Relevant bibliographies by topics / Muscle blood flow / Books

Books on the topic 'Muscle blood flow'

To see the other types of publications on this topic, follow the link: Muscle blood flow.
Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 32 books for your research on the topic 'Muscle blood flow.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse books on a wide variety of disciplines and organise your bibliography correctly.

1

Monteiro, Andre Antonio. Blood flow change in human masseter muscle elicited by voluntary isometric contraction. Stockholm: Karolinska Institutet, 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Margaliot, Zvi. Measurement of microvascular blood flow in skin and skeletal muscle using ultrasound contrast agents and a negative-bolus indicator-dilution technique. Ottawa: National Library of Canada, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

F, Nielsen Poul M., Miller Karol, and SpringerLink (Online service), eds. Computational Biomechanics for Medicine: Soft Tissues and the Musculoskeletal System. New York, NY: Springer Science+Business Media, LLC, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Dawson, Judith Mary. Responses of the microcirculation in metabolically different skeletal muscles to increased or reduced blood flow. Birmingham: University of Birmingham, 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Cole, Mark Aaron. The effects of acute and prolonged low frequency electrical stimulation on blood flow and fatigue in the human triceps surae and tibialis anterior muscles. Birmingham: University of Birmingham, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

The relationship between skeletal muscle blood flow and blood lactate concentrations during exercise in rats. 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Carey, Michael Francis. Observations on the autoregulation of blood flow and capillary filtration in human skeletal muscle. 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

The relationships among exercise blood lactate response, muscle blood flow, and oxidative adaptation to endurance training in the rat. 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

The relationships among exercise blood lactate response, muscle blood flow, and oxidative adaptation to endurance training in the rat. 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Differential control of blood flow to muscles composed predominantly of different fiber types. 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
11

Differential control of blood flow to muscles composed predominantly of different fiber types. 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
12

Bochaton-Piallat, Marie-Luce, Carlie J. M. de Vries, and Guillaume J. van Eys. Vascular smooth muscle cells. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0007.

Full text
Abstract:
To understand the function of arteries in the regulation of blood supply throughout the body it is essential to realize that the vessel wall is composed predominantly of smooth muscle cells (SMCs) with only one single layer of luminal endothelial cells. SMCs determine the structure of arteries and are decisive in the regulation of blood flow. This review describes the reason for the large variation of SMCs throughout the vascular tree. This depends on embryonic origin and local conditions. SMCs have the unique capacity to react to these conditions by modulating their phenotype. So, in one situation SMCs may be contractile in response to blood pressure, in another situation they may be synthetic, providing compounds to increase the strength of the vascular wall by reinforcing the extracellular matrix. This phenotypic plasticity is necessary to keep arteries functional in fulfilling the metabolic demands in the various tissues of the body.
APA, Harvard, Vancouver, ISO, and other styles
13

Andromeda. Cardiovascular System, Module 3: Cardiac Muscle Action and Blood Flow (CD-ROM for Windows & Macintosh, Individual Version). Andromeda Interactive Inc, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
14

Reading, Jeffrey Lawrence. Changes in cardiac function and skeletal muscle blood flow with endurance exercise training following coronary artery bypass surgery. 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
15

Influence of reactive hyperemia in muscle during exercise. 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
16

Influence of reactive hyperemia in muscle during exercise. 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
17

Influence of reactive hyperemia in muscle during exercise. 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
18

Influence of reactive hyperemia in muscle during exercise. 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
19

van Hinsbergh, Victor W. M. Physiology of blood vessels. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0002.

