|
Showing 1 - 14 of
14 matches in All Departments
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.
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.
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.
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.
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.
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. Angiotensin II Receptor Blockade: Physiological and
Clinical Implications focuses on the most recent developments in
the molecular biology, cellular physiology and structure-function
relationships of angiotensin II and its receptors. In addition,
this volume covers the current therapeutic uses for angiotensin
receptor antagonists and considers their potential future
applications. This volume will be a valuable resource for
scientists, practising clinicians and students who are attempting
to extend their knowledge in the field of hypertension and heart
failure, and who are devoted to improving cardiovascular health.
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.
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.
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.
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.
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."
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.Angiotensin II Receptor Blockade: Physiological and
Clinical Implications focuses on the most recent developments in
the molecular biology, cellular physiology and structure-function
relationships of angiotensin II and its receptors. In addition,
this volume covers the current therapeutic uses for angiotensin
receptor antagonists and considers their potential future
applications. This volume will be a valuable resource for
scientists, practising clinicians and students who are attempting
to extend their knowledge in the field of hypertension and heart
failure, and who are devoted to improving cardiovascular health.
A concise, in-depth analysis of the status of the sympathetic
system in heart diseases
This book summarizes the functional status of the sympathetic
neural system in cardiological diseased states and highlights
aspects of sympathetic neural activity that are important to an
overall understanding of the pathophysiology process. Critical
reviews of methods for evaluating sympathetic activity are
discussed, existing data is closely scrutinized, and attempts are
made to delineate the factors derived from increased sympathetic
activity. The book provides a physiologically and clinically based
approach to the investigation of the involvement of catecholamines
in cardiovascular diseases, which makes it a valuable addition to
the reference collections of researchers, clinical scientists, and
graduate students.
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.
|
|