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Preface. Part One: Pathophysiology of ischemia and reperfusion. 1. Moderate ischemic injury and myocardial stunning; M.E. Zughaib, P.B. McCay, M.O. Jeroudi, C. Hartley, Jian-Zhong Sun, S. Seikili, Xiao-Ying Li, R. Bolli. 2. Severe ischemic injury and the oxygen paradox; H.M. Piper, B. Siegmund, K.-D. Schluter. 3. Role of leukocytes in reperfusion injury; S.L. Hale, R.A. Kloner. 4. Ischemia of the neonatal heart; F.M. Lupinetti. Part Two: Concepts of cardioplegia. 5. Cardioplegia with an intracellular formulation; C.J. Preusse. 6. Cardioplegia with an extracellular formulation; D.J. Chambers, M.V. Braimbridge. 7. Blood cardioplegic strategies during adult cardiac operations; G.D. Buckberg, B.S. Allen, F. Beyersdorf. Part Three: Clinical application of cardioplegia. 8. High volume perfusion; I.B. Krukenkamp, C.A. Caldarone, P. Burns, S. Levitsky. 9. Intermittent coronary perfusion; H.D. Schulte. 10. Retrograde perfusion; P. Menasche. 11. Cardiac arrest by ventricular fibrillation; C.W. Akins. 12. Myocardial preservation in the immature heart; J.E. Mayer, Jr. Part Four: Evaluation of cardioplegic methodology. 13. High-energy phosphates and their catabolites; J.W. de Jong, T. Huizer, M. Janssen, R. Krams, M. Tavenier, P.D. Verdouw. 14. Lactate monitoring during and after cardiopulmonary bypass: an approach implicating a perioperative measure for cardiac energy metabolism; E.-G. Krause, D. Pfeiffer, U. Wollenberger, H.-G. Wollert. 15. Myocardialtissue pH in the assessment of the extent of myocardial ischemia and the adequacy of myocardial protection; M.B. Tantillo, S.F. Khuri. 16. Morphology of the acute and chronic ischemic myocardium in man; M. Borgers, W. Flameng. 17. Muscle birefringence; S. Darracott-Cankovic. 18. How to measure cardiac energy expenditure; M.Takaki, T. Namba, J. Araki, K. Ishioka, H. Ito, T. Akashi, Ling Yun Zhao, Dan Dan Zhao, Miao Liu, W. Fujii, M. Takaki, H. Suga. 19. Cardioplegia and cardiac function; D. Baumgart, R. Schulz, T. Ehring, G. Heusch. Index.
With this volume results become generally available of a recent conference that was the first to discuss properties of isolated heart muscle cells from the adult myocardium as a new cardio- logical research tool. The conference was held as an International Erwin Riesch Symposium un- der the auspices of the Deutsche Gesellschaft fUr Herz- und Kreislaufforschung at Spangenberg Castle, March 22-25, 1984. It was made possible through funding by the Erwin Riesch Foun- dation and the Bayer AG which deserve our gratitude for their generosity. It may not be fully reflected in this collection of papers that the atmosphere of this meeting was unique. The reason for this resided apparently in the still rudimentary experiences with the adult cardiocyte model that is now widely acknowledged to be very promising. Thus, quite basic inter- ests brought together experts from different biological disciplines who in respect to this new mod- el were all still "beginners". It was noteworthy that such common interests exerted a unifying effect upon otherwise rather separated fields of science. The main task of the years to come will certainly consist in improving isolation and culturing conditions for adult myocytes in order to fully establish the isolated cell model in heart research.
In the cardiovascular sciences, an increasing demand for the use of modern methods of cell biology has developed. The use of specific cell culture models of the various tissues involved is essential for most of these novel approaches. This book meets the demand for acomprehensive and easy accessible source for cell cul- ture methods in cardiovascular research as it was not previously available. The basic methods for cultures of cardiomyocytes (embryonic and adult), endothelial cells (micro- and macrovascular), smooth muscle cells and pericytes are described in detail by an international selection of experts. Special chapters discuss the use of growth factors and attachment substrates, techniques for co-cultures, cultures on permeable filter membranes and microcarrier cultures. The methodological descriptions are sufficiently detailed for an immediate application in the laboratory. All chapters also contain a critical evaluation of alternative approaches.
In industrialized countries, ischemic heart disease is by far the most common organ-specific cause of death. The thrombotic occlusion of a coronary artery which had previously been severely altered by atherosclerosis, is the most frequent cause of ischemic deterioration of myocardial tissue, i. e. myocardial infarction. Death of the human individual occurs when myocardial ischemia causes a critical impairment of cardiac pump function. The failure of a heart with an ischemic area may be due to the amount and location of contractile tissue becoming paralyzed or even necrotic, or to arrhythmias provoked by the ischemic condition, or by a combination of both factors. Considerable progress has been made in the development of antiarrythmic therapy. Effective tools have been developed to reperfuse ischemic myocar dial tissue as soon as the patient reaches hospital. However, therapeutical principles for the ischemic-reperfused myocardium which would specifically interfere with the state of injury of the ischemic tissue at the onset of reperfusion, and avoid the apparent hazards of the reperfusion process itself, have yet to be established. But not only approved therapeutical concepts are lacking, the pathophysiology of myocardial cell injury in pro gressive ischemia and under reperfusion is in itself only partly understood."
In industrialized countries, ischemic heart disease is by far the most common organ-specific cause of death. The thrombotic occlusion of a coronary artery which had previously been severely altered by atherosclerosis, is the most frequent cause of ischemic deterioration of myocardial tissue, i. e. myocardial infarction. Death of the human individual occurs when myocardial ischemia causes a critical impairment of cardiac pump function. The failure of a heart with an ischemic area may be due to the amount and location of contractile tissue becoming paralyzed or even necrotic, or to arrhythmias provoked by the ischemic condition, or by a combination of both factors. Considerable progress has been made in the development of antiarrythmic therapy. Effective tools have been developed to reperfuse ischemic myocar dial tissue as soon as the patient reaches hospital. However, therapeutical principles for the ischemic-reperfused myocardium which would specifically interfere with the state of injury of the ischemic tissue at the onset of reperfusion, and avoid the apparent hazards of the reperfusion process itself, have yet to be established. But not only approved therapeutical concepts are lacking, the pathophysiology of myocardial cell injury in pro gressive ischemia and under reperfusion is in itself only partly understood.
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