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Taschenbuch. Zustand: Neu. Myocardial Ischemia | Proceedings of a Satellite Symposium of the Thirtieth International Physiological Congress July 8-11, 1986, Winnipeg, Canada | Naranjan S. Dhalla (u. a.) | Taschenbuch | xiv | Englisch | 2013 | Springer | EAN 9781461292210 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - Whenever the coronary flow is inadequate to provide enough oxygen to meet the energy demands of the tissue, the heart becomes ischemic. Manifestations of myocardial ischemia include depression in contractile activity, changes in metabolic pattern, abnormalities in ultrastructure, and alterations in membrane potential. Ischemic changes during the early phase are reversible but as the period of ischemia is extended, the injury becomes irreversible. The transition from reversible to irreversible ischemic injury is usually associated with some membrane defects. It is worthwhile to consider that the irreversible damage to the ischemic myocardium occurs when the sarcolemmal membrane is altered in suoh a way that it would promote 2 a net gain of ca + in the cardiac cell upon reinstitution of blood flow. Suoh a lesion could result when mechanisms for the entry as well as removal 2 of ca + from the myocardial oell become defective. In this regard, 2 depression of the sarcolemmal ca + pump would favour the oocurrenoe of 2 intracellular ca + overload. Furthermore, inhibition of the Na+-K+ pump would lead to elevation of myoplasmic Na+ which oould then increase the 2 2 intracellular concentration of ca + through the sarcolemmal Na+-ca + exchange mechanism. In faot recent studies have revealed an inhibition of 2 the sarcolemmal Na+-ca + exchange mechanism in the ischemic heart and this 2 change could also contribute towards the occurrence of intracellular ca + 2 overload.

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Taschenbuch. Zustand: Neu. Heart Function and Metabolism | Proceedings of the Symposium held at the Eighth Annual Meeting of the American Section of the International Society for Heart Research, July 8-11, 1986, Winnipeg, Canada | Naranjan S. Dhalla (u. a.) | Taschenbuch | xiv | Englisch | 2011 | Springer | EAN 9781461292203 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - In the course of the last two decades, it has become increasingly evident that the sarcolemmal, sarcoplasmic reticular and mitochondrial membrane systems play an important role in determining the status of heart funotion in health and disease. These organelles have been shown to be intimately involved in the regulation of cation movements during the contraotion-relaxation cycle. Various proteins imbedded in the phospholipid 2+ + - + + bilayers of these membranes control Ca ,Na, Cl ,K and H concentrations within the oytoplasm by indirect or direct means. Cationic channels, Na+, + 2+ 2+ 2+ + 2+ + + K -ATPase, Ca IMg ATPase, Ca pump, Na -Ca exchanger, Na -II exchanger and adenylate cyclase affect myocardial funotion and viability through their role as regulators of specific ion movements. However, proteins are not the only important constituents of the membrane. Any disturbance in the interaction between proteins and phospholipids in the membrane has been suggested to alter the funotion of the organelles, upset ionic homeostasis and precipitate the development of abnormalities in oardiac performance. It is, therefore, orucial to understand the faotors whioh regulate membrane funotion in their totality if we are to oomprehend the nature of heart performanoe in healthy subjects. Similarly, the study of membrane dysfunotion in a wide variety of experimental models of heart disease at various stages of failure is essential if we are to fully understand the pathogenesis of heart dysfunotion and improve its treatment.

Taschenbuch. Zustand: Neu. Neuware - Mechanisms of Heart Failure is based on papers selected from poster presentations made at the International Conference on Heart Failure, Winnipeg, May 20-23, 1994. Although the entire book is one continuous discussion of subcellular mechanisms of heart failure and its treatment, the presentation has been divided into three sections: the opening section on the subcellular basis of heart failure includes discussions of cytokines, signal transduction, metabolism, extracellular matrix, organ level changes and newer approaches to understanding the pathogenesis of heart failure. The second section focuses on the pathophysiological aspects of cardiomyopathies and their treatment. In the final section, medical, surgical and pharmacological approaches to the treatment of heart failure are discussed in clinical and animal laboratory settings.

