Relevant bibliographies by topics / Arterial heterogeneity

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Arterial heterogeneity'

Author: Grafiati
Published: 26 April 2025

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Journal articles on the topic "Arterial heterogeneity"

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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Arterial heterogeneity"

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Le, Corvec Tom. "Mécanismes moléculaires de l’hétérogénéité des plaques d’athérosclérose et des calcifications dans les artères périphériques : régulation des miRs dans les calcifications vasculaires des artères périphériques." Electronic Thesis or Diss., Nantes Université, 2024. http://www.theses.fr/2024NANU1041.

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Le premier objectif de ce travail était d'identifier les miRs associés aux calcifications vasculaires (CV), de caractériser leur implication dans la minéralisation des CMLVs, et de déterminer leurs gènes cibles. Le second objectif était d’étudier les mécanismes de l’hétérogénéité artérielle en comparant le phénotype des CMLVs carotides et fémorales, et leur réponse aux stimuli pro-athérosclérotiques. Premièrement, nous avons utilisé des artères athéromateuses humaines calcifiées et non calcifiées (Biocoll.ECLAGEN) pour identifier les miRs associés aux CV en combinant une analyse miRNomique (puces microfluidiques) et transcriptomique pour sélectionner des miRs candidats et leurs gènes cibles prédits. Nous avons ensuite validé le rôle fonctionnel des miRs candidats dans la minéralisation cellulaire des CMLVs humaines aortiques. Deuxièmement, nous avons extrait des CMLVs d’artères carotides et fémorales saines (Biocoll.ECLA-H) pour étudier les différences phénotypiques (marqueurs contractiles/inflammatoires, migration, contractilité, captation des lipides) à l’état basal et après stimulation par des cytokines pro-inflammatoires (IL1β, IL6) ou pro-fibrosantes (TGFβ et PDGF). Notre étude a d’abord permis l’identification de 12 miRs associés aux CV. Parmi eux, nous avons montré que l'expression des miR136, miR155 et miR183 était régulée pendant la minéralisation des CMLVs, que leur surexpression induisait la minéralisation des CMLVs et des modifications phénotypiques transcriptionnelles. L'analyse croisée a conduit à l'identification des voies CD73 et Smad3 comme gènes cibles prédits responsables de la fonction pro-minéralisante du miR155. Dans un deuxième temps, l’étude phénotypique comparative des CMLVs carotides et fémorales nous a permis de montrer certaines différences transcriptionnelles, l’expression des marqueurs d’activation (ICAM-1, VCAM-1) était supérieure dans le territoire carotidien, l’expression des marqueurs contractiles (ACTA2, SM22α, SMMHC) était supérieure dans le territoire fémoral. Les expériences préliminaires d’analyse de contractilité et de réponse au stress lipidique suggéraient une tendance à une contractilité et une captation de lipides plus importante dans le territoire fémoral. Nous n’avons pas montré de différence lors de l’analyse des switch phénotypiques et de la migration cellulaire. Ces résultats montrent le bénéfice potentiel de l'inhibition du miR155 pour limiter le développement des calcifications vasculaires dans les lésions athéromateuses des artères périphériques
The first objective of this work was to identify the miRs associated with vascular calcification (VC), to characterise their involvement in the mineralisation of VSMCs, and to determine their target genes. The second objective was to study the mechanisms of arterial heterogeneity by comparing the phenotype of carotid and femoral VSMCs and their response to pro-atherosclerotic stimuli. Firstly, we used calcified and non-calcified human atheromatous arteries (Biocoll.ECLAGEN) to identify VC-associated miRs by combining miRNomic (microfluidic arrays) and transcriptomic analysis to select candidate miRs and their predicted target genes. We then validated the functional role of candidate miRs in cell mineralisation of human aortic VSMCs. Secondly, we extracted VSMCs from healthy carotid and femoral arteries (Biocoll.ECLA-H) to study phenotypic differences (contractile/inflammatory markers, migration, contractility, lipid uptake) in the basal state and after stimulation with pro-inflammatory (IL1β, IL6) or pro-fibrotic cytokines (TGFβ and PDGF). In our study, we first identified 12 miRs associated with VC. Among them, we showed that the expression of miR136, miR155 and miR183 was regulated during VSMC mineralisation and that their overexpression induced VSMC mineralisation and phenotypic transcriptional changes. Cross-analysis led to the identification of the CD73 and Smad3 pathways as predicted target genes responsible for the pro-mineralising function of miR155. Secondly, a comparative phenotypic study of carotid and femoral VSMCs allowed us to demonstrate several transcriptional differences, with higher expression of activation markers (ICAM-1, VCAM-1) in the carotid territory and higher expression of contractile markers (ACTA2, SM22α, SMMHC) in the femoral territory. Preliminary experiments analysing contractility and response to lipid stress suggested a trend towards greater contractility and lipid uptake in the femoral territory. No difference was observed when phenotypic switches and cell migration were analysed. These results demonstrate the potential benefit of miR155 inhibition in limiting the development of VC in atheromatous lesions of peripheral arteries
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Books on the topic "Arterial heterogeneity"

