Myocardial ischemia and subsequent reperfusion of the ischemic myocardium represent complex phenomena encompassing numerous physiological processes. This book aims at enhancing our understanding of these processes and stresses recent important developments in this very active area of research. The concise, state-of-the-art reviews cover recent advances in many fields important to the area of myocardial ischemia and reperfusion including physiology, pathology, pharmacology, biochemistry and molecular biology with reference to clinical relevance and applicability of these findings. Major areas which are highlighted include vascular mechanisms resulting in myocardial ischemia, cellular events in the ischemic, postinfarcted and reperfused myocardium as well as new exciting developments in cardiac protection that involve both novel pharmacological approaches as well as endogenous cardioprotective mechanisms such as preconditioning. Aimed at both the basic and clinical cardiovascular investigator, the book comprehensively reviews the rapid progress made in recent years in understanding the etiology of myocardial ischemia and reperfusion. It will further serve as an authoritative reference for all those interested in learning about the important developments in the treatment of myocardial ischemic and reperfusion disorders.

I am extremely honored and pleased to have the opportunity to write a few introductory words for this timely volume on Na + /It exchange. This is a field of investigation that I entered into by challenge and necessity, embraced with passion and fmally left in my quest for new discoveries in growth control. Ten years, one third of my scientific life, has been devoted to uncovering the mysteries of intracellular pH (PH;) regulation with respect to growth factor action. I got started on this new topic in 1980, when I heard a rather provocative hypothesis presented by Enrique Rozengurt at an ICN-UCLA Keystone meeting on "Cell Surface and Malignancy." He showed that all mitogens induced amiloride-sensitive Na + entry into resting cells and proposed that, if a compound stimulates Na + influx, it could be a mitogen. In support of his proposal Enrique reported that the amphipathic polypeptide, mellitin, which induced Na+ influx, was indeed mitogenic for 3T3 cells. This was only correlation at this stage. However, I was fascinated by this talk. I immediately approached Enrique to inform him of my skepticism about this beautiful story, and to indicate that I would only be convinced when I succeeded in isolating mutant fibroblasts lacking the amiloride-sensitive Na+ transporter. ''Good luck " was his response.

How to protect against ischemia/reperfusion damage is one of the most urgent problems in medicine. It is known that ischemic damage can be attenuated by improving the oxygen balance of the ischemic heart, but the damage-producing mechanism is not yet fully understood. This book provides the latest information on the pathophysiology of ischemia/reperfusion damage and presents new ideas for more effective methods for protection. In the first two sections, the roles of such factors as various ions and phospholipids that modulate ischemia/reperfusion damage are explored, providing a clear and updated explanation of the mechanisms involved. In the third section, the myocardial and vascular remodeling procedure in hearts that have undergone ischemia/reperfusion is explained in terms of signal transduction, enabling a new understanding of the remodeling process. In the final section, a new approach to protection against ischemia/reperfusion damage is presented.

I am extremely honored and pleased to have the opportunity to write a few introductory words for this timely volume on Na + /It exchange. This is a field of investigation that I entered into by challenge and necessity, embraced with passion and fmally left in my quest for new discoveries in growth control. Ten years, one third of my scientific life, has been devoted to uncovering the mysteries of intracellular pH (PH;) regulation with respect to growth factor action. I got started on this new topic in 1980, when I heard a rather provocative hypothesis presented by Enrique Rozengurt at an ICN-UCLA Keystone meeting on "Cell Surface and Malignancy." He showed that all mitogens induced amiloride-sensitive Na + entry into resting cells and proposed that, if a compound stimulates Na + influx, it could be a mitogen. In support of his proposal Enrique reported that the amphipathic polypeptide, mellitin, which induced Na+ influx, was indeed mitogenic for 3T3 cells. This was only correlation at this stage. However, I was fascinated by this talk. I immediately approached Enrique to inform him of my skepticism about this beautiful story, and to indicate that I would only be convinced when I succeeded in isolating mutant fibroblasts lacking the amiloride-sensitive Na+ transporter. ''Good luck " was his response.

How to protect against ischemia/reperfusion damage is one of the most urgent problems in medicine. It is known that ischemic damage can be attenuated by improving the oxygen balance of the ischemic heart, but the damage-producing mechanism is not yet fully understood. This book provides the latest information on the pathophysiology of ischemia/reperfusion damage and presents new ideas for more effective methods for protection. In the first two sections, the roles of such factors as various ions and phospholipids that modulate ischemia/reperfusion damage are explored, providing a clear and updated explanation of the mechanisms involved. In the third section, the myocardial and vascular remodeling procedure in hearts that have undergone ischemia/reperfusion is explained in terms of signal transduction, enabling a new understanding of the remodeling process. In the final section, a new approach to protection against ischemia/reperfusion damage is presented.