Full text
Abstract:
This chapter covers two major fields of the blood circulation: ‘distribution’ and ‘exchange’. After a short survey of the types of vessels, which form the circulation system together with the heart, the chapter describes how hydrostatic pressure derived from the heartbeat and vascular resistance determine the volume of blood that is locally delivered per time unit. The vascular resistance depends on the length of the vessel, blood viscosity, and, in particular, on the diameter of the vessel, as formulated in the Poiseuille-Hagen equation. Blood flow can be determined in vivo by different imaging modalities. A summary is provided of how smooth muscle cell contraction is regulated at the cellular level, and how neuronal, humoral, and paracrine factors affect smooth muscle contraction and thereby blood pressure and blood volume distribution among tissues. Subsequently the exchange of solutes and macromolecules over the capillary endothelium and the contribution of its surface layer, the glycocalyx, are discussed. After a description of the Starling equation for capillary exchange, new insights are summarized(in the so-called glycocalyx cleft model) that led to a new view on exchange along the capillary and on the contribution of oncotic pressure. Finally mechanisms are indicated in brief that play a role in keeping the blood volume constant, as a constant volume is a prerequisite for adequate functioning of the circulatory system.
APA, Harvard, Vancouver, ISO, and other styles
20

Montgomery, Hugh, and Rónan Astin. Normal physiology of the cardiovascular system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0128.

Full text
Abstract:
Preload modulates contractile performance, and is determined by end-diastolic volume (EDV) and ventricular compliance. Compliance falls with increasing preload, muscle stiffness or ventricular hypertrophy, making central venous pressure (CVP) a poor surrogate for EDV. Responsiveness to fluid loading can be identified by seeking a change in stroke volume (SV) with changes in cardiac loading. Afterload, the force to be overcome before cardiac muscle can shorten to eject blood, rises with transmural pressure and end-diastolic radius, and inversely with wall thickness. Afterload, being the tension across the ventricular wall, is influenced by pleural pressure. Reductions in afterload increase SV for any cardiac work, as do reductions in vascular resistance. Resistance is modified by changes in arteriolar cross-sectional area. A rise in resistance increases blood pressure and microvascular flow velocity. Increased resistance may reduce CO if cardiac work cannot be augmented sufficiently. Flow autoregulationis the ability of vascular beds to maintain constant flow across varied pressures by adjusting local resistance.
APA, Harvard, Vancouver, ISO, and other styles
21

Anderson, Claudia. Red Light Therapy: The Secrets of Using near Infrared Light to Relieve Muscle Spasms, Slow the Aging Process, Accelerate Weight Loss, Improve Blood Flow, Reduce Inflammation, Gain Muscles, and Optimize All Body Parts Naturally. Hades, 2019.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
22

Anderson, Claudia. Red Light Therapy: The Secrets of Using Near Infrared Light to Relieve Muscle Spasms, Slow the Aging Process, Accelerate Weight Loss, Improve Blood Flow, Reduce Inflammation, Gain Muscles, and Optimize All Body Parts Naturally. Hades, 2019.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
23

Harrison, Mark. Basic cellular physiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198765875.003.0032.

Full text
Abstract:
This chapter describes basic cellular physiology as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of homeostasis, compartments and fluid spaces, cell structure and function, vessel fluid dynamics, blood flow, neurological action potential, generated action potential, parasympathetic nervous systems, and muscle physiology. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.
APA, Harvard, Vancouver, ISO, and other styles
24

Hedenstierna, Göran, and Hans Ulrich Rothen. Physiology of positive-pressure ventilation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0088.

Full text
Abstract:
During positive pressure ventilation the lung volume is reduced because of loss of respiratory muscle tone. This promotes airway closure that occurs in dependent lung regions. Gas absorption behind the closed airway results sooner or later in atelectasis depending on the inspired oxygen concentration. The elevated airway and alveolar pressures squeeze blood flow down the lung so that a ventilation/perfusion mismatch ensues with more ventilation going to the upper lung regions and more perfusion going to the lower, dependent lung. Positive pressure ventilation may impede the return of venous blood to the thorax and right heart. This raises venous pressure, causing an increase in systemic capillary pressure with increased capillary leakage and possible oedema formation in peripheral organs. Steps that can be taken to counter the negative effects of mechanical ventilation include an increase in lung volume by recruitment of collapsed lung and an appropriate positive end-expiratory pressure, to keep aerated lung open and to prevent cyclic airway closure. Maintaining normo- or hypervolaemia to make the pulmonary circulation less vulnerable to increased airway and alveolar pressures, and preserving or mimicking spontaneous breaths, in addition to the mechanical breaths, since they may improve matching of ventilation and blood flow, may increase venous return and decrease systemic organ oedema formation (however, risk of respiratory muscle fatigue, and even overexpansion of lung if uncontrolled).
APA, Harvard, Vancouver, ISO, and other styles
25

Chokroverty, Sudhansu, and Sushanth Bhat. Physiological changes in sleep. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0006.

