Masatsugu Hori – författare

It has been almost 15 years since the fIrst reports appeared indicating that adenosine exerted a .protective effect in ischemic and reperfused myocardium. Numerous experimental studies have shown that adenosine (both exogenous and endogenous adenosine) delays the onset of ischemic contracture, modulates myocardial metabolism during ischemia, attenuates reversible postischemic ventricular dysfunction (myocardial stunning), and reduces myocardial infarct size. Initial studies on adenosine's cardioprotective effect were based on its ability to stimulate postischemic ATP resynthesis, increase coronary blood flow, and reduce heart rate. Although these actions of adenosine are undoubtedly benefIcial to the ischemic/reperfused heart, it now appears that adenosine's cardioprotective effect may be exclusive of these properties. The immense growth in the number of articles on adenosine cardioprotection in the last several years has been related in large part to the hypothesis that adenosine plays a role in ischemic preconditioning.Ischemic preconditioning is the phenomenon in which a brief period of ischemia (and reperfusion) prior to a more prolonged occlusion reduces myocardial infarct size. This form of myocardial protection has received much interest because ischemic preconditioning has been shown to be the most potent means of reducing infarct size in all animal models thus far tested. In fact prior to studies implicating adenosine's role in ischemic preconditioning, adenosine's infarct reducing effect was not well recognized.

It has been almost 15 years since the fIrst reports appeared indicating that adenosine exerted a .protective effect in ischemic and reperfused myocardium. Numerous experimental studies have shown that adenosine (both exogenous and endogenous adenosine) delays the onset of ischemic contracture, modulates myocardial metabolism during ischemia, attenuates reversible postischemic ventricular dysfunction (myocardial stunning), and reduces myocardial infarct size. Initial studies on adenosine's cardioprotective effect were based on its ability to stimulate postischemic ATP resynthesis, increase coronary blood flow, and reduce heart rate. Although these actions of adenosine are undoubtedly benefIcial to the ischemic/reperfused heart, it now appears that adenosine's cardioprotective effect may be exclusive of these properties. The immense growth in the number of articles on adenosine cardioprotection in the last several years has been related in large part to the hypothesis that adenosine plays a role in ischemic preconditioning.Ischemic preconditioning is the phenomenon in which a brief period of ischemia (and reperfusion) prior to a more prolonged occlusion reduces myocardial infarct size. This form of myocardial protection has received much interest because ischemic preconditioning has been shown to be the most potent means of reducing infarct size in all animal models thus far tested. In fact prior to studies implicating adenosine's role in ischemic preconditioning, adenosine's infarct reducing effect was not well recognized.

Advances in cellular physiology and molecular biology have now disclosed the metabolic changes and adaptational responses of the heart to various kinds of stresses. Topics covered in this volume include the regulation of myocardial proteins in mechanical overload, the alteration of adrenoceptors in the stressed heart, metabolic adaptation in cardiac hypertrophy, intracellular calcium metabolism in the ischemia-reperfused myocardium, calcium overload as a cause of myocardial stunning, acquisition of ischemic tolerance by ischemic preconditioning, factors that accelerate myocardial injury, and ventricular remodeling in the ischemic heart. As an update of the latest findings in basic cardiology, this book will benefit both researchers and clinical practitioners.

Cardiac performance is regulated not only by cardiac muscle properties but also by several other factors, including those associated with the neurohumoral system and the mechanical characteristics of the peripheral circulation. New information con­ cerning these regulatory factors has furthered our understanding of the pathophysi­ ology of cardiac dysfunction. However, controversy remains, along with a need to integrate these multidisciplinary findings. It was with this in mind, together with my continuing interest in the response of the normal and diseased heart to variations in loading conditions, that the satellite symposium entitled "Interactions Between Car­ diac Function and Vascular Dynamics" was organized and dedicated to my mentor, Dr. T. Takishima. The symposium was held in Fukushima, Japan, in 1992 following the Tenth Inter­ national Conference of the Cardiovascular Systems Dynamics Society in Kobe, Japan, which was organized by the then president of the society, Dr. Masatsugu Hori. The Fukushima symposium and the Kobe conference were stimulating and informative. To commemorate these events, Dr. Hori, Dr. Janicki, and I decided to publish this book. It covers topics that were presented then as well as pertinent new material. As a result, the book includes not only updated reviews but also up-to-date findings that were not considered at the two scientific sessions. The high level attained in this book is due to the outstanding contributions from internationally renowned scientists. This final product of their efforts should prove to be a valuable source of information to the reader.

Cardiovascular dynamics is a field in which modelling and systems analysis have formed an extremely important discipline. For example, understanding of even such a fundamental function of the circulation as the relationship between central venous pressure apd cardiac output has required evolution of a pertinent model based on years of exhaustive ex­ perimental investigations by Starling, Starr, and Guyton. Hemodynamic analyses of pulsatile pressures and flows in the arteries and veins have been a continuing challenge taken up by champions of fluid dynamics such as Frank, Wetterer, Taylor, and Wormersley, just to mention a few names, and some kind of model was always proposed as a conceptual framework. An even greater challenge to cardiovascular dynamicists was how to analyze the intermittent coupling of the ventricle and the arterial or venous vasculature through the valve. The availability of numerical solutions by computer and the recently evolved ventricular model with a time-varying elastance and a pressure-dependent internal resistance opened the way to analysis of this coupling. The ever­ increasing speed of computers has also facilitated trips between the fre­ quency and the time domain, even on-line for some experimental studies. This book contains many analyses dedicated to the interactions between the heart and the vasculature, providing the reader with findings at the cutting edge of current research in this field.

Research centering on blood flow in the heart continues to hold an important position, especially since a better understanding of the subject may help reduce the incidence of coronary arterial disease and heart attacks. This book summarizes recent advances in the field; it is the product of fruitful cooperation among international scientists who met in Japan in May, 1990 to discuss the regulation of coronary blood flow.

Advances in cellular physiology and molecular biology have now disclosed the metabolic changes and adaptational responses of the heart to various kinds of stresses. Topics covered in this volume include the regulation of myocardial proteins in mechanical overload, the alteration of adrenoceptors in the stressed heart, metabolic adaptation in cardiac hypertrophy, intracellular calcium metabolism in the ischemia-reperfused myocardium, calcium overload as a cause of myocardial stunning, acquisition of ischemic tolerance by ischemic preconditioning, factors that accelerate myocardial injury, and ventricular remodeling in the ischemic heart. As an update of the latest findings in basic cardiology, this book will benefit both researchers and clinical practitioners.