Henk Keurs – författare

The Third International Symposium on Excitation-Contraction Coupling in Skeletal, Cardiac, and Smooth Muscle, organized by George Frank, C. Paul Bianchi, and Henk E. DJ. ter Keurs, was held in Banff Centre, Banff, Alberta, Canada during June 26 to June 30, 1991. The theme of these symposia has been to recognize the similarities and dissimilarities of excitation-contraction coupling in skeletal, cardiac, and smooth muscle. Cross fertilization of concepts of excitation-contraction coupling in these three types of muscle has occurred since the early studies in the late fifties and early sixties on skeletal muscle. Investigators in each field meet only at specialized symposia which exclude investigators in the other fields. The purpose of the symposia has been to bring together international investigators studying excitation-contraction coupling in skeletal, cardiac, and smooth muscle so that we may learn from each other and hence provide a more global concept of excitation-contraction. The Third International Symposia has accomplished its objective as we recognize that calcium channels of the sarcolemma and the sarcoplasmic reticulum play key essential roles in excitation-contraction coupling in all three types of muscles. In skeletal muscle the recognition that E-C coupling consists of two parallel mechanisms, one dependent upon a dihydropyridine voltage-sensitive sensors coupled to calcium release from the terminal cisternae via the ryanodine sensitive channel in the foot structure of the triad.

This volume constitutes the proceedings of a satellite symposium of the XXXth congress of the International Union of Physiological Sciences. The symposium has been held In Banff, Alberta Canada July 9-11 1986. The program was organized to provide a selective overview of current developments in cardiac biophysics, biochemistry, and physiology. In order to highlight areas of develop­ ing ideas and to stimulate the participants' inquisitiveness into the nature and complexity of the integrated cardiovascular system, lectures and discussions were presented that emphasized evolving and sometimes provocative concepts in the field. With the same goal in mind we have, for the readers of this volume, briefly summarized the general discussions. We would like to thank several individuals whose dedication made this sym­ posium and publication of the proceedings possible. Mrs. Lois Kokoski and Mrs. Madeleine Aldridge of the Conference Office of the University of Calgary seemingly effortlessly handled the details of the symposium. Peter de Tombe, Dr. Peter Backx and Dr. Jeroen Bucx transcribed the general discussions. Finally, we appreciate the extra effort of our secretaries, Lenore Doell and Gregory Douglas, and the work of Anna Tyberg who prepared the final manuscripts for publication. Henk E.D.J. ter Keurs, M.D. Ph.D. John V. Tyberg, M.D. Ph.D.

The Third International Symposium on Excitation-Contraction Coupling in Skeletal, Cardiac, and Smooth Muscle, organized by George Frank, C. Paul Bianchi, and Henk E. DJ. ter Keurs, was held in Banff Centre, Banff, Alberta, Canada during June 26 to June 30, 1991. The theme of these symposia has been to recognize the similarities and dissimilarities of excitation-contraction coupling in skeletal, cardiac, and smooth muscle. Cross fertilization of concepts of excitation-contraction coupling in these three types of muscle has occurred since the early studies in the late fifties and early sixties on skeletal muscle. Investigators in each field meet only at specialized symposia which exclude investigators in the other fields. The purpose of the symposia has been to bring together international investigators studying excitation-contraction coupling in skeletal, cardiac, and smooth muscle so that we may learn from each other and hence provide a more global concept of excitation-contraction. The Third International Symposia has accomplished its objective as we recognize that calcium channels of the sarcolemma and the sarcoplasmic reticulum play key essential roles in excitation-contraction coupling in all three types of muscles. In skeletal muscle the recognition that E-C coupling consists of two parallel mechanisms, one dependent upon a dihydropyridine voltage-sensitive sensors coupled to calcium release from the terminal cisternae via the ryanodine sensitive channel in the foot structure of the triad.

The Third International Symposium on Excitation-Contraction Coupling in Skeletal, Cardiac, and Smooth Muscle, organized by George Frank, C. Paul Bianchi, and Henk E. DJ. ter Keurs, was held in Banff Centre, Banff, Alberta, Canada during June 26 to June 30, 1991. The theme of these symposia has been to recognize the similarities and dissimilarities of excitation-contraction coupling in skeletal, cardiac, and smooth muscle. Cross fertilization of concepts of excitation-contraction coupling in these three types of muscle has occurred since the early studies in the late fifties and early sixties on skeletal muscle. Investigators in each field meet only at specialized symposia which exclude investigators in the other fields. The purpose of the symposia has been to bring together international investigators studying excitation-contraction coupling in skeletal, cardiac, and smooth muscle so that we may learn from each other and hence provide a more global concept of excitation-contraction. The Third International Symposia has accomplished its objective as we recognize that calcium channels of the sarcolemma and the sarcoplasmic reticulum play key essential roles in excitation-contraction coupling in all three types of muscles. In skeletal muscle the recognition that E-C coupling consists of two parallel mechanisms, one dependent upon a dihydropyridine voltage-sensitive sensors coupled to calcium release from the terminal cisternae via the ryanodine sensitive channel in the foot structure of the triad.

H. E. D. J. TER KEURS & M. I. M. NOBLE The "Starling''s Law of the Heart" and "The Frank-Starling Mechanism" have long been the cornerstone of cardiac mechanical physiology. It is often forgotten that Frank and Starling carried out fundamentally different exper­ iments. Frankl measured the isovolumic pressure developed by frog heart at different volumes. He therefore discovered the pressure-volume-volume rela­ tionship which depends directly on the force-length relationship of the 2 sarcomeres. Starling ,3 studied cardiac shortening as manifest by cardiac output and its relationship to end-diastolic conditions as manifest by right atrial pressure. Thus he was studying the ability of cardiac muscle to shorten more at a given load from a greater initial length. Starling in the promulga­ 4 tions of his law implied a common mechanism for these two phenomena and spoke of the "energy liberated" being a function of initial muscle fiber length. However, there has been much confusion about the interrelationship between the two different aspects studied by Frank and Starling. The 1960s saw the era of isolated cardiac muscle mechanics, beginning with 5 the paper of Abbott and Mommaerts. Whole muscle length-tension relations were equated with sarcomere-length-tension relations by fixation of muscle at a particular point on the curve and determination of sarcomere length by electronmicroscopy.