Gebunden. Zustand: New. Proceedings of the Symposium held at the 8th Annual Meeting of the American Section of the International Society for Heart Research, July 8-11, 1986, Winnipeg, Canada It is indeed ironical that in the absence of a complete knowledge of Pathophysio.

Gebunden. Zustand: New. Mechanisms of Heart Failure is based on papers selected from poster presentations made at the International Conference on Heart Failure, Winnipeg, May 20-23, 1994. Although the entire book is one continuous discussion of subcellular mechanisms o.

Gebunden. Zustand: New. Proceedings of the Symposium held at the 8th Annual Meeting of the American Section of the International Society for Heart Research, July 8-11, 1986, Winnipeg, Canada A. Special Lecture.- 1. Molecular Biology and Cardiac Function, Past, Present and Fu.

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Taschenbuch. Zustand: Neu. Angiotensin II Receptor Blockade Physiological and Clinical Implications | Naranjan S Dhalla (u. a.) | Taschenbuch | Einband - flex.(Paperback) | Englisch | 2012 | Springer Us | EAN 9781461376316 | Verantwortliche Person für die EU: Springer Nature Customer Service Center GmbH, Europaplatz 3, 69115 Heidelberg, productsafety[at]springernature[dot]com | Anbieter: preigu.

Taschenbuch. Zustand: Neu. Pathophysiology of Heart Failure | Naranjan S. Dhalla (u. a.) | Taschenbuch | Developments in Cardiovascular Medicine | xlii | Englisch | 2011 | Humana | EAN 9781461285250 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.

Taschenbuch. Zustand: Neu. Heart Hypertrophy and Failure | Naranjan S. Dhalla (u. a.) | Taschenbuch | xlii | Englisch | 2011 | Springer | EAN 9781461285267 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.

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Buch. Zustand: Neu. Neuware - It is indeed ironical that in the absence of a complete knowledge of Pathophysiology, clinical cardiologists are left with no choice but to do the best they can to help the patient with the armamentarium of drugs at their disposal. But nothing could be further from truth than to treat the diagnosed end point of a disease process without a full understanding of its patho physiology. This point was eloquently made by Dr. Arnold Katz in his Presidential Address (Chapter 1) at the 8th Annual Meeting of the American Section of the International Society for Heart Research held in Winnipeg, Canada, July 8-11, 1986. This volume represents a part of the scientific proceedings of this Meeting. From a reading of this treatise it will become evident that discoveries of newer scientific facts as well as a better understanding of pathophysiology are continuously influencing/ improving our therapeutic approaches in modern medicine. In this book, latest biochemical, physiological and pharmacological findings on different experimental models such as Myocaridal hypertrophy, Hypertension and heart failure, Diabetes, Cardio myopathies and Cardiac function in shock are described by internationally recognised experts. Hopefully information presented here will provide another building block to the edifice of Science of Cardiology which we all are trying to create. Acknowledgements We are grateful to the following Agencies and Foundations for their generous financial support of the Symposium, which formed the basis of this book. A. Major Contributors: 1. Manitoba Heart Foundation 2. Sterling-Winthrop Research Institute 3. Squibb Canada, Inc.

