodney C. G. Franklin, and Rosemary Radley-Smith. "The real fate of pulmonary arteries after bidirectional superior cavopulmonary anastomosis: is there a need for concern?" Cardiology in the Young 9, no. 1 (January 1999): 6–10. http://dx.doi.org/10.1017/s1047951100007319.

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AbstractControversy remains about the growth of the pulmonary arteries following a bidirectional superior cavopulmonary anastomosis in children with complex cyanotic congenital cardiac malformations. This is partially due to the morphological heterogeneity of the patients, and partially due to methodological differences in series published so far. It is further complicated by the variable use, in different centres, of additional sources of pulmonary blood flow. We believe that the fate of these arteries preoperatively is significantly influenced by the amount of pulmonary blood flow and the initial size of the arteries. Separate assessment of the pulmonary arterial development postoperatively is recommended for those who, initially, had relatively small as opposed to larger than normal pulmonary arteries. Measurement of the diameters of both pulmonary arteries just prior to their first point of branching, together with the use of Z-score evaluation rather than the Nakata index, is discussed. It remains to be established whether, over time, the bidirectional cavopulmonary anastomosis is effective in developing adequately the pulmonary arteries in preparation for an ultimate total cavopulmonary connection, or even as isolated long-term palliation. A prospective, multi-institutional study involving sequential non-invasive assessment of pulmonary arterial development (using, for example, magnetic resonance imaging) is required to solve the outstanding problems.
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40

Schortgen, Frédérique, and Caroline Le Bec. "Invasive Arterial Pressure Monitoring: Are We Confident Making Decisions Based on Reliable Values?" Critical Care Explorations 7, no. 2 (February 2025): e1216. https://doi.org/10.1097/cce.0000000000001216.

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A prerequisite for accurate invasive arterial pressure measurement is familiarity with measurement principles and pitfalls. Using an electronic survey, we assessed knowledge about invasive arterial pressure monitoring and current invasive arterial pressure monitoring practices in the ICU. The questionnaire was sent to nurses and physicians who are members of the French Intensive Care Society and the Réseau Européen de Recherche en Ventilation Artificielle network. Three hundred nine nurses and 76 physicians responded. We identified considerable gaps in knowledge and differences in practices that can significantly impact the reliability of invasive arterial pressure measurement, mainly the confusion between zeroing and leveling the transducer and the heterogeneity in external landmarks choice for the phlebostatic axis. In modern critical care, where mean arterial pressure targets are recommended and where patients are awake and/or frequently mobilized, standardized invasive arterial pressure monitoring is required.
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41

Hou, Siyuan, Zongcheng Li, Ji Dong, Yun Gao, Zhilin Chang, Xiaochen Ding, Shuaili Li, et al. "Heterogeneity in endothelial cells and widespread venous arterialization during early vascular development in mammals." Cell Research 32, no. 4 (January 25, 2022): 333–48. http://dx.doi.org/10.1038/s41422-022-00615-z.

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AbstractArteriogenesis rather than unspecialized capillary expansion is critical for restoring effective circulation to compromised tissues in patients. Deciphering the origin and specification of arterial endothelial cells during embryonic development will shed light on the understanding of adult arteriogenesis. However, during early embryonic angiogenesis, the process of endothelial diversification and molecular events underlying arteriovenous fate settling remain largely unresolved in mammals. Here, we constructed the single-cell transcriptomic landscape of vascular endothelial cells (VECs) during the time window for the occurrence of key vasculogenic and angiogenic events in both mouse and human embryos. We uncovered two distinct arterial VEC types, the major artery VECs and arterial plexus VECs, and unexpectedly divergent arteriovenous characteristics among VECs that are located in morphologically undistinguishable vascular plexus intra-embryonically. Using computational prediction and further lineage tracing of venous-featured VECs with a newly developed Nr2f2CrexER mouse model and a dual recombinase-mediated intersectional genetic approach, we revealed early and widespread arterialization from the capillaries with considerable venous characteristics. Altogether, our findings provide unprecedented and comprehensive details of endothelial heterogeneity and lineage relationships at early angiogenesis stages, and establish a new model regarding the arteriogenesis behaviors of early intra-embryonic vasculatures.
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42

Wang, Peichun, Daniels Konja, Sandeep Singh, Beijia Zhang, and Yu Wang. "Endothelial Senescence: From Macro- to Micro-Vasculature and Its Implications on Cardiovascular Health." International Journal of Molecular Sciences 25, no. 4 (February 6, 2024): 1978. http://dx.doi.org/10.3390/ijms25041978.

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Endothelial cells line at the most inner layer of blood vessels. They act to control hemostasis, arterial tone/reactivity, wound healing, tissue oxygen, and nutrient supply. With age, endothelial cells become senescent, characterized by reduced regeneration capacity, inflammation, and abnormal secretory profile. Endothelial senescence represents one of the earliest features of arterial ageing and contributes to many age-related diseases. Compared to those in arteries and veins, endothelial cells of the microcirculation exhibit a greater extent of heterogeneity. Microcirculatory endothelial senescence leads to a declined capillary density, reduced angiogenic potentials, decreased blood flow, impaired barrier properties, and hypoperfusion in a tissue or organ-dependent manner. The heterogeneous phenotypes of microvascular endothelial cells in a particular vascular bed and across different tissues remain largely unknown. Accordingly, the mechanisms underlying macro- and micro-vascular endothelial senescence vary in different pathophysiological conditions, thus offering specific target(s) for therapeutic development of senolytic drugs.
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43

Achim, Alexandru, Orsolya Ágnes Péter, Mihai Cocoi, Adela Serban, Stefan Mot, Alexandra Dadarlat-Pop, Attila Nemes, and Zoltan Ruzsa. "Correlation between Coronary Artery Disease with Other Arterial Systems: Similar, Albeit Separate, Underlying Pathophysiologic Mechanisms." Journal of Cardiovascular Development and Disease 10, no. 5 (May 11, 2023): 210. http://dx.doi.org/10.3390/jcdd10050210.