This volume constitutes the proceedings of a satellite symposium of the XXXth congress of the International Union of Physiological Sciences. The symposium has been held In Banff, Alberta Canada July 9-11 1986. The program was organized to provide a selective overview of current developments in cardiac biophysics, biochemistry, and physiology. In order to highlight areas of develop­ ing ideas and to stimulate the participants'' inquisitiveness into the nature and complexity of the integrated cardiovascular system, lectures and discussions were presented that emphasized evolving and sometimes provocative concepts in the field. With the same goal in mind we have, for the readers of this volume, briefly summarized the general discussions. We would like to thank several individuals whose dedication made this sym­ posium and publication of the proceedings possible. Mrs. Lois Kokoski and Mrs. Madeleine Aldridge of the Conference Office of the University of Calgary seemingly effortlessly handled the details of the symposium. Peter de Tombe, Dr. Peter Backx and Dr. Jeroen Bucx transcribed the general discussions. Finally, we appreciate the extra effort of our secretaries, Lenore Doell and Gregory Douglas, and the work of Anna Tyberg who prepared the final manuscripts for publication. Henk E.D.J. ter Keurs, M.D. Ph.D. John V. Tyberg, M.D. Ph.D.

Left ventricular hypertrophy (LVH) is usually considered to be a compen­ satory adjustment of heart muscle to an inreased work load. LVH develops in the course of valvular or congenital heart disease, or when part of the myocardium is damaged by long-standing ischemia or infarction. In the hypertrophied heart the muscle fibers increase in size, not in number. The fibers are found to contain a larger number of myofibrils and the cell organelles are larger. From epidemiologic studies it is known that even mild LVH is associated with myocardial ischemia, ventricular arrhythmias, and sudden cardiac death. Most cases of LVH show focal degenerative tissue changes including cellular atrophy, myofibrillar disorganization, interstitial fibrosis, and loss of intracellular connections. Myocardial dysfunction develops and, unlike the functional adaptive changes found in pure hypertrophy, is not reversible by surgical treatment of the valvular heart disease or medical correction of hypertension. Interstitial fibrosis, intracellular changes of musc Ie cells, and loss of contract ile tissue lead to poor mechanical function and undoubtedly increase the risk of ischemia, arrhythmias, or sudden death, a well-recognized problem in patients with a variety of heart diseases. Even When successfully treated, the patients may remain at risk if the compensatory hypertrophy is not fully reversed. Epidemiologic studies conducted in the Framingham population in the early 1950'' s demonstrated LVH according to electrocardiographic criteria in 1. 5% of the population; 2% of the population had LVH according to chest X-ray criteria.

Left ventricular hypertrophy (LVH) is usually considered to be a compen­ satory adjustment of heart muscle to an inreased work load. LVH develops in the course of valvular or congenital heart disease, or when part of the myocardium is damaged by long-standing ischemia or infarction. In the hypertrophied heart the muscle fibers increase in size, not in number. The fibers are found to contain a larger number of myofibrils and the cell organelles are larger. From epidemiologic studies it is known that even mild LVH is associated with myocardial ischemia, ventricular arrhythmias, and sudden cardiac death. Most cases of LVH show focal degenerative tissue changes including cellular atrophy, myofibrillar disorganization, interstitial fibrosis, and loss of intracellular connections. Myocardial dysfunction develops and, unlike the functional adaptive changes found in pure hypertrophy, is not reversible by surgical treatment of the valvular heart disease or medical correction of hypertension. Interstitial fibrosis, intracellular changes of musc Ie cells, and loss of contract ile tissue lead to poor mechanical function and undoubtedly increase the risk of ischemia, arrhythmias, or sudden death, a well-recognized problem in patients with a variety of heart diseases. Even When successfully treated, the patients may remain at risk if the compensatory hypertrophy is not fully reversed. Epidemiologic studies conducted in the Framingham population in the early 1950' s demonstrated LVH according to electrocardiographic criteria in 1. 5% of the population; 2% of the population had LVH according to chest X-ray criteria.

H. E. D. J. TER KEURS & M. I. M. NOBLE The "Starling's Law of the Heart" and "The Frank-Starling Mechanism" have long been the cornerstone of cardiac mechanical physiology. It is often forgotten that Frank and Starling carried out fundamentally different exper­ iments. Frankl measured the isovolumic pressure developed by frog heart at different volumes. He therefore discovered the pressure-volume-volume rela­ tionship which depends directly on the force-length relationship of the 2 sarcomeres. Starling ,3 studied cardiac shortening as manifest by cardiac output and its relationship to end-diastolic conditions as manifest by right atrial pressure. Thus he was studying the ability of cardiac muscle to shorten more at a given load from a greater initial length. Starling in the promulga­ 4 tions of his law implied a common mechanism for these two phenomena and spoke of the "energy liberated" being a function of initial muscle fiber length. However, there has been much confusion about the interrelationship between the two different aspects studied by Frank and Starling. The 1960s saw the era of isolated cardiac muscle mechanics, beginning with 5 the paper of Abbott and Mommaerts. Whole muscle length-tension relations were equated with sarcomere-length-tension relations by fixation of muscle at a particular point on the curve and determination of sarcomere length by electronmicroscopy.