Titlebook: Cardiac Remodeling and Failure; Pawan K. Singal (Professor),Ian M. C. Dixon (Assoc Book 2003 Springer Science+Business Media New York 2003

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https://doi.org/10.1007/978-94-009-9260-3y discussed. In isolated muscle strips from end-stage failing human hearts, we have recently demonstrated an inverse correlation of Na.?Ca. exchanger expression with the occurrence of diastolic dysfunction. Moreover, it has been hypothesized that different phenotypes of failing human hearts with res

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https://doi.org/10.1007/978-94-009-9260-3A- as well as the protein levels of the sarcoplasmic reticulum (SR) Ca. ATPase (encoded by SERCA2 gene) are reduced in hypertrophied and failing myocardium. On the other hand, investigations on phospholamban (PLB) knock-out and phospholamban transgenic mice have proven that the expression ratio of P

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Normen als Grund bilateraler Au?enpolitikpies that arrest or reverse structural abnormalities produce the most striking improvements in patient outcome. Cardiac myocytes comprise about 75% of the heart mass and provide mechanical force for contraction. Consequently, structural changes in these cells are likely to play a key role in heart f

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Normen als Grund bilateraler Au?enpolitiko investigate at what level these vascular changes can be recognized, a comparison study of vessel continuity using 3-dimensional reconstruction was performed. The eighteen hearts of acute, chronic myocarditis, and control obtained at autopsy were examined to detect the differences of the microvascu

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Walter Winkler,Paul Schwarzenbergercise, exacerbation of hemodynamic abnormalities, neurohumoral activation and perturbed NO bioavailability could exhaust coronary flow reserve and thereby impair myocardial O. supply. We tested this hypothesis in swine with a 2–3 week old myocardial infarction (MI) and determined whether a loss of NO

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