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Books on the topic 'Cardiac receptors'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Gesellschaft für Fortschritte auf dem Gebiet der Inneren Medizin. Symposium. Cardiovascular receptors: New pharmacological and clinical aspects : 18th Symposium of the Gesellschaft für Fortschritte auf dem Gebiet der Inneren Medizin, Düsseldorf, December 1984 (chairman: Paul Schölmerich with collaboration of Erland Erdmann and Hasso Scholz). Stuttgart: G. Thieme, 1986.

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2

van, Zwieten P. A., and Schönbaum E, eds. Receptors in the cardiovascular system: Proceedings of a symposium, organized by the Dutch Pharmacological Society in OSS, the Netherlands, May 31, 1985. New York: G. Fischer Varlag, 1986.

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3

Cardiac Glycoside Receptors and Positive Inotropy: Evidence for More Than One Receptor? Springer, 1986.

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4

Rosenbaum, Larry C. Structural characterization of the cardiac muscarinic acetylcholine receptor. 1987.

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5

Ernst E. van der Wall, P. K. Blanksma, and M. G. Niemeyer. Cardiac Positron Emission Tomography: Viability, Perfusion, Receptors and Cardiomyopathy. Springer, 2012.

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6

Chidiac, Peter. Cardiac muscarinic receptors and G proteins: mechanism of interaction. 1992.

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7

Wall, Ernst E. van der, P. K. Blanksma, M. G. Niemeyer, and A. M. Paans. Cardiac Positron Emission Tomography: Viability, Perfusion, Receptors and Cardiomyopathy. Springer, 2012.

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8

Cardiac positron emission tomography: Viability, perfusion, receptors, and cardiomyopathy. Dordrecht: Kluwer Academic Publishers, 1995.

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9

Blanksma, P. K., A. M. Paans, Ernst E. van der Wall, and M. G. Niemeyer. Cardiac Positron Emission Tomography: Viability, Perfusion, Receptors and Cardiomyopathy. Springer London, Limited, 2012.

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10

Green, Marty Anne *. The binding properties of muscarinic receptors in washed cardiac membranes. 1988.

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11

Cardiac Adaptations Molecular Mechanisms. Springer, 2012.

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12

Induced heterogeneity of cardiac muscarinic receptors: Cooperativity in the binding of antagonists. Ottawa: National Library of Canada, 1996.

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13

Erdmann, Erland, R. Jacob, and W. Schaper. Cardiac Glycoside Receptors and Positive Inotropy: Evidence for more than one receptor? Symposium, Munich, October 26-29, 1983. Steinkopff, 2011.

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14

Erdmann, Erland, R. Jacob, and W. Schaper. Cardiac Glycoside Receptors and Positive Inotropy: Evidence for More Than One Receptor? - Symposium, Munich, October 26-29 1983. Steinkopff, Dietrich, 2011.

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15

Erdmann, E., R. Jacob, and W. Schaper. Cardiac Glycoside Receptors and Positive Inotropy: Evidence for More Than One Receptor? Symposium, Munich, October 26-29 1983. Steinkopff, Dietrich, 2013.

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16

E.E. van der Wall (Editor), P. K. Blanksma (Editor), M. G. Niemeyer (Editor), and A. M. Paans (Editor), eds. Cardiac Positron Emission Tomography: Viability, Perfusion, Receptors and Cardiomyopathy (Developments in Cardiovascular Medicine). Springer, 1995.

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17

Re, Richard N., and Edward D. Frohlich. Local Cardiac Renin-Angiotensin Aldosterone System. Springer, 2006.

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18

Re, Richard N., and Edward D. Frohlich. Local Cardiac Renin-Angiotensin Aldosterone System. Springer London, Limited, 2009.

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19

Re, Richard N., and Edward D. Frohlich. Local Cardiac Renin-Angiotensin Aldosterone System. Springer, 2014.

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20

Latency and G protein-sensitive heterogeneity in reconstituted cardiac muscarinic receptors: Implications for co-operativity. Ottawa: National Library of Canada, 2000.

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21

Re, Richard N., and Edward D. Frohlich. The Local Cardiac Renin-Angiotensin Aldosterone System. Springer, 2009.

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22

Re, Richard N., and Edward D. Frohlich. The Local Cardiac Renin-Angiotensin Aldosterone System. Springer, 2010.