1

Galiè, Nazzareno, Alessandra Manes, and Massimiliano Palazzini. Pulmonary hypertension. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0065.

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Pulmonary hypertension is a haemodynamic and pathophysiological condition defined as an increase in the mean pulmonary arterial pressure of ≥25 mmHg at rest, as assessed by right heart catheterization. In fact, while transthoracic echocardiography may provide clues on the presence of pulmonary hypertension, the haemodynamic evaluation offers a more precise and comprehensive assessment. Pulmonary hypertension is heterogeneous from a pathophysiological point of view, and the diversity is reflected in the haemodynamic definitions. The different haemodynamic forms of pulmonary hypertension can be found in multiple clinical conditions which have been classified into six main groups and at least twenty-six subgroups. Each main clinical group shows specific pathological changes in the lung distal arteries, capillaries, and small veins. If we combine the haemodynamic and clinical heterogeneity, we understand the complexity of an accurate diagnosis in the individual patient which is crucial for the prognostic assessment and treatment strategy. In addition, the concomitant presence of different haemodynamic and clinical mechanisms cannot be excluded in individual cases (e.g. in patients with congestive heart failure and associated lung diseases). The presence of pulmonary hypertension, as defined above, is always an ominous prognostic sign, even if the severity may differ according to the haemodynamic changes and underlying clinical condition. The therapeutic approach also is markedly different, according to the clinical group, and symptomatic and haemodynamic severity. For these reasons, the four more frequent clinical groups are discussed individually, while the classifications are described in the Introduction section.
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Denton, Christopher P., and Pia Moinzadeh. Systemic sclerosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0121.

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The term 'scleroderma' describes a group of conditions in which the development of thickened, fibrotic skin is a cardinal feature. This includes localized forms of scleroderma (e.g. morphoea) and also systemic forms of the disease that are more correctly termed systemic sclerosis. Systemic sclerosis (SSc) is a multiorgan, autoimmune disease that has a high clinical burden and mortality, due to affecting the skin as well as internal organs. As with other related diseases there is a female predominance and marked clinical diversity. The pathogenesis of SSc is not fully elucidated; it includes endothelial cell injury fibroblast activation and autoimmunity that lead to skin and internal organ manifestations. The majority of cases exhibit characteristic serum autoantibodies. Some of these antibodies are scleroderma-specific reactivities including anti-centromere (ACA), anti-topoisomerase-1 (ATA or Scl 70) or anti-RNA polymerase III antibodies. These anti-nuclear antibody (ANA) patterns are generally mutually exclusive and serve as useful clinical markers of disease subgroups. Additional subsetting of scleroderma cases, based on the extent of skin sclerosis, permits classification into limited and diffuse subsets. Because of the heterogeneity of the disease patients may suffer from different organ manifestations, such as lung fibrosis, hypertensive renal crisis, severe cardiac disease, gastrointestinal involvement, and pulmonary arterial hypertension. Although outcomes have improved recently, systemic sclerosis still has the highest case-specific mortality of any of the autoimmune rheumatic diseases and requires careful and systematic investigation, management and follow-up. Treatment includes symptomatic strategies with attention to each involved organ system; it is still an area where therapeutic progress and better understanding of pathogenesis is increasingly anticipated.
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Farmakis, Dimitrios, John Parissis, and Gerasimos Filippatos. Acute heart failure: epidemiology, classification, and pathophysiology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0051.

