Recent Progress in Failing Heart Syndrome

345 Pages·1991·21.411 MB·English

by  Seiryo Sugiura, Hiroshi Yamashita (auth.), Shigetake Sasayama M.D., Hiroyuki Suga M.D., D.M. SC. (eds.)

S. Sasayama · H. Suga
(Eds.)
Recent Progress in
Failing Heart Syndrome
With 159 Figures
Springer-Verlag
Tokyo Berlin Heidelberg
New York London Paris
Hong Kong Barcelona
SmGETAKE SASAYAMA, M.D.
Professor of Medicine, The Second Department of Internal Medicine, Toyama Medical
and Pharmaceutical University, 2630 Sugitani, Toyama, 930-01 Japan
HIROYUKI SUGA, M.D., D.M. SC.
Professor of Physiology, Okayama University Medical School, 2-5-1, Shikata-cho,
Okayama, 700 Japan
ISBN-13:978-4-431-68019-2 e-ISBN-13:978-4-431-67955-4
DOl: 10.1007/978-4-431-67955-4
Library of Congress Cataloging-in-Publication Data
Recent progress in failing heart syndrome I S. Sasayama, H. Suga (eds). p. cm. Compilation
of scientific results of a three year project for research on heart failure organized by the Japanese
Circulation Society from 1988 to 1991. Includes bibliographical references and index.
ISBN-13:978-4-431-68019-2 1. Congestive heart failure.
2. Heart failure. I. Sasayama, Shigetake, 1937- . II. Suga, H. (Hiroyuki), 1941- .
III. Nihon Junkanki Gakkai. [DNLM: 1. Heart-physiopathology. 2. Heart Failure, Congestive.
3. Myocardial Contraction. WG 370 R295] RC685.C53R43 1991, 616.1'29-dc20, DNLM/DLC,
for Library of Congress 91-5067
© Springer-Verlag Tokyo 1991
Softcover reprint of the hardcover 1st edition 1991
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Preface
Heart failure is a syndrome caused by a heart dysfunction that leads to insuf
ficient blood in the peripheral tissues for their metabolic demands. This syn
drome still remains an obscure clinical entity and even its definition is disputed.
It has become increasingly apparent that heart failure may relate not only to
cardiac dysfunction but also to other physiological alterations involved in the
maintenance of circulatory homeostasis.
In 1988, the Japanese Circulation Society organized a three-year project for
research on heart failure. The research group consisted of ten investigators,
all relatively young but well recognized internationally for their research
accomplishments.
This book represents a compilation of the achievements by this group during
the past three years which have led to new insights into the pathophysiologic
mechanisms of heart failure, and diagnosis, evaluation and treatment of this
syndrome. Contents include research into the cellular biology of congestive
heart failure, and a framework of pressure-volume relationships enabling
assessment of ventricular contraction energetics or coupling of ventricular
properties and arterial load. This conceptual framework is of vital significance,
particularly when we consider the failing heart as an energy-depleted state.
An understanding of the neuroendocrine responses to explain the pathophy
siology of congestive heart failure is perhaps the most important advance, and
has led to new developments in therapy.
This book also includes an analysis of mechanical factors, including both
regional, and global ventricular functions, and this is related to the under
standing of the pathophysiology of congestive heart failure.
With such an increase in knowledge concerning the biological and physio
logical bases of congestive heart failure, its management has become more
complex than before. The therapeutic implications of selective stimulation of
high-affinity ~l-receptors are outlined, as well as use of the left ventricular
assist system as a viable alternative.
v
VI Preface
The materials presented in this book summarize the latest knowledge on
heart failure syndrome, from basic science to treatment. We hope this book
will describe the current state of research on heart failure in Japan and serve
as a stimulus for further investigation.
