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In 1883, Ringer found that the frog heart was inhibited by potassium and stimulated by calcium. Little did he know that nearly a century later we would be doing similar things to more than 200,000 human hearts per year.This book, collating more than 1,300 references, defines the critical factors that determine cardioplegic actions and efficacy. It delineates many practical guidelines and identifies several areas of uncertainty. And despite the complexity of this subject, the book is written with exemplary clarity.Myocardial protection stems from two lines of thought: the concept of the reversibility of tissue injury after reperfusion, and the supposition that cellular metabolism can be manipulated to salvage cells that might otherwise have died. The myocardial cell and the surgeon, however, may exhibit conflicting requirements. Cells like blood, while surgeons don't—at least not while they sew. Surgeons like a heart that takes over circulatory work soon after the

DURING a study on the sub-microscopic appearance of the myocardium of rats, we have observed well delineated membrane bound structures, circular to elliptical in shape, entering into myocardial cells in the area of the intercalated disk. These contours appeared to assume an intimate relationship with elements of the sarcoplasmic reticulum.

and if so, would explain in large part the prolonged QT interval. Equally as interesting would be studies on myocardial cell permeability changes during the cardiac cycle which would reveal intracellular and extracellular electrolyte concentrations during the cardiac cycle. Acknowledgments.-The research for this project was done while the author held a summer research grant from the California Foundation for Biochemical Research. The

Excerpt Mechanisms responsible for the documented cardiotoxicity of nicotine are unknown and are complicated by the diverse effects of this complex agent. It has been shown to release catecholamine...

High sensitive troponin T (hsTnT) is a highly specific marker of myocardial injury and one of the keystones in the diagnosis of acute coronary syndrome. Although hsTnT is thought to be released by myocardial cell damage, recent studies reported elevated levels after exercise testing and endurance sports. The exact mechanism of this phenomenon is discussed controversially. CMR stress testing is widely used for detection of myocardial ischemia. The kinetic of troponin release after CMR stress testing has not been studied previously.