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Acute heart failure is defined as the rapid development or change of symptoms and signs of heart failure that requires urgent medical attention and usually hospitalization. Acute heart failure is the first reason for hospital admission in individuals aged 65 or more and accounts for nearly 70% of the total health care expenditure for heart failure. It is characterized by an adverse prognosis, with an in-hospital mortality rate of 4-7%, a 2-3-month post-discharge mortality of 7-11%, and a 2-3-month readmission rate of 25-30%. The majority of patients have a previous history of heart failure and present with normal or increased blood pressure, while about half of them have a preserved left ventricular ejection fraction. A high prevalence of cardiovascular or non-cardiovascular comordid conditions is further observed, including coronary artery disease, arterial hypertension, atrial fibrillation, diabetes mellitus, renal dysfunction, chronic lung disease, and anaemia. Different classification systems have been proposed for acute heart failure, reflecting the clinical heterogeneity of the syndrome; the categorization to acutely decompensated chronic heart failure vs de novo acute heart failure and to hypertensive, normotensive, and hypotensive acute heart failure are among the most widely used and clinically relevant classifications. The pathophysiology of acute heart failure involves several pathogenetic mechanisms, including volume overload, pressure overload, myocardial loss, and restrictive filling, while several cardiovascular and non-cardiovascular causes or precipitating factors lead to acute heart failure through a single of these mechanisms or a combination of them. Regardless of the underlying mechanism, peripheral and/or pulmonary congestion is the hallmark of acute heart failure, resulting from fluid retention and/or fluid redistribution. Myocardial injury and renal dysfunction are also involved in the precipitation and progression of the syndrome.
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Cahill, Thomas J., and Paul R. Riley. Epicardial and coronary vascular development. Edited by Miguel Torres. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0009.

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The coronary circulation is essential for human life. In embryonic development, abnormal formation of the coronary vasculature can cause death in utero or after birth. In adulthood, atherosclerosis of the coronary arteries is the commonest cause of death worldwide. The last decade has witnessed significant strides forward in our understanding of coronary development. Multiple sources of coronary endothelial cells have been identified using genetic tools for fate mapping. The epicardium, the outermost layer of the developing heart, has emerged as both a source of cell progenitors and key signalling mediators. Knowledge of the specific genes underlying formation, function, and heterogeneity of the epicardium is expanding. Significant challenges remain, however, in understanding the spatiotemporal signalling patterns required for organized migration, differentiation, and patterning of the vasculature. In addition, dissecting how coronary development is perturbed in patients with congenital coronary anomalies is a major ongoing focus of research.
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Book chapters on the topic "Arterial heterogeneity"

1

Unkeless, Jay C. "Heterogeneity of Murine and Human Fcγ Receptors." In Molecular Biology of the Arterial Wall, 88–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-83118-8_28.

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Murtada, Sae-Il, and Jay D. Humphrey. "Regional Heterogeneity in the Regulation of Vasoconstriction in Arteries and Its Role in Vascular Mechanics." In Advances in Experimental Medicine and Biology, 105–28. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96445-4_6.

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Morrell, Nicholas W. "Structure and function of the pulmonary circulation." In Oxford Textbook of Medicine, edited by Jeremy Dwight, 3691–95. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0373.

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The normal pulmonary circulation distributes deoxygenated blood at low pressure and high flow to the pulmonary capillaries for the purposes of gas exchange. The structure of pulmonary blood vessels varies with their function—from large elastic conductance arteries, to small muscular arteries, to thin-walled vessels involved in gas exchange. Pulmonary vascular resistance is about one-tenth of systemic vascular resistance, with the small muscular and partially muscular arteries of 50–150 µm diameter being the site of the greatest contribution to resistance. In the normal pulmonary circulation, a large increase in cardiac output causes only a small rise in mean pulmonary arterial pressure because pulmonary vascular resistance falls on exercise. Pulmonary blood flow is heterogeneous: gravity causes increased blood flow in the more dependent parts of the lung; within a horizontal region—or within an acinus—blood-flow heterogeneity is imposed by the branching pattern of the vessels.
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Hsia Connie C.W. "Pulmonary Diffusion, Ventilation-Perfusion Ratio and Arterial Oxygen Homeostasis." In Biomedical and Health Research. IOS Press, 2010. https://doi.org/10.3233/978-1-60750-497-9-95.