Full text
Abstract:
It is important for clinicians to be conversant with the physiological changes that occur in various organ systems during sleep, and the impact that sleep fragmentation and sleep deprivation have on the normal functioning of these systems. This chapter therefore strives to provide a brief overview of the physiological changes associated with sleep that occur in the central nervous system (CNS), the autonomic nervous system (ANS), the neuromuscular system, the respiratory system (including changes in the control of breathing during various stages of sleep) and cardiovascular systems, the gastrointestinal tract, the endocrine system, and the systems controlling thermoregulation and immune regulation. Additionally, the mechanisms underlying muscle hypotonia in sleep, as well as sleep-related changes in cerebral blood flow and cytokine function are discussed.
APA, Harvard, Vancouver, ISO, and other styles
26

Lutgens, Esther, Marie-Luce Bochaton-Piallat, and Christian Weber. Atherosclerosis: cellular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0013.

Full text
Abstract:
Atherosclerosis is a lipid-driven, chronic inflammatory disease of the large and middle-sized arteries that affects every human being and slowly progresses with age. The disease is characterized by the presence of atherosclerotic plaques consisting of lipids, (immune) cells, and debris that form in the arterial intima. Plaques develop at predisposed regions characterized by disturbed blood flow dynamics, such as curvatures and branch points. In the past decades, experimental and patient studies have revealed the role of the different cell-types of the innate and adaptive immune system, and of non-immune cells such as platelets, endothelial, and vascular smooth muscle cells, in its pathogenesis. This chapter highlights the roles of these individual cell types in atherogenesis and explains their modes of communication using chemokines, cytokines, and co-stimulatory molecules.
APA, Harvard, Vancouver, ISO, and other styles
27

Differential control of blood flow to muscles composed predominantly of different fiber types. 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
28

Douglas, Kenneth. Bioprinting. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780190943547.001.0001.

Full text
Abstract:
Abstract: This book describes how bioprinting emerged from 3D printing and details the accomplishments and challenges in bioprinting tissues of cartilage, skin, bone, muscle, neuromuscular junctions, liver, heart, lung, and kidney. It explains how scientists are attempting to provide these bioprinted tissues with a blood supply and the ability to carry nerve signals so that the tissues might be used for transplantation into persons with diseased or damaged organs. The book presents all the common terms in the bioprinting field and clarifies their meaning using plain language. Readers will learn about bioink—a bioprinting material containing living cells and supportive biomaterials. In addition, readers will become at ease with concepts such as fugitive inks (sacrificial inks used to make channels for blood flow), extracellular matrices (the biological environment surrounding cells), decellularization (the process of isolating cells from their native environment), hydrogels (water-based substances that can substitute for the extracellular matrix), rheology (the flow properties of a bioink), and bioreactors (containers to provide the environment cells need to thrive and multiply). Further vocabulary that will become familiar includes diffusion (passive movement of oxygen and nutrients from regions of high concentration to regions of low concentration), stem cells (cells with the potential to develop into different bodily cell types), progenitor cells (early descendants of stem cells), gene expression (the process by which proteins develop from instructions in our DNA), and growth factors (substances—often proteins—that stimulate cell growth, proliferation, and differentiation). The book contains an extensive glossary for quick reference.
APA, Harvard, Vancouver, ISO, and other styles
29

Fervenza, Fernando C. Evaluation of Kidney Function, Glomerular Disease, and Tubulointerstitial Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0472.