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23

(Editor), Edward D. Frohlich, and Richard N. Re (Editor), eds. The Local Cardiac Renin Angiotensin-Aldosterone System (Basic Science for the Cardiologist). Springer, 2005.

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24

R, Hainsworth, McWilliam P. N, Mary, D. A. S. G., and University of Leeds. Department of Cardiovascular Studies., eds. Cardiogenic reflexes: Report of an international symposium. Oxford: Oxford University Press, 1987.

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25

Cardiogenic reflexes: Report of an international symposium organized by the Department of Cardiovascular Studies, University of Leeds, and held in Leeds, 16-20 September 1985. Oxford: Oxford University Press, 1987.

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26

Dhaun, Neeraj, and David J. Webb. Endothelins and their antagonists in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0114_update_001.

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The endothelins (ETs) are a family of related peptides of which ET-1 is the most powerful endogenous vasoconstrictor and the predominant isoform in the cardiovascular and renal systems. The ET system has been widely implicated in both cardiovascular disease and chronic kidney disease (CKD). ET-1 contributes to the pathogenesis and maintenance of hypertension and arterial stiffness, as well endothelial dysfunction and atherosclerosis. By reversal of these effects, ET antagonists, particularly those that block ETA receptors, may reduce cardiovascular risk. In CKD patients, antagonism of the ET system may be of benefit in improving renal haemodynamics and reducing proteinuria, effects seen both in animal models and in some human studies. Data suggest a synergistic role for ET receptor antagonists with angiotensin-converting enzyme inhibitors in lowering blood pressure, reducing proteinuria, and in animal models in slowing CKD progression. However, in clinical trials, fluid retention or cardiac failure has caused concern and these agents are not yet ready for general use for risk reduction in CKD.

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27

Rathore, Hargovind S. Studies on cardiotonic steroids and their receptor Nað́,Kð́-ATPase. 1985.

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28

Dierdorf, Stephen F. Hypocalcemia/Hypercalcemia. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0038.

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Calcium is critical to many vital physiologic functions. These functions include cardiac rhythm and contractility, neuromuscular transmission, and skeletal muscle contractility. 45% of the calcium in the blood is ionized, which is more revalent to the physiologic function of calcium as opposed to the fraction that is bound. Serum ionized calcium levels are closely regulated by the parathyroid gland via calcium-sensing receptors and parathormone secretion. Low or high levels of calcium can result in life-threatening cardiac dysrhythmias and skeletal muscle weakness leading to respiratory failure. The anesthesiologist must be aware of the clinical conditions that place patients at risk for calcium abnormalities. This will allow for early recognition of the signs and symptoms, so that measurements can take place and rapid treatment can be given.

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29

Sum, Chi Shing. Mechanism of binding and activation in the cardiac muscarinic receptor. 2002.

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30

1948-, Deedwania Prakash C., ed. Beta-blockers and cardiac arrhythmias. New York: M. Dekker, 1992.

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31

Kararigas, Georgios, and Dawn A. Lowe, eds. New Insights into Estrogen/Estrogen Receptor Effects in the Cardiac and Skeletal Muscle. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-707-2.

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32

Pannabecker, Thomas Lloyd. Intracellular messages associated with octopamine receptors and adipokinetic hormone release in the locust corpus cardiacum. 1988.

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33

Adler, Adam C., and Mehernoor Watcha. Postoperative Nausea and Vomiting in Patients with Prolonged QTc. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0067.

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Postoperative nausea and vomiting (PONV) is a very common complication after a general anesthetic. In some cases the feeling of nausea has been accredited to being worse than the actual pain. There are a number of medications that can be utilized to combat PONV. Of note, some of these agents can lead to cardiac arrhythmias. It is imperative to know which drugs may predispose patients to arrhythmias such as prolonged QT intervals as well as how to prevent or treat PONV in the patient with prolonged QT interval. This chapter discusses the basics of cardiac electrophysiology regarding the QT interval and the risks to the patient when it becomes prolonged, explains the potential effects of first- and second-generation 5-HT3 receptor antagonists on cardiac repolarization, and reviews currently used antiemetics and anticipated future developments in this field.