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Atherosclerosis is a multifactorial systemic disease that affects the entire arterial tree, although some areas are more prone to lipid deposits than others. Moreover, the histopathological composition of the plaques differs, and the clinical manifestations are also different, depending on the location and structure of the atherosclerotic plaque. Some arterial systems are correlated with each other more than in that they simply share a common atherosclerotic risk. The aim of this perspective review is to discuss this heterogeneity of atherosclerotic impairment in different arterial districts and to investigate the current evidence that resulted from studies of the topographical interrelations of atherosclerosis.
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44

Del Giorno, Rosaria, Ania Maddalena, Stefano Bassetti, and Luca Gabutti. "Association between Alcohol Intake and Arterial Stiffness in Healthy Adults: A Systematic Review." Nutrients 14, no. 6 (March 12, 2022): 1207. http://dx.doi.org/10.3390/nu14061207.

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Background: Arterial stiffness as assessed by Pulse Wave Velocity (PWV) represents an independent predictor of cardiovascular disease. Several dietary compounds and lifestyle factors could influence arterial stiffness. The debate on the significance of the correlation between alcohol consumption and arterial stiffness is still open, given that the relationship is complex and potentially affected by several factors such as alcohol type, consumption levels, gender and age differences. Objective: This systematic literature review aims to examine the evidence supporting an association between alcohol use and PWV, in electronic databases including PubMed/MEDLINE and the Cochrane Library, from January 2010 to November 2020. Screening and full-text reviews were performed by three investigators and data extraction by two. Considering the significant heterogeneity of data only a qualitative analysis (systematic review) was performed. Results: A total of 13 studies met the inclusion criteria. Alcohol consumption was independently associated with arterial stiffness in a J-shaped way in most of the studies included. A benefit of alcohol consumption on arterial stiffness was found in four experimental studies, whilst an unfavorable increasing linear association was found in four others. Associations were confirmed with both oscillometric and tonometric PWV assessment methods. In some studies, a gender and age correlation was found with a more pronounced association in older males. In all studies elevated levels of alcohol consumption were associated with a worsening of arterial stiffness. Conclusions: Despite the variable findings across studies, the current review provides preliminary evidence that light-to-moderate alcohol consumption is associated with arterial stiffness values lower than expected, and evidence that high doses accelerate arterial ageing. These findings could be useful for clinicians who provide recommendations for patients at cardiovascular (CV) risk. Nevertheless, given the heterogeneity of study designs, interventions, measurement methods and statistical evaluations, the protective role of moderate alcohol consumption on arterial stiffness is likely but not certain, warranting additional trials and evidence.
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45

Kitazawa, Toshio, and Kazuyo Kitazawa. "Size-dependent heterogeneity of contractile Ca2+sensitization in rat arterial smooth muscle." Journal of Physiology 590, no. 21 (October 15, 2012): 5401–23. http://dx.doi.org/10.1113/jphysiol.2012.241315.

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46

Simmons, Grant H., and Jaume Padilla. "Shear-induced vascular adaptations: therapeutic insights and heterogeneity throughout the arterial tree." Journal of Physiology 588, no. 14 (July 15, 2010): 2527–28. http://dx.doi.org/10.1113/jphysiol.2010.191882.

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47

Killam, A. L., S. S. Nikam, G. M. Lambert, A. R. Martin, and D. L. Nelson. "Comparison of two different arterial tissues suggests possible 5-hydroxytryptamine2 receptor heterogeneity." Journal of Pharmacology and Experimental Therapeutics 252, no. 3 (March 1990): 1083–89. https://doi.org/10.1016/s0022-3565(25)20164-1.

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48

Inoue, Shinya, Hiroyuki Koyama, Tetsuro Miyata, and Hiroshi Shigematsu. "Pathogenetic heterogeneity of in-stent lesion formation in human peripheral arterial disease." Journal of Vascular Surgery 35, no. 4 (April 2002): 672–78. http://dx.doi.org/10.1067/mva.2002.122021.

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49

Corbett, Richard W., Lorenza Grechy, Francesco Iori, Jeremy S. Crane, Paul E. Herbert, Pierpaolo Di Cocco, Wady Gedroyc, Peter E. Vincent, Colin G. Caro, and Neill D. Duncan. "Heterogeneity in the nonplanarity and arterial curvature of arteriovenous fistulas in vivo." Journal of Vascular Surgery 68, no. 6 (December 2018): 152S—163S. http://dx.doi.org/10.1016/j.jvs.2018.04.045.

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50

Chung, Ick-Mo. "THE ADJACENT ARTERIAL SEGMENTS HAVE HETEROGENEITY IN GENE EXPRESSION AND PHYSIOLOGICAL FUNCTION." Journal of the American College of Cardiology 59, no. 13 (March 2012): E1471. http://dx.doi.org/10.1016/s0735-1097(12)61472-7.

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