S. SASAYAMA
H. SUGA
Table of Contents
Preface.......................................................... V
List of Contributors ............................................... IX
1 Reconstitution of Actin-Myosin Interaction In Vitro:
Its Application to Cardiac Physiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
SEIRYO SUGIURA, HIROSHI YAMASHITA, TAKASHI SERIZAWA,
MASAHIKO IIZUKA
2 Molecular Basis for Cardiac Adaptation to Overload. . . . . . . . . . . . . . .. 19
YOSHIO YAZAKI, MASAHIKO KURABAYASHI, ISSEI KOMURO
3 Role of Ca2+ Overload in Myocardial Contractile Dysfunction 43
MASATSUGU HORl, YUKIHIRO KORETSUNE, MASAFUMI KITAKAZE,
HIDEO KUSUOKA, EDUARDO MARBAN, MICHITOSHI INOUE
4 Cardiac Oxygen Costs of Contractility (Emax) and Mechanical
Energy (PVA): New Key Concepts in Cardiac Energetics. . . . . . . . . . .. 61
HIROYUKI SUGA, Y OICHI GOTO
5 Left Ventricular Regional Mechanics and Energetics Assessed in
the Wall Tension-Regional Area Diagram ......................... 117
YOICHI GOTO, HIROYUKI SUGA
6 Myocardial Energetics of Hypertrophied Heart of Spontaneously
Hypertensive Rat and Stroke-Prone Spontaneously
Hypertensive Rat .............................................. 151
KEIJIRO KUSUNOKI, YASUYUKI NAKAMURA, TAKASHI KONISHI,
MASATO MATSUNAGA, CHUICHI KAWAI
VII
VIII Table of Contents
7 Optimal Left Ventricle Versus Optimal Afterload .................. 161
KENJI SUNAGAWA, KIYOSHI HAYASHIDA, MASARU SUGIMACHI,
KOJI TODAKA, TORU KUBOTA, RYOICHI ITAYA, CHISHAKI AKIKO,
AKIRA TAKESHITA
8 Coupling Between Ventricluar and Arterial Properties .............. 187
SHIGETAKE SASAYAMA, HIDETSUGU ASANOI
9 Neurohumoral Mechanisms in Chronic Heart Failure. . . . . . . . . . . . . . .. 221
MASATSUGU HORI, TOSHIFUMI KAGIYA, HIDEYUKI SATO, HIROSHI SATO,
AKIRA KITABATAKE, MASATAKE FUKUNAMI, NORITAKE HOKI,
MICHITOSHI INOUE
10 Effects of Rapid Pacing Stress on Ventricular Function of
Hypertrophied Human Heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 241
YASUYUKI NAKAMuRA, TAKASHI KONISHI, TOSHIAKI KUMADA,
CHUICHI KAWAI
11 Regional Work of the Left Ventricle and Contractility Index
Independent of Ventricular Size .................................. 257
MOTOAKI SUGAWARA, KIYOHARU NAKANO, MASATOSHI KAWANA,
JUN UMEMURA, SHIGETAKE SASAYAMA, BLASE A. CARABELLO
12 Selective Stimulation of High-Affinity PI-Receptors: Its Implication
in the Treatment of Mild Heart Failure. . . . . . . . . . . . . . . . . . . . . . . . . . .. 281
TERUYUKI YANAGISAWA, KUNIAKI ISHII, HITOSHI YOKOYAMA,
HID EO KUROSAWA, NORIO TAIRA
13 Hemodynamic and Histopathological Consideration of Left
Ventricular Assist System on Acute Myocardial Infarction:
Experimental and Clinical Investigation . . . . . . . . . . . . . . . . . . . . . . . . . .. 303
HISATERU TAKANO, TAKESHI NAKATANI
14 Therapeutic Effects of the Left Ventricular Assist System on
Myocardial Ischemia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 325
TAKESHI NAKATANI, HISATERU TAKANO, HIROYUKI NODA,
MASAYUKI KINOSHITA
Index ............................................................ 341
List of Contributors
Akiko, C. 161 Komuro, I. 19 Sato, Hideyuki 221
Asanoi, H. 187 Konishi, T. 151,241 Sato, Hiroshi 221
Carabello, B.A. 257 Koretsune, Y. 43 Serizawa, T. 1
Fukunami, M. 221 Kubota, T. 161 Suga, H. 61, 117
Goto, Y. 61, 117 Kumada, T. 241 Sugawara, M. 257
Hayashida, K. 161 Kurabayashi, M. 19 Sugimachi, M. 161
Hoki, N. 221 Kurosawa, H. 281 Sugiura, S. 1
Hori, M. 43, 221 Kusunoki, K. 151 Sunagawa, K. 161
Iizuka, M. 1 Kusuoka, H. 43 Taira, N. 281
Inoue, M. 43, 221 Marban, E. 43 Takano, H. 303, 325
Ishii, K. 281 Matsunaga, M. 151 Takeshita, A. 161
Itaya, R. 161 Nakamura, Y. 151, Todaka, K. 161
Kagiya, T. 221 241 Umemura, J. 257
Kawai, C. 151,241 Nakano, K. 257 Yamashita, H. 1
Kawana, M. 257 Nakatani, T. 303, 325 Yanagisawa, T. 281
Kinoshita, M. 325 Noda, H. 325 Yazaki, Y. 19
Kitabatake, A. 221 Sasayama, S. 187, 257 Yokoyama, H. 281
Kitakaze, M. 43
IX
1
Reconstitution of Actin-Myosin Interaction In
Vitro: Its Application to Cardiac Physiology
SEIRYO SUGIURA1 , HIROSHI YAMASHITA 1, TAKASHI SERIZAW AI,
MASAHIKO IIZUKA2
Summary. Recently, biochemical studies have revealed that heart muscle can
change the structure of contractile protein under various physiological or
pathophysiological conditions. To examine the functional significance of these
changes at the molecular level, we applied an in vitro motility assay technique
and measured the sliding velocity of cardiac myosin in vitro.
First, various methods to assay in vitro motility are reviewed. These tech
niques enabled us to study the mechanical aspect of acto-myosin interaction
under controlled conditions and thus showed many intriguing results.
Secondly, our preliminary results using rabbit cardiac myosin are presented.
We used an assay system in which polystyrene beads coated with cardiac
myosin obtained from either normal or hyperthyroid rabbit were made to slide
on actin cables of an alga Nitellopsis obtusa in the presence of Mg-A TP. The
movement observed under photo microscope was smooth and its velocity was
related to the biochemical characteristics of myosin. The velocity changed
under various experimental conditions, suggesting that the sliding observed in
this system is physiological in nature.
We consider that in vitro motility assay techniques can help us understand
the relation between biochemistry and physiology.
Key words: Cardiac myosin - In vitro motility assay - Sliding velocity
Introduction
While recent advances in biochemistry and biotechnology have attracted the
interest of researchers studying heart muscle [1, 2], less attention has been
paid to the physiological aspect of this field. Of course, continuous efforts have
1 The Second Department of Internal Medicine, Faculty of Medicine, University of
Tokyo, Bunkyo-ku, Tokyo, 113 Japan
2The First Department of Internal Medicine, Dokkyo University, School of Medicine,
Mibu, Tochigi, 321 Japan
1
2 S. Sugiura et al.
been made towards complete understanding of the mechanical properties [3-6]
and energetics [7] of the muscle, but most of these studies are still within the
conceptual framework of the "cross-bridge theory" which was first proposed
in 1957 [8] and later revised.
This theory has been used for many years to account for experimental results
but recently, serious challenges have been made against its basic assumptions.
Researchers are now questioning whether one cross-bridge cycling is rigidly
coupled to one ATP hydrolysis cycle, and whether a single cross-bridge always
exerts a constant force under any loading conditions.
This drastic change in thinking was made possible by the development of in
vitro motility assays which allow visualization of the interaction of contractile
proteins using light microscopy [9-18]. Direct visualization of acto-myosin
interaction eliminates the complex deduction process by providing us with
direct results on the fundamental mechanisms of muscle contraction.
In this article, we will review the techniques and results of in vitro motility
assays and the application of these techniques in cardiac physiology. Finally,
the significance and future direction of these techniques in cardiology will be
discussed.
Motility Assay Using Algae
Historical Overview
The first version of the in vitro motility assay was developed independently by
Sheetz and Spudich in 1983 [17] and Shimmen and Yano in 1984 [18]. This type
of assay is characterized by use of the algae Characeae, of which the species
Chara and Nitella are well known. These algae consist of cylindrical internodal
cells, about 1 mm in diameter and several cm in length, that are connected in
series. The inner surface of the cell wall is covered with well-organized rows
of chloroplasts running longitudinally, and the endoplasm inside (sol phase)
streams actively (sometimes the rate is as fast as 100Ilm/s).
As a mechanism for cytoplasmic streaming, Kamiya and Kuroda proposed
that the shear stress was generated by the interaction of the cytoplasm and the
inner surface of the chloroplast rows (sol-gel interface) [19]. Interestingly, this
discovery coincided with the publication of the cross-bridge theory. Later
research identified bundles of actin filaments running on the chloroplast rows
[20]. These filaments can be decorated with heavy meromyosin (HMM) to
form arrow heads. The direction of cytoplasmic streaming is opposite to the
pointed end which is similar to the relative sliding of acto-myosin in muscle
sarcomeres. Currently, molecular motors are classified into two categories:
actin-based and microtubule-based [21]. In the actin-based molecular motor,
myosins are coupled. Indeed, Kato and Tonomura [22] isolated myosin from
Nitella flexilis. Furthermore, small bodies having myosin-like activities (ATPase
activity, generating motive force for the sliding movement) were found to exist
on the endoplasmic organelles [23].