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34

Miller, Aaron E., and Teresa M. DeAngelis. Myasthenia Gravis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0022.

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Myasthenia gravis (MG) is an autoimmune disorder that results in loss of functional acetylcholine receptors (AChR) on the postsynaptic membrane of the neuromuscular junction caused by the presence of antibodies to the AChR. In this chapter, we review the cardinal clinical findings of MG, the standard diagnostic testing including electrophysiological features, and the medical and surgical treatment recommendations.

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35

Cónsole-Avegliano, Gloria Miriam. Embriología molecular de las cardiopatías congénitas. Editorial de la Universidad Nacional de La Plata (EDULP), 2018. http://dx.doi.org/10.35537/10915/71653.

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La presente obra pretende integrar aspectos embriológicos, genéticos y moleculares del desarrollo cardíaco humano normal y patológico. Se han reunido trabajos de embriólogos, genetistas, especialistas en imágenes, pediatras y cirujanos pediátricos involucrados en el tratamiento de las cardiopatías congénitas. La obra aporta una exhaustiva revisión de la Embriología cardíaca humana clásica y molecular que conlleva a una mejor comprensión del desarrollo de las principales cardiopatías congénitas. Además, resulta de interés conocer los nuevos genes involucrados en la cardiogénesis y analizar los programas de expresión génica cámara-específicos mediados por los factores de transcripción y las moléculas receptoras. En el ciclo lectivo 1965 comencé a enseñar Embriología Humana como Ayudante alumna de la Cátedra de Biología-Embriología a cargo del Prof. Dr. Herberto Prieto Díaz y desde entonces, siento especial inclinación por el estudio embriológico y por los avances moleculares y genéticos que se han incorporado. Hice mi aporte al tema al redactar el capítulo 18: Desarrollo del corazón y grandes vasos de la obra Embriología Humana (Atlas y Texto) del maestro Prof. Dr. César L.A. Gómez Dumm (2003). Con esta obra deseo presentar los avances moleculares, genéticos y de terapia génica para que los profesionales de la salud actualicen sus conocimientos sobre los procesos del desarrollo cardíaco y optimicen las estrategias terapéuticas.

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36

Lameire, Norbert. Prevention of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0224_update_001.

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The prevention of acute kidney injury (AKI) should start with an assessment of the risk to develop AKI, by identification of co-morbidities, use of potentially nephrotoxic medications, and early recognition of acute reversible risk factors associated with AKI. This chapter discusses first the most relevant general risk factors for AKI and describes the recent introduction of several surveillance systems. In addition, some specific risk factors play a role in the pathogenesis of post-cardiac surgery AKI. Finally risks associated with commonly used drugs such as non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, statins, and warfarin are considered.

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37

Vergnaud, Sophie, David Dobarro, and John Wort. Pulmonary vasculature. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199657742.003.0017.

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A 16-year-old girl with a diagnosis of diffuse cutaneous systemic sclerosis is referred to a specialist pulmonary hypertension centre with a history of progressive breathlessness, reduced exercise tolerance, and raised pulmonary pressures on transthoracic echocardiogram. She is found to have pulmonary arterial hypertension on right cardiac catheterization and is started on sildenafil, a phosphodiesterase-5 inhibitor, which stabilizes her condition. An endothelin receptor antagonist is added, which provides some initial symptomatic improvement. She continues to deteriorate over a period of 5 years, ultimately requiring intravenous prostanoids, the only treatment to provide a real symptomatic and haemodynamic improvement. This chapter explores the physiology and pathophysiology of pulmonary arterial hypertension, its classification, the means of investigation and diagnosis, who to refer to specialist centres, and the concepts behind current and future treatment strategies.

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38

Zoccali, Carmine, Davide Bolignano, and Francesca Mallamaci. Left ventricular hypertrophy in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0107_update_001.