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The lung derives from two distinct embryonic origins, has two separate circulations, undergoes extensive branching morphogenesis, experiences the highest blood flow and the largest continuous distortion among organs due to wide fluctuations in ventilation, perfusion and mechanical stresses. The inflated lung volume consists of about 85% air and 15% cells, fibers, matrix and blood. Both gravitation-dependent and -independent gradients contribute to spatial heterogeneity in structure and function. Dynamic factors such as surface folding, the surfactant layer, and capillary erythrocytes distribution greatly influence the physical properties of the organ. These unique features pose challenges for the optimization of lung function in health and disease. Oxygen uptake across the lung begins with O2flow into the lungs via negative pressure generated by diaphragm contraction, followed by convective distribution among airways, diffusive distribution within intra-acinar air spaces and across the blood-gas barrier, diffusion across plasma and capillary erythrocyte membrane and finally chemical reaction with hemoglobin. Efficiency of O2transfer depends on appropriate matching between diffusion interfaces, allosteric interaction with hemoglobin, and regulation of hematological volumes and flow. This chapter briefly reviews: 1. Structural determinants of gas exchange. 2. Physiological determinants of gas exchange, including distributive and diffusive factors, the methods of measurement and interpretation of results. 3. Arterial oxygen homeostasis, including optimization of alveolar-arterial O2tension gradient during exercise via regulation of hematological volumes and allosteric control of the oxyhemoglobin dissociation curve.
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Palazzini, Massimiliano, Nazzareno Galiè, and Alessandra Manes. "Pulmonary hypertension." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 839–48. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0063.

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Pulmonary hypertension is a haemodynamic and pathophysiological condition defined as an increase in the mean pulmonary arterial pressure of ?25 mmHg at rest, as assessed by right heart catheterization. Recently, a new definition has been proposed as mean pulmonary arterial pressure >20 mmHg combined with pulmonary vascular resistance ? 3 Wood units. While transthoracic echocardiography may provide clues on the presence of pulmonary hypertension, the haemodynamic evaluation offers a more precise and comprehensive assessment. Pulmonary hypertension is heterogeneous from a pathophysiological point of view, and the diversity is reflected in the haemodynamic definitions. The different haemodynamic and clinical forms of pulmonary hypertension can be found in multiple clinical conditions which have been classified into five main groups and at least twenty-six subgroups. Each main clinical group shows specific pathological changes in the lung distal arteries, capillaries, and small veins. If we combine the haemodynamic and clinical heterogeneity, we understand the complexity of an accurate diagnosis in the individual patient which is crucial for the prognostic assessment and treatment strategy. In addition, the concomitant presence of different haemodynamic and clinical mechanisms cannot be excluded in individual cases (e.g. in patients with congestive heart failure and associated lung diseases). The presence of pulmonary hypertension, as defined above, is always an ominous prognostic sign, even if the severity may differ according to the haemodynamic changes and underlying clinical condition. The therapeutic approach also is markedly different, according to the clinical group, and symptomatic and haemodynamic severity. For these reasons, the four more frequent clinical groups are discussed individually, while the classifications are described in the Introduction section.
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6

Denton, Christopher P., and Pia Moinzadeh. "Systemic sclerosis." In Oxford Textbook of Rheumatology, 971–88. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0121_update_001.

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The term ’scleroderma’ describes a group of conditions in which the development of thickened, fibrotic skin is a cardinal feature. This includes localized forms of scleroderma (e.g. morphoea) and also systemic forms of the disease that are more correctly termed systemic sclerosis. Systemic sclerosis (SSc) is a multiorgan, autoimmune disease that has a high clinical burden and mortality, due to affecting the skin as well as internal organs. As with other related diseases there is a female predominance and marked clinical diversity. The pathogenesis of SSc is not fully elucidated; it includes endothelial cell injury fibroblast activation and autoimmunity that lead to skin and internal organ manifestations. The majority of cases exhibit characteristic serum autoantibodies. Some of these antibodies are scleroderma-specific reactivities including anti-centromere (ACA), anti-topoisomerase-1 (ATA or Scl 70) or anti-RNA polymerase III antibodies. These anti-nuclear antibody (ANA) patterns are generally mutually exclusive and serve as useful clinical markers of disease subgroups. Additional subsetting of scleroderma cases, based on the extent of skin sclerosis, permits classification into limited and diffuse subsets. Because of the heterogeneity of the disease patients may suffer from different organ manifestations, such as lung fibrosis, hypertensive renal crisis, severe cardiac disease, gastrointestinal involvement, and pulmonary arterial hypertension. Although outcomes have improved recently, systemic sclerosis still has the highest case-specific mortality of any of the autoimmune rheumatic diseases and requires careful and systematic investigation, management and follow-up. Treatment includes symptomatic strategies with attention to each involved organ system; it is still an area where therapeutic progress and better understanding of pathogenesis is increasingly anticipated.
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7