Buch. Zustand: Neu. Neuware - In the course of the last two decades, it has become increasingly evident that the sarcolemmal, sarcoplasmic reticular and mitochondrial membrane systems play an important role in determining the status of heart funotion in health and disease. These organelles have been shown to be intimately involved in the regulation of cation movements during the contraotion-relaxation cycle. Various proteins imbedded in the phospholipid 2+ + - + + bilayers of these membranes control Ca ,Na, Cl ,K and H concentrations within the oytoplasm by indirect or direct means. Cationic channels, Na+, + 2+ 2+ 2+ + 2+ + + K -ATPase, Ca IMg ATPase, Ca pump, Na -Ca exchanger, Na -II exchanger and adenylate cyclase affect myocardial funotion and viability through their role as regulators of specific ion movements. However, proteins are not the only important constituents of the membrane. Any disturbance in the interaction between proteins and phospholipids in the membrane has been suggested to alter the funotion of the organelles, upset ionic homeostasis and precipitate the development of abnormalities in oardiac performance. It is, therefore, orucial to understand the faotors whioh regulate membrane funotion in their totality if we are to oomprehend the nature of heart performanoe in healthy subjects. Similarly, the study of membrane dysfunotion in a wide variety of experimental models of heart disease at various stages of failure is essential if we are to fully understand the pathogenesis of heart dysfunotion and improve its treatment.

Buch. Zustand: Neu. Neuware - Mechanisms of Heart Failure is based on papers selected from poster presentations made at the International Conference on Heart Failure, Winnipeg, May 20-23, 1994. Although the entire book is one continuous discussion of subcellular mechanisms of heart failure and its treatment, the presentation has been divided into three sections: the opening section on the subcellular basis of heart failure includes discussions of cytokines, signal transduction, metabolism, extracellular matrix, organ level changes and newer approaches to understanding the pathogenesis of heart failure. The second section focuses on the pathophysiological aspects of cardiomyopathies and their treatment. In the final section, medical, surgical and pharmacological approaches to the treatment of heart failure are discussed in clinical and animal laboratory settings.

Gebunden. Zustand: New. The relationship between angiotensin II and hypertension was established in 1898 when angiotensin II was shown to modulate systemic blood pressure. Over the intervening decades, a complete characterization of the renin-angiotensin system (RAS) has been achi.

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - The relationship between angiotensin II and hypertension was established in 1898 when angiotensin II was shown to modulate systemic blood pressure. Over the intervening decades, a complete characterization of the renin-angiotensin system (RAS) has been achieved, and our understanding of its biochemistry and physiology has led to the directed development of agents such as ACE inhibitors and receptor antagonists capable of controlling hypertension. More recently, it was shown that angiotensin II is secreted within certain tissues and that these tissue-specific systems operate independently of the systemic RAS. The novel concept that angiotensin II regulates a number of cardiovascular processes that are unrelated to blood pressure has renewed the interest of both basic and clinical scientists in angiotensin II. The association between angiotensin II and cardiac growth, in particular, has indicated that therapies currently in use for hypertension may have direct application to the treatment of heart failure. The Manitoba Cardiovascular Forum on Angiotensin Receptor Blockade in Winnipeg was convened October 18-20, 1996 to examine the clinical and basic aspects of angiotensin receptor biology as they apply to hypertension and heart failure. In addition, the potential treatment of these conditions using specific angio tensin receptor antagonists was addressed within the context of their immediate therapeutic application and future potential.

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - Pathophysiology of Heart Failure brings together leading basic scientists and clinicians, presenting new approaches to this complex problem, involving cardiomyopathic processes and ischemia perfusion injury. The result is a synthesis of state-of-the-art information on molecular biology, cellular physiology and structure-function relationships in the cardiovascular system. The role which excess intracellular calcium plays in the genesis of cardiac dysfunction is described as a fundamental mechanism underlying heart failure; one which may lead to improved prevention and treatment. Audience: Clinical and experimental cardiologists will find the book a helpful source of ideas and inspiration.

Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - Heart Hypertrophy and Failure brings together leading basic scientists and clinicians, presenting improved knowledge of the pathophysiology and treatment of the condition. The result is a synthesis of state-of-the-art information on molecular biology, cellular physiology and structure-function relationships in the cardiovascular system in health and disease. The papers presented describe fundamental mechanisms underlying changes in the cellular machinery during the development of cardiac hypertrophy and heart failure. Audience: Students, scientists, clinical and experimental cardiologists who seek to understand and manage the perplexing problems of hypertrophy and heart failure.