Full text
Abstract:
Several measures are used to evaluate kidney function: serum creatinine, urinalysis, renal clearance, and renal imaging. Creatinine is an end product of muscle catabolism and is commonly used as a filtration marker. Dysmorphic erythrocytes in the urinary sediment indicate bleeding in the upper urinary tract. A urine pH less than 5.5 excludes type 1 renal tubular acidosis. A pH greater than 7 suggests infection. Acidic urine is indicative of a high-protein diet, acidosis, and potassium depletion. Alkaline urine is associated with a vegetarian diet, alkalosis and urease-producing bacteria. Clearance of p-aminohippurate is a measure of renal blood flow. Kidney function is evaluated to determine disease states such as glomeruluar disease or tubulointerstitial disease. Clinical manifestations of glomerular injury can vary from the finding of isolated hematuria or proteinuria, or both. In addition, some patients who present with advanced renal insufficiency, hypertension, and shrunken, smooth kidneys are presumed to have chronic glomerulonephritis. Acute and chronic interstitial disease preferentially involves renal tubules.
APA, Harvard, Vancouver, ISO, and other styles
30

Guzik, Tomasz J., and Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.

Full text
Abstract:
Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.
APA, Harvard, Vancouver, ISO, and other styles
31

Golper, Thomas A., Andrew A. Udy, and Jeffrey Lipman. Drug dosing in acute kidney injury. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0364.

Full text
Abstract:
Drug dosing in acute kidney injury (AKI) is one of the broadest topics in human medicine. It requires an understanding of markedly altered and constantly changing physiology under many disease situations, the use of the drugs to treat those variety of diseases, and the concept of drug removal during blood cleansing therapies. Early in AKI kidney function may be supraphysiologic, while later in the course there may be no kidney function. As function deteriorates other metabolic pathways are altered in unpredictable ways. Furthermore, the underlying disorders that lead to AKI alter metabolic pathways. Heart failure is accompanied by vasoconstriction in the muscle, skin and splanchnic beds, while brain and cardiac blood flow proportionally increase. Third spacing occurs and lungs can become congested. As either kidney or liver function deteriorates, there may be increased or decreased drug sensitivity at the receptor level. Acidosis accompanies several failing organs. Protein synthesis is qualitatively and quantitatively altered. Sepsis affects tissue permeability. All these abnormalities influence drug pharmacokinetics and dynamics. AKI is accompanied by therapeutic interventions that alter intrinsic metabolism which is in turn complicated by kidney replacement therapy (KRT). So metabolism and removal are both altered and constantly changing. Drug management in AKI is exceedingly complex and is only beginning to be understood. Thus, we approach this discussion in a physiological manner. Critically ill patients pass through phases of illness, sometimes rapidly, other times slowly. The recognition of the phases and the need to adjust medication administration strategies is crucial to improving outcomes. An early phase involving supraphysiologic kidney function may be contributory to therapeutic failures that result in the complication of later AKI and kidney function failure.
APA, Harvard, Vancouver, ISO, and other styles
32

Groeneveld, A. B. J., and Alexandre Lima. Vasodilators in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0035.

Full text
Abstract:
Vasodilators are commonly used in the intensive care unit (ICU) to control arterial blood pressure, unload the left or the right heart, control pulmonary artery pressure, and improve microcirculatory blood flow. Vasodilator refers to drugs acting directly on the smooth muscles of peripheral vessel walls and drugs are usually classified based on their mechanism (acting directly or indirectly) or site of action (arterial or venous vasodilator). Drugs that have a predominant effect on resistance vessels are arterial dilators and drugs that primarily affect venous capacitance vessels are venous dilators. Drugs that interfere with sympathetic nervous system, block renin-angiotensin system, phosphodiesterase inhibitors, and nitrates are some examples of drugs with indirect effect. Vasodilator drugs play a major therapeutic role in hypertensive emergencies, primary and secondary pulmonary hypertension, acute left heart, and circulatory shock. This review discusses the main types of vasodilators drugs commonly used in the ICU.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Muscle blood flow' for other source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography