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TitleBiochemistry of Signal Transduction in Myocardium
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BIOCHEMISTRY OF SIGNAL TRANSDUCTION IN MYOCARDIUM

Page 2

Developments in Molecular and Cellular Biochemistry

Series Editor: Naranjan S. Dhalla, Ph.D., FACC

1. V.A. Najjar (ed.): Biological Effects o/Glutamic Acid and Its Derivatives. 1981 ISBN 90-6193-841-4
2. V.A. Najjar (ed.): Immunologically Active Peptides. 1981 ISBN 90-6193-842-2
3. V.A. Najjar (ed.): Enzyme Induction and Modulation. 1983 ISBN 0-89838-583-0
4. V.A. Najjar and L. Lorand (eds.): Transglutaminase. 1984 ISBN 0-89838-593-8
5. GJ. van der Vusse (ed.): Lipid Metabolism in Normoxic and Ischemic Heart. 1989 ISBN 0-7923-0479-9
6. IF.C. Glatz and GJ. van der Vusse (eds.): Cellular Fatty Acid-Binding Proteins. 1990

ISBN 0-7923-0896-4
7. H.E. Morgan (ed.): Molecular Mechanisms o/Cellular Growth. 1991 ISBN 0-7923-1183-3
8. GJ. van der Vusse and H. Stam (eds.): Lipid Metabolism in the Healthy and Diseased Heart. 1992

ISBN 0-7923-1850-1
9. Y. Yazaki and S. Mochizuki (eds.): Cellular Function and Metabolism. 1993 ISBN 0-7923-2158-8

10. I.F.C. Glatz and G.I. van der Vusse (eds.): Cellular Fatty-Acid-Binding Proteins, II. 1993
ISBN 0-7923-2395-5

11. R.L. Khandelwal and I.H. Wang (eds.): Reversible Protein Phosphorylation in Cell Regulation. 1993
ISBN 0-7923-2637-7

12. l Moss and P. Zahradka (eds.): ADP-Ribosylation: Metabolic Effects and RegUlatory Functions. 1994
ISBN 0-7923-2951-1

13. V.A. Saks and R. Ventura-Clapier (eds.): Cellular Bioenergetics: Role o/Coupled Creatine Kinases. 1994
ISBN 0-7923-2952-X

14. I. Slezak and A. ZiegelhOffer (eds.): Cellular Interactions in Cardiac Pathophysiology. 1995
ISBN 0-7923-3573-2

15. I.A. Barnes, H.G. Coore, A.H. Mohammed and R.K. Sharma (eds.): Signal Transduction Mechanisms.
1995 ISBN 0-7923-3663-1

16. A.K. Srivastava and I.-L. Chiasson (eds.): Vanadium Compounds: Biochemical and Therapeutic Applica-
tions. 1995 ISBN 0-7923-3763-8

17. lMJ. Lamers and P.D. Verdouw (eds.): Biochemistry 0/ Signal Transduction in Myocardium. 1996
ISBN 0-7923-4067-1

KLUWER ACADEMIC PUBLISHERS - DORDRECHT / BOSTON / LONDON

Page 131

134

signal transduction mechanism is involved. Myocardial
ischemia is accompanied by an increase in cell volume that
finally leads to disruption of the sarcolemma and cell death
[36]. Cell swelling occurs within the first minutes of ischemia
and becomes more severe when hypoxia continues. Increased
intracellular osmolarity and consequently cell swelling has
been recognized as a potential factor involved in the transi-
tion from reversible to irreversible damage of cardiac tissue
and may thus be of clinical importance [36]. Recently, a time-
and voltage-independent current activated by cell swelling
has been described in cardiomyocytes that could be blocked
by the Cl- channel inhibitors anthracene-9-carboxilic acid (9-
AC) and 5-nitro-2-(3-phenylpropylamino )-benzoic acid
(NPPB) [37]. The current was found to be independent of
intracellular Ca2+ and not affected by the protein kinase in-
hibitor H-S. Interestingly, inhibition of this type of Cl- cur-
rent leads to an immediate increase in the diameter of atrial
cells by approx. 12% [30]. Taken together, these observations
suggest that an active mechanism of cellular volume regula-
tion is not only beneficial during pathological conditions such
as myocardial ischemia but may also be essential during
normal heart function.

In conclusion, neonatal rat cardiomyocytes express several
classes of Cl- channels that are involved in generation and
modulation of action potentials as well as in cell volume regu-
lation. Pharmacological manipulation of the activity of se-
lective classes of channels, either activation or inhibition, may
therefore be of therapeutic significance in limiting or prevent-
ing cardiac diseases.

Acknowledgements

The authors wish to express their gratitude to Dr lA. Post
(Institute of Molecular Biology and Medical Technology,
University of Utrecht, the Netherlands) for preparing puri-
fied sarcolemma. B.C.T. is a fellow of the Royal Dutch Acad-
emy of Sciences, The Netherlands.

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Page 261

Cardiac Energetics: From Emax
to Pressure-Volume Area
edited by Martin M. LeWinter, Director, Cardiology Unit, University of Vermont,
Burlington, USA; Hiroyuki Suga, Dept. of Physics, Okayama University Medical
School, Japan; Matthew W. Watkins, Cardiology Unit, University of Vermont,
Burlington, USA

DEVELOPMENTS IN CARDIOVASCULAR MEDICINE 177

Most of the progress in cardiac energetics in recent years has been spurred by
the pressure volume area concept, the natural extension into energetics of
earlier pioneering work delineating the time-varying elastance framework for
ventricular contraction. The book draws together a broad spectrum of researchers
basic, applied and clinical having a shared interest in the energetics of cardiac
muscle and ventricle, providing an overview of the current state of the art.

Contents and Contributors:
List of contributors. Preface; MM LeWinter, et al. 1. Energy costs of PYA and
Emax: constancy and variability; H. Suga, et al. 2. Kinetic property of cardiac
myosin in vitro; S. Sugiura, et al. 3. Thin filament regulation and cardiac
energetics; R.J. Solaro. 4. Explaining load-dependent ventricular performance
and energetics based on a model of E-C coupling; D. Bur/(hoff, et al. 5. Cardiac
contractions. PYA and energetic considerations determined from a cardiac
muscle crossbridge model; T. W. Taylor, et al. 6. Normalization of Em ax and PYA;
M Sugawara, et al. 7. Observations on the relation of PYA and MV02 in closed
chest dogs; G.L. Freeman, S.D. Prabhu. 8. Regional myocardial contraction
coupled with energetics; Y. Goto, etal. 9. Energetics during ventricular fibrillation;
H. Kusuoka, E. Marbab. 10. Influence of preload on non-mechanical V0 2
assessed with 2,3-butanedione monoxime; M.M. LeWinter, et al. 11. Emax and
myocardial microcirculation; F. Kajiya, et al. 12. Efficiency of ventricular-arterial
coupling and baroreflex regulation of blood pressure; K. Sunagawa, et al. 13.
Ventriculo-arterialload matching of failing hearts; H. Asanoi, et al. 14. Calcium
signalling and pharmacology of cardiotonic agents; M. Endoh. 15. Effect of
inotropic agents on mechanoenergetics in human diseased heart; M Takeuchi,
et al. 16. Effects of various inotropic agents on the relation between
ventriculoarterial coupling and myocardial energetics in patients with idiopathic
dilated cardiomyopathy; M Yokota, et al. Index.

1995, 256 pp. ISBN 0-7923-3721-2
Hardbound NLG 200.00 I USD 117.00 I GBP 79.75

P.O. Box 322, 3300 AH Dordrecht, The Netherlands
P.O. Box 358, Accord Station, Hingham,

MA 02018-0358,U.S.A.

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