Pathophysiology of Heart Failure brings together leading basic scientists and clinicians, presenting new approaches to this complex problem, involving cardiomyopathic processes and ischemia perfusion injury. The result is a synthesis of state-of-the-art information on molecular biology, cellular physiology and structure-function relationships in the cardiovascular system. The role which excess intracellular calcium plays in the genesis of cardiac dysfunction is described as a fundamental mechanism underlying heart failure; one which may lead to improved prevention and treatment. Audience: Clinical and experimental cardiologists will find the book a helpful source of ideas and inspiration.

Inhalt

I. Cardiomyopathy and Contractile Dysfunction.- 1. Experimental models of heart failure and cardiomyopathy.- 2. Role of tissue and circulating substance P in cardiovascular injury associated with Mg-deficiency.- 3. Functional and metabolic effects of norepinephrine on the rat heart.- 4. Interventions in experimentally induced diabetic cardiomyopathy.- 5. Diabetes as a risk factor for cardiovascular disease: Experimental models.- 6. Ethanol-induced hypertension: the role of Acetaldehyde.- 7. Abnormalities in cardiac contractile proteins and cardiac dysfunction.- 8. Role of the slow sodium channel in hereditary cardiomyopathy.- 9. Cardiac contractile failure caused by disturbances in myofibrillar energy supply and pathogenesis of cardiomyopathies.- 10. Changes in contractile proteins under oxidative stress.- 11. Antioxidants and the heart.- 12. Gene expression of cardiac myocytes: a pharmacologic target for the failing heart?.- II. Calcium-Related Events and Heart Dysfunction.- 13. Regulation of slow Ca2+ channels of myocardial cells by cyclic nucleotides and phosphorylation.- 14. Multiple roles for the membrane-associated Ca2+/calmodulin-dependent protein kinase in the regulation of sarcoplasmic reticulum function in heart muscle.- 15. Calreticulin, a multifunctional Ca2+ binding protein of smooth muscle sarcoplasmic reticulum membranes.- 16. Intracellular Ca2+ transients in response to step length changes in aequorin-injected ferret papillary muscles.- 17. Initial changes in ?-adrenergic receptor function during development of rapid ventricular pacing-induced heart failure.- 18. Impaired cellular signaling of the adenylyl cyclase and the phosphoinositide pathway in septic cardiomyopathy.- 19. Defective G-protein expression and adenylyl cyclase in genetic and experimental hypertension.- 20. Electrophysiological studies of wild-type and mutant Na+-Ca2+ exchange proteins.- 21. Cardiac sarcolemmal Na+/H+ exchange after a myocardial infarction in the rat.- 22. Myocardial Na, K-ATPase concentration and heart failure.- 23. The cytosolic calcium-force relation of vascular smooth muscle during the contraction and the relaxation.- III. Ischemia and Cellular Interactions.- 24. Ventricular remodeling following coronary artery constriction and hypertension.- 25. Collagenous proteins in scar tissue subsequent to myocardial infarction.- 26. Structural remodeling and functional changes in chronic hypoxia-induced right ventricular hypertrophy.- 27. Mechanism of openings and role of the ATP-sensitive K+ channels during myocardial ischemia/reperfusion.- 28. The contribution of K+ currents to electrical heterogeneity across the canine ventricular wall under normal and ischemic conditions.- 29. Diabetic state reduces ischemic K+ loss and H+ efflux in isolated rat hearts.- 30. Divergent effects of receptor- and nonreceptor-mediated activators of sodium-hydrogen exchange on reperfusion-induced contractile dysfunction.- 31. Heart cells in culture for studying anoxia and "simulated ischemia" at the cellular level.- 32. Cardioprotection and basic fibroblast growth factor.- 33. The heart and nitric oxide.- 34. The endothelium and the regulation of coronary blood flow.- 35. Signal transduction in vascular smooth muscle: synergistic interactions between receptors and transduction pathways.- 36. Modulation of peak aerobic capacity by the peripheral circulation during the course of the syndrome of congestive heart failure.