Farmakis, Dimitrios, and Gerasimos Filippatos. "Acute heart failure: epidemiology, classification, and pathophysiology." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 603–16. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0046.

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Acute heart failure (AHF) is defined as the rapid development or change of symptoms and signs of heart failure that requires urgent medical attention and usually hospitalization. it represents the first reason for hospital admission in individuals aged 65 or more and accounts for nearly 70% of the total healthcare expenditure for heart failure. It is generally characterized by adverse prognosis, with an in-hospital mortality rate of 4-7%, a 2 to 3-month post-discharge mortality of 7-11% and a 2 to 3-month readmission rate of 25-30%. The majority of patients have a previous history of heart failure and present with symptoms and/or signs of congestion and normal or increased blood pressure, while about half of them have preserved left ventricular ejection fraction. A high prevalence of cardiovascular or non-cardiovascular comorbidities is further observed, including coronary artery disease, arterial hypertension, atrial fibrillation, diabetes mellitus, renal dysfunction, chronic lung disease, anemia and iron deficiency. Different classification criteria have been proposed for AHF, reflecting the clinical heterogeneity of the syndrome. Classifications according to the past history of heart failure (acutely decompensated chronic or de novo), the systolic blood pressure upon presentation (hypertensive, normotensive or hypotensive) and the presence or absence of congestion and peripheral hypoperfusion are among the most widely used. The pathophysiology of AHF involves several mechanisms, including volume overload, pressure overload, myocardial loss and restrictive filling, while several cardiovascular and non-cardiovascular precipitating factors lead to AHF. Regardless of the underlying mechanism, peripheral and/or pulmonary congestion is present in the vast majority of AHF, resulting from fluid retention and/or fluid redistribution, while a marked reduction in cardiac output with peripheral hypoperfusion occurs in a minority of cases. Myocardial injury and renal dysfunction are important factor involved in the precipitation and progression of the syndrome.
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Cahill, Thomas J., and Paul R. Riley. "Epicardial and coronary vascular development." In ESC CardioMed, edited by Miguel Torres, 52–56. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0009_update_001.

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The coronary circulation is essential for human life. In embryonic development, abnormal formation of the coronary vasculature can cause death in utero or after birth. In adulthood, atherosclerosis of the coronary arteries is the commonest cause of death worldwide. The last decade has witnessed significant strides forward in our understanding of coronary development. Multiple sources of coronary endothelial cells have been identified using genetic tools for fate mapping. The epicardium, the outermost layer of the developing heart, has emerged as both a source of cell progenitors and key signalling mediators. Knowledge of the specific genes underlying formation, function, and heterogeneity of the epicardium is expanding. Significant challenges remain, however, in understanding the spatiotemporal signalling patterns required for organized migration, differentiation, and patterning of the vasculature. In addition, dissecting how coronary development is perturbed in patients with congenital coronary anomalies is a major ongoing focus of research.
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Cahill, Thomas J., and Paul R. Riley. "Epicardial and coronary vascular development." In ESC CardioMed, edited by Miguel Torres, 52–56. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0009_update_002.