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Alterations in left ventricular (LV) mass and geometry and LV dysfunction increase in prevalence from stage 2 to stage 5 in CKD. Nuclear magnetic resonance is the most accurate and precise technique for measuring LV mass and function in patients with heart disease. Quantitative echocardiography is still the most frequently used means of evaluating abnormalities in LV mass and function in CKD. Anatomically, myocardial hypertrophy can be classified as concentric or eccentric. In concentric hypertrophy, the muscular component of the LV (LV wall) predominates over the cavity component (LV volume). Due to the higher thickness and myocardial fibrosis in patients with concentric LVH, ventricular compliance is reduced and the end-diastolic volume is small and insufficient to maintain cardiac output under varying physiological demands (diastolic dysfunction). In those with eccentric hypertrophy, tensile stress elongates myocardiocytes and increases LV end-diastolic volume. The LV walls are relatively thinner and with reduced ability to contract (systolic dysfunction). LVH prevalence increases stepwisely as renal function deteriorates and 70–80% of patients with kidney failure present with established LVH which is of the concentric type in the majority. Volume overload and severe anaemia are, on the other hand, the major drivers of eccentric LVH. Even though LVH may regress after renal transplantation, the prevalence of LVH after transplantation remains close to that found in dialysis patients and a functioning renal graft should not be seen as a guarantee of LVH regression. The vast majority of studies on cardiomyopathy in CKD are observational in nature and the number of controlled clinical trials in these patients is very small. Beta-blockers (carvedilol) and angiotensin receptors blockers improve LV performance and reduce mortality in kidney failure patients with LV dysfunction. Although current guidelines recommend implantable cardioverter-defibrillators in patients with ejection fraction less than 30%, mild to moderate symptoms of heart failure, and a life expectancy of more than 1 year, these devices are rarely offered to eligible CKD patients. Conversion to nocturnal dialysis and to frequent dialysis schedules produces a marked improvement in LVH in patients on dialysis. More frequent and/or longer dialysis are recommended in dialysis patients with asymptomatic or symptomatic LV disorders if the organizational and financial resources are available.

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39

Erlinge, David, and Göran Olivecrona. Diagnosis and management of non-STEMI coronary syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0146.

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Acute coronary syndromes are classified as ST segment elevation myocardial infarction (STEMI), non-STEMI (NSTEMI) or unstable angina. Most patients with NSTEMI present with a history of chest pain that has subsided spontaneously before or soon after arrival at the emergency room, but with positive cardiac markers (usually troponin T or I) indicative of myocardial infarction. NSTEMI has a risk of recurrent myocardial infarction of 15–20% and a 15% chance of 1-year mortality. Patients with non-STE-acute coronary syndromes are at similar risk as a STEMI patient at 1 year. The strongest objective signs of NSTEMI are a positive troponin and ST segment depression. NSTEMI should be acutely treated with aspirin, an adenosine diphosphate-receptor antagonist, and an anticoagulant (fondaparinux or low molecular weight heparins). NSTEMI should be investigated with coronary angiography within 72 hours. Curative treatment is percutaneous coronary intervention or coronary artery bypass grafting.

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40

Dilsizian, Vasken, Ines Valenta, and Thomas H. Schindler. Myocardial Viability Assessment. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0021.

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Heart failure may be a consequence of ischemic or non-ischemic cardiomyopathy. Etiologies for LV systolic dysfunction in ischemic cardiomyopathy include; 1) transmural scar, 2) nontransmural scar, 3) repetitive myocardial stunning, 4) hibernating myocardium, and 5) remodeled myocardium. The LV remodeling process, which is activated by the renin-angiotensin system (RAS), stimulates toxic catecholamine actions and matrix metalloproteinases, resulting in maladaptive cellular and molecular alterations5, with a final pathway to interstitial fibrosis. These responses to LV dysfunction and interstitial fibrosis lead to progressive worsening of LV function. Established treatment options for ischemic cardiomyopathy include medical therapy, revascularization, and cardiac transplantation. While there has been continuous progress in the medical treatment of heart failure with beta-blockers, angiotensin-converting enzyme (ACE) inhibition, angiotensin II type 1 receptor (AT1R) blockers, and aldosterone to beneficially influence morbidity and mortality, the 5-years mortality rate for heart failure patients remains as high as 50%. Revascularization procedures include percutaneous transluminal coronary artery interventions (PCI) including angioplasty and endovascular stent placement and coronary artery bypass grafting (CABG). Whereas patents with heart failure due to non-coronary etiologies may best benefit from medical therapy or heart transplantation, coronary revascularization has the potential to improve ventricular function, symptoms, and long term survival, in patients with heart failure symptoms due to CAD and ischemic cardiomyopathy.

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41

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.

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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.

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