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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Pathophysiology of Heart Failure: Role of Oxygen Free Radicalsin chronic volume overload heart failure might be due to an increased level of OFRs and/or decrease in the antioxidant status. We, therefore, studied the effects of chronic volume overload in the absence and presence of vitamin E (antioxidant) on cardiac function and contractility, cardiac malondial

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Therapeutics in Congestive Heart Failure: From Hemodynamics to Neurohormonespheral perfusion, sodium retention, increased ventricular afterload, and progressively deteriorating left ventricular pumping capacity. In new or decompensated heart failure, this hemodynamic paradigm predicts acute clinical improvement. Chronically, however, treatment based fundamentally on inotrop

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Dilated Cardiomyopathies and Congestive Heart Failurestinguished: dilated, hypertrophic, restrictive, right ventricular, and non-classifiable cardiomyopathies with distinct hemodynamic properties. The new WHO/WHF definition also comprises inflammatory cardiomyopathy, defined as myocarditis in association with cardiac dysfunction. Idiopathic, autoimmun

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The Failing SHHF Rat Hearted to the SHR (spontaneously hypertensive rat), but unlike the SHR, all animals, male and female, develop fatal congestive heart failure, most in the second year of life. SHHF rats are now being widely used by the pharmaceutical industry to evaluate potential therapeutic agents for preventing the ma

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Sarcoplasmic Reticulum Gene Expression of Ca2+-Cycling Proteins as a Target for the Treatment of Heatrin (CQS) are known to determine the function of cardiac sarcoplasmic reticulum (SR). Protein kinase A is known to phosphoryate PLB and RyR whereas Ca./calmodulin kinase phosphorylates PLB, SERCA2a and RyR and thus these regulatory proteins have been shown to alter the activities of SR Ca.-cycling

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