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Abstract:
The coronary circulation is essential for human life. In embryonic development, abnormal formation of the coronary vasculature can cause death in utero or after birth. In adulthood, atherosclerosis of the coronary arteries is the commonest cause of death worldwide. The last decade has witnessed significant strides forward in our understanding of coronary development. Multiple sources of coronary endothelial cells have been identified using genetic tools for fate mapping. The epicardium, the outermost layer of the developing heart, has emerged as both a source of cell progenitors and key signalling mediators. Knowledge of the specific genes underlying formation, function, and heterogeneity of the epicardium is expanding. Significant challenges remain, however, in understanding the spatiotemporal signalling patterns required for organized migration, differentiation, and patterning of the vasculature. In addition, dissecting how coronary development is perturbed in patients with congenital coronary anomalies is a major ongoing focus of research.
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"Heterogeneity of EDHF-type relaxations of rabbit and rat arteries analysed with peptides homologous to the extracellular loops of connexins 37, 40 and 43." In Edhf 2000, 90–102. CRC Press, 2003. http://dx.doi.org/10.1201/b12802-14.

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Conference papers on the topic "Arterial heterogeneity"

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Wan, Shu-Yen, Denise A. Reyes, William E. Higgins, and Erik L. Ritman. "Heterogeneity of coronary arterial branching geometry." In Medical Imaging 2000, edited by Chin-Tu Chen and Anne V. Clough. SPIE, 2000. http://dx.doi.org/10.1117/12.383435.

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Burrowes, Kelly S., Merryn H. Tawhai, and Peter J. Hunter. "Evaluation of arterial blood flow heterogeneity via an image-based computational model." In Medical Imaging, edited by Amir A. Amini and Armando Manduca. SPIE, 2005. http://dx.doi.org/10.1117/12.600718.

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Frantz, RP, RJ Barst, M. Turner, P. Wason, and MD McGoon. "Regional Heterogeneity in Prostanoid Utilization for Pulmonary Arterial Hypertension in the United States." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3350.

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Wu, T. H., G. Peng, A. Tian, T. Guan, and M. R. Nicolls. "Single-Cell RNA-seq Analysis Reveals Endothelial Heterogeneity of Inflammation-Induced Pulmonary Arterial Hypertension Under Bmpr2 Dysfunction." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2681.

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Pan, H. M., R. McClelland, J. Moutchia, D. Appleby, J. S. Fritz, J. Holmes, J. Minhas, et al. "Heterogeneity of Treatment Effects by Predicted Risk in Pulmonary Arterial Hypertension: An Individual Participant Data Meta-analysis." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1180.

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VanEpps, J. Scott, and David A. Vorp. "Calculation of a Shear Strain Parameter for a Three-Dimensional Fung-Type Exponential Model of the Arterial Wall Under Torsion." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176658.

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The distribution of atherosclerotic lesions within the coronary arteries is highly localized, despite the fact that risk factors (e.g., dyslipidemia) are systemic nature. The biomechanical milieu of the coronary arteries is unique in that in addition to cyclic pressure, circumferential distension and shear stress, they experience mechanical deformations of twisting, bending, and longitudinal stretching due to their tethering to the dynamic epicardial surface [1]. Biplane cineangiographic reconstruction studies have demonstrated that the coronary arteries experience as much as 20° of torsion during a cardiac cycle [2]. Spatial variations in shear and mural stresses caused by this deformation could account for the heterogeneity of atherosclerotic plaques.
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Yamasaki, Y., Y. Asari, K. Tsuchida, K. Suzuki, YJ Akashi, T. Okazaki, S. Ozaki, and H. Yamada. "SAT0369 Heterogeneity in the underlining pathogenesis in patients with connective tissue disease-associated borderline mean pulmonary arterial pressure and its distinctive hemodynamic characteristics from those with normal pulmonary arterial pressure." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3592.

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Kim, Jungsil, and Seungik Baek. "Spatial Variations in the Mechanical Properties of the Porcine Thoracic Aorta." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53329.

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Characterization of the mechanical properties of a blood vessel is essential in understanding the progression of a vascular disease and for computational studies of vascular adaptation. For example, stiffness of vascular tissue is one of the major indicators to diagnose the vascular disease and make a clinical decision. Although previous studies reported the heterogeneity of the mechanical properties of arterial wall along the arterial tree [2], little was taken account for its circumferential variations. With the lack of experimental studies for investigating the circumferential variation, the aortic wall is typically assumed to have uniform deformation. Our previous study, however, has observed that there are circumferential variations in aortic wall stress and stiffness [1]. In addition to our previous study, we investigate further regional variations of the porcine thoracic aorta in both circumferential and longitudinal directions during the inflation test. Hence, we additionally test the distal thoracic aorta at each anterior and posterior side, respectively, and compare with the proximal thoracic aorta.
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Moraes, Emilly Reis de Albuquerque, Adna Cristina da Silva Pereira, Aline Ferreira Mendes, Andreia Sena Sousa Aguiar, Jamil dos Santos Neto, João Pedro Pimentel Abreu, Kauã Manuel Costa Araújo, Pedro Washington Nascimento de Souza, Lydia Kedine Leite Chicar, and Vinicius José da Silva Nina. "Epidemiological profile of patients undergoing myocardial revascularization surgery with extracorporeal circulation in a reference hospital in Maranhão." In IV Seven International Congress of Health. Seven Congress, 2024. http://dx.doi.org/10.56238/homeivsevenhealth-045.

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Myocardial revascularization is a procedure indicated in situations in which there are significant obstructions in the coronary arteries. Therefore, given the heterogeneity of the Brazilian population, the objective was to analyze the epidemiological profile of patients undergoing myocardial revascularization surgery with cardiopulmonary bypass in Maranhão. This is an analytical, longitudinal, descriptive and retrospective cohort study, carried out in the Cardiovascular Surgery Service of a reference hospital in São Luís - Maranhão. The study was approved by the Research Ethics Committee under consolidated opinion no. 6,678,093. With a sample consisting of 104 patients who underwent surgery between January 2022 and July 2023. The exclusion criteria were patients in whom cardiopulmonary bypass was not used and who underwent associated cardiac surgery, such as valve replacement and congenital corrections. During the period analyzed, 102 individuals aged between 41 and 88 years were evaluated, with an average of 63.9 years. The cardiovascular risk factors found were: systemic arterial hypertension (81.40%), diabetes mellitus (52.90%), dyslipidemia (25.50%), smoking (40.20%) and alcohol consumption (33.30%) . A history of acute myocardial infarction was identified in 36.30% of cases. Predominance of male patients (65.69%) and mixed race. The observed mortality was 12.70%. The data analyzed are consistent with the literature. However, some articles state that the ethnicity is predominantly white, which goes against the present study, with a predominance of brown ethnicity. The possible hypothesis to justify this finding is the fact that hypertension, a comorbidity with the highest incidence, is predominant in black or brown ethnicities. Therefore, this discovery highlights the importance of continuous investigations into epidemiological characteristics and social aspects that are determinant for this variation, in order to accurately identify these changes and improve the clinical outcomes of future diagnoses in Maranhão.
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Dosualdo, Caique Alberto. "Reversible posterior encephalopathy syndrome as a rare complication of oxaliplatin chemotherapy: a case report." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.399.

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Introduction: The reversible posterior encephalopathy syndrome corresponds to a clinical and radiological diagnosis marked by headache, altered mental status, reduced visual acuity and seizures, associated with vasogenic edema mainly in posterior white matter. It presents a large heterogeneity of etiologies, such as cytotoxic drugs, eclampsia, vasculitis, and nephropathies, with arterial hypertension being the most important. In that way, quick diagnostic investigation is necessary to provide a better prognosis. Case report: Case report of a patient who was in adjuvance combined chemotherapy, wich includes oxaliplatin, after pancreatic tumor resection, and presented reversible posterior encephalopathy as a treatment complication. The article was developed from data collection through literature review on the subject, as well as analysis of the patient’s medical records. We found the history of a patient with pancreatic ductal adenocarcinoma resection, who underwent adjuvant FOLFIRINOX combined chemotherapy, which contain oxaliplatin. After the first dose, the patient developed severe headache, mental confusion, left-sided motor deficit, and reentrant epileptic seizures, requiring orotracheal intubation due to a non-convulsive status epilepticus. Patient was investigated with brain resonance, wich showed cortical and subcortical hypersignal lesions in the bilateral parieto-occipital lobes, as well as in the thalamus and right insula, and normal cerebrospinal fluid at the first and seventh day. She was also investigated with a panel for autoimmune encephalitis antibodies, with a negative result. After withdrawal of chemotherapy, the patient evolved with a gradual improvement of symptoms and resolution of seizures within twenty days, and was referred for motor rehabilitation at discharge. Conclusion: Early diagnosis and treatment of the etiology contribute to a better prognosis for patients with reversible posterior encephalopathy